Vestibular Rehabilitation, Dizziness, Balance, and Associated Issues in Physical TherapyIndependent Study Course 17.3.3

Cervicogenic Dizziness and Differential Diagnosis of Dizziness in the OrthopaedicPhysical Therapy Setting

An Independent Study Course Designed for Individual Continuing Education

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, MTC, CSCS, FAAOMPT, FCAMTUniversity of St Augustine for Health SciencesSt Augustine, Florida The Journal of Manual and Manipulative TherapyForest Grove, Oregon Shelbourne Physiotherapy ClinicVictoria, British ColumbiaDynamic Physical TherapyCadillac, Michigan

Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPTMercy Rehab AssociatesDarby, PennsylvaniaSpecialized Physical Therapy, LLCCherry Hill, New JerseyUniversity of St Augustine for Health SciencesSt Augustine, FloridaUniversity of the Sciences in PhiladelphiaPhiladelphia, Pennsylvania

Dear Colleague,

I am pleased to welcome you to Cervicogenic Dizziness and Differential Diagnosis of Dizziness in the Orthopaedic Physical Therapy Setting, authored by Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, MTC, CSCS, FAAOMPT, FCAMT, and Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPT, as part of the Independent Study Course entitled Vestibular Rehabilitation, Dizziness, Balance, and Associated Issues in Physical Therapy.

Dr Peter A. Huijbregts received a diploma in physiotherapy from the Hogeschool Eindhoven in 1990, an MSc degree in manual therapy from the Vrije Universiteit Brussel in 1994, an MHSc degree in physical therapy from the University of Indianapolis in 1997, and a DPT degree in 2001 from the University of St Augustine for Health Sciences in St Augustine, Florida. He is currently clinically employed as a consultant physiotherapist at Shelbourne Physiotherapy Clinic in Victoria, British Columbia, and is assistant professor of online education at the University of St Augustine for Health Sciences. He is also Editor-in-Chief of The Journal of Manual and Manipulative Therapy and serves as a manuscript reviewer for Physiotherapy Canada. He is a member of the scientific board of the Rehabilitacja Medyczna Journal and also serves as a consulting editor for Jones and Bartlett Publishers in Sudbury, Massachusetts. He has been a previous author of many other independent study course monographs for the Orthopaedic Section.

Dr Paul G. Vidal received his MPT degree from Philadelphia College of Pharmacy and Science and his DPT degree from the University of St Augustine for Health Sciences. His areas of expertise include orthopaedics, manual physical therapy, and vestibular rehabilitation. He is owner of Specialized Physical Therapy, LLC, in Cherry Hill, New Jersey, and also is employed at Mercy Rehab Associates, in Darby, Pennsylvania. He has been a frequent presenter at national conferences on the topic of physical therapy management of cervicogenic dizziness. He has also published in the peer-reviewed publications Journal of Orthopaedic and Sports Physical Therapy and Journal of Manual and Manipulative Therapy.

The authors present a thorough review of the physiology and etiology of cervicogenic dizziness and other pathologies potentially causing dizziness and present an evaluation scheme that applies a 4-category diagnostic classification system and leads to the management of cervicogenic dizziness and other types of dizziness amenable to physical therapy management. The classification system facilitates proper diagnosis and helps the clinician distinguish between those patients who can benefit from physical therapy intervention and those who require medical-surgical referral.

The authors also discuss performance, scoring, and interpretation of tests and measures used in evaluating dizziness. Vertigo, presyncope, and dysequilibrium are specifically defined according to the structures affected and the presentation of the patient’s symptoms.

After reviewing the monograph, I am sure you will find the information practical and readily applicable to effectively evaluating and treating your patients who present with dizziness as a symptom.

Sincerely,

Christopher Hughes PT, PhD, OCS, CSCSEditor

Vestibular Rehabilitation, Dizziness, Balance, and Associated Issues in Physical TherapyChristopher Hughes, PT, PhD, OCS—Editor

2920 East Avenue South, Suite 200 | La Crosse, WI 54601Office 608-788-3982 | Toll Free 800-444-3982 | Fax 608-788-3965

TABLE OF CONTENTS

LEARNING OBJECTIVES ..................................................................................................................................................1

CERVICOGENIC DIZZINESS ...........................................................................................................................................1

Dizziness Originating in the Cervical Spine ............................................................................................................1

Cervicogenic Dizziness...........................................................................................................................................2

Diagnostic Criteria and Differential Diagnosis.........................................................................................................2

Physical Therapy Management of Cervicogenic Dizziness .......................................................................................3

DIAGNOSTIC CLASSIFICATION SYSTEM ........................................................................................................................4

Vertigo ....................................................................................................................................................................4

Presyncope .............................................................................................................................................................4

Dysequilibrium .......................................................................................................................................................4

Other Dizziness ......................................................................................................................................................5

Challenges to the Diagnostic Classification System .................................................................................................5

VERTIGO ........................................................................................................................................................................5

Peripheral Vestibular Disorders ...............................................................................................................................5

Benign paroxysmal positional vertigo ...............................................................................................................5

Ménière disease ...............................................................................................................................................6

Acute peripheral vestibulopathy .......................................................................................................................6

Otosclerosis .....................................................................................................................................................6

Head trauma ....................................................................................................................................................7

Cerebellopontine angle tumor ..........................................................................................................................7

Toxic vestibulopathies ......................................................................................................................................7

Acoustic neuropathy .........................................................................................................................................7

Perilymphatic fistula .........................................................................................................................................7

Autoimmune disease of the inner ear................................................................................................................7

Central Vestibular Disorders ....................................................................................................................................7

Drug intoxication .............................................................................................................................................7

Wernicke encephalopathy ................................................................................................................................8

Inflammatory disorders .....................................................................................................................................8

Multiple sclerosis .............................................................................................................................................8

Alcoholic cerebellar degeneration ....................................................................................................................8

Phenytoin-induced cerebellar degeneration ......................................................................................................9

Hypothyroidism ................................................................................................................................................9

Paraneoplastic cerebellar degeneration .............................................................................................................9

Hereditary spinocerebellar degenerations .........................................................................................................9

Ataxia-telangiectasia ........................................................................................................................................9

Wilson disease .................................................................................................................................................9

Creutzfeldt-Jakob disease .................................................................................................................................9

Posterior fossa tumors .......................................................................................................................................9

Posterior fossa malformations ...........................................................................................................................9

Familial paroxysmal ataxia .............................................................................................................................10

PRESYNCOPE ................................................................................................................................................................10

Pancerebral Hypoperfusion ...................................................................................................................................10

Vasovagal presyncope ....................................................................................................................................10

Cardiovascular presyncope .............................................................................................................................10

Migraine .........................................................................................................................................................10

Benign paroxysmal vertigo of childhood .........................................................................................................11

Takayasu disease ............................................................................................................................................11

Carotid sinus syndrome ..................................................................................................................................11

Orthostatic hypotension .................................................................................................................................11

Hyperventilation ............................................................................................................................................11

Cough-related syncope ...................................................................................................................................11

Micturition syncope .......................................................................................................................................11

Glossopharyngeal neuralgia ...........................................................................................................................12

Hypoglycemia ................................................................................................................................................12

Brainstem Hypoperfusion ......................................................................................................................................12

Vertebrobasilar insufficiency...........................................................................................................................12

Vertebrobasilar infarction ...............................................................................................................................13

Basilar-type migraine ......................................................................................................................................14

Vertebrobasilar migraine ................................................................................................................................14

Vestibular migraine ........................................................................................................................................14

Subclavian steal syndrome .............................................................................................................................14

DYSEQUILIBRIUM ........................................................................................................................................................14

Visual Impairment.................................................................................................................................................15

Somatosensory Impairment ...................................................................................................................................15

Myelopathy ....................................................................................................................................................15

Landsickness and mal de debarquement syndrome ........................................................................................15

Musculoskeletal Impairment .................................................................................................................................16

Basal Ganglia Impairment .....................................................................................................................................16

OTHER DIZZINESS .......................................................................................................................................................16

Psychogenic Dizziness ..........................................................................................................................................16

Panic disorder .................................................................................................................................................16

Phobic postural vertigo ...................................................................................................................................16

Tilting of the Environment .....................................................................................................................................17

PHYSICAL THERAPY VERSUS MEDICAL DIFFERENTIAL DIAGNOSIS ...........................................................................17

HISTORY .......................................................................................................................................................................19

Symptoms .............................................................................................................................................................20

Symptom description ......................................................................................................................................20

Symptom behavior .........................................................................................................................................28

Pertinent Past and Present Medical History ............................................................................................................29

Patient demographics .....................................................................................................................................29

Medical history ..............................................................................................................................................29

Family history .................................................................................................................................................30

Medication history .........................................................................................................................................30

PHYSICAL EXAMINATION ............................................................................................................................................30

Observation ..........................................................................................................................................................30

Skin ................................................................................................................................................................30

Posture ...........................................................................................................................................................31

Eyes ................................................................................................................................................................31

Vital Signs .............................................................................................................................................................32

Blood pressure ...............................................................................................................................................32

Heart rate .......................................................................................................................................................32

Auscultation ...................................................................................................................................................32

Gait Assessment ....................................................................................................................................................32

Vestibulospinal Examination .................................................................................................................................33

Single-leg stance ............................................................................................................................................33

Romberg and sharpened Romberg ..................................................................................................................33

Modified Clinical Test of Sensory Integration of Balance .................................................................................33

Fukuda step test ..............................................................................................................................................34

Cranial Nerve Examination ...................................................................................................................................34

Oculomotor Examination ......................................................................................................................................34

Observation for spontaneous nystagmus .........................................................................................................35

Saccadic eye movements ................................................................................................................................35

Smooth pursuit testing ....................................................................................................................................35

Hearing Examination ............................................................................................................................................36

Weber test ......................................................................................................................................................36

Rinne test .......................................................................................................................................................36

Active Range-of-motion Tests ................................................................................................................................36

Limb Ataxia Tests ..................................................................................................................................................36

Passive Range-of-motion Tests ...............................................................................................................................37

Strength Tests ........................................................................................................................................................37

Reflex Tests ...........................................................................................................................................................38

Sensation Tests ......................................................................................................................................................38

Vertebrobasilar Insufficiency Tests .........................................................................................................................38

De Kleyn-Nieuwenhuyse test .........................................................................................................................38

Sustained cervical rotation test .......................................................................................................................39

Hautant test ....................................................................................................................................................39

Vestibulo-ocular Tests ............................................................................................................................................39

Dynamic visual acuity ....................................................................................................................................39

Autorotation test .............................................................................................................................................40

Doll’s head test ...............................................................................................................................................40

Head-shaking nystagmus test ..........................................................................................................................40

Head-thrust test ..............................................................................................................................................40

Benign Paroxysmal Positional Vertigo Tests ............................................................................................................40

Opinions expressed by the authors are their own and do not necessarily reflect the views of the Orthopaedic Section.

The publishers have made every effort to trace the copyright holders for borrowed material.If we have inadvertently overlooked any, we would be willing to correct the situation at the first opportunity.

© 2007, Orthopaedic Section, APTA, Inc.

Course content is not intended for use by participants outside the scope of their license or regulations. Subsequent use of management is physical therapy only when performed by a PT or a PTA in accordance with Association policies, posi-

tions, guidelines, standards, and ethical principals and standards.

Hallpike-Dix maneuver ..................................................................................................................................40

Straight head-hanging test ..............................................................................................................................41

Roll test ..........................................................................................................................................................41

Walk-rotate-walk test ......................................................................................................................................41

Cervicogenic Dizziness Testing .............................................................................................................................41

Breathing-related Tests ..........................................................................................................................................42

Hyperventilation test ......................................................................................................................................42

Valsalva test....................................................................................................................................................42

HISTORY AND PHYSICAL EXAMINATION ...................................................................................................................42

CASE STUDIES ..............................................................................................................................................................42

Case Study 1 .........................................................................................................................................................42

Subjective information ....................................................................................................................................42

Objective findings ..........................................................................................................................................43

Physical therapy diagnosis ..............................................................................................................................43

Guide to Physical Therapist Practice diagnosis ................................................................................................44

Physical therapy management and outcomes..................................................................................................44

Case Study 2 .........................................................................................................................................................44

Subjective information ....................................................................................................................................44

Objective findings ..........................................................................................................................................45

Physical therapy diagnosis ..............................................................................................................................45

Guide to Physical Therapist Practice diagnosis ................................................................................................46

Physical therapy management and outcomes..................................................................................................46

ACKNOWLEDGEMENTS ...............................................................................................................................................47

REFERENCES .................................................................................................................................................................47

REVIEW QUESTIONS ....................................................................................................................................................56

1

Cervicogenic Dizziness and Differential Diagnosis of Dizziness in the Orthopaedic Physical Therapy Setting

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, MTC, CSCS, FAAOMPT, FCAMTUniversity of St Augustine for Health SciencesSt Augustine, Fla

The Journal of Manual and Manipulative TherapyForest Grove, Ore

Shelbourne Physiotherapy ClinicVictoria, British Columbia

Dynamic Physical TherapyCadillac, Mich

Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPTMercy Rehab AssociatesDarby, Pa

Specialized Physical Therapy, LLCCherry Hill, NJ

University of St Augustine for Health SciencesSt Augustine, Fla

University of the Sciences in PhiladelphiaPhiladelphia, Pa

LEARNING OBJECTIVESUpon completion of this monograph, the course par-

ticipant will be able to discuss:1. The underlying pathophysiology, diagnostic criteria,

and physical therapy management of cervicogenic dizziness.

2. A 4-category diagnostic classification system for the differential diagnosis of patients complaining of dizzi-ness.

3. Pathologies organized to conform to this diagnostic classification system potentially responsible for a pa-tient report of dizziness.

4. The performance, scoring, and interpretation of tests and measures used in the history and physical exami-nation of patients complaining of dizziness.

5. The characteristics of patients that may respond to conservative interventions within the physical therapy scope of practice versus patients that require medical-surgical referral for medical differential diagnosis and medical-surgical management.

CERVICOGENIC DIZZINESSDizziness Originating in the Cervical Spine

Multiple different dysfunctions or diseases of the cervical spine can result in a patient report of dizziness. Three pathophysiologic mechanisms have been proposed for dizziness originating in the cervical spine1-3:1. Ischemic processes affecting the vertebrobasilar sys-

tem.2. Vasomotor changes caused by irritation of the cervical

sympathetic nervous system.

3. Altered proprioceptive input from the upper cervical region.Mechanical compression, tension, dissection, or steno-

sis of one or both vertebral arteries as they course through the cervical spine will cause decreased vertebrobasilar blood flow and may cause hindbrain and brainstem isch-emia resulting in dizziness. Faulty head and neck posture, congenital cervical deformities, cervical thrust manipula-tion, and traumatic or degenerative instabilities are among the causes that have been implicated for the mechanical compromise leading to vertebrobasilar ischemia.1,2,4-6 The previous monograph has discussed vertebral artery compromise in detail.

The cervical sympathetic ganglia are located along-side the blood vessels and muscles anterolateral to the vertebral bodies. The superior cervical ganglion, located at the level of C2-C3, is the largest of the cervical sympa-thetic ganglia. It is formed by coalescence of the cranial 4 sympathetic ganglia.7 Upper cervical dysfunction has been hypothesized to negatively impact this ganglion.1,2 This might affect the sympathetic innervations of both the vertebral and internal carotid arteries with subsequent hypoperfusion of the brain resulting in a report of dizzi-ness.7,8 However, Bogduk et al9 noted no effect of electri-cal stimulation of the cervical sympathetic trunk and the vertebral nerve on vertebral artery blood flow in monkeys. Likewise, Brandt and Bronstein10 discounted this proposed pathophysiologic mechanism and reported that there is no scientific support for this proposed cervical sympathetic irritation in the etiology of cervicogenic dizziness.

There are extensive efferent and afferent connections between especially the upper cervical spine and other structures involved in balance control.11 The vestibulocer-vical reflex counteracts angular rotation of the head by reflexively producing opposite head and neck rotation.12 The hair cells in the semicircular canals (SCCs) provide afferent information for the vestibulocervical reflex to the neck and proximal trunk muscles.12 The otolithic maculae may also contribute to this vestibulocervical reflex by supplying afferent information to the sternocleidomastoid muscle.13 The upper cervical spine contains a great den-sity of muscle and joint mechanoreceptors with a role in postural control.14,15 Muscle spindle density is especially high in the deep, short intervertebral neck muscles.10 Af-ferent input from these mechanoreceptors into the central vestibular system and integration with vestibular (and visual) afferent information allows for a true perception of head and trunk position in space.10 Abnormal stimu-lation of these proprioceptors due to cervical whiplash trauma, spondylosis, disk herniations, and head trauma has been hypothesized to lead to a sensory mismatch at the level of the central vestibular apparatus of the cervi-cal proprioceptive with the vestibular and visual input.6 Ryan and Cope16 also implicated iatrogenic injury in the form of cervical traction. Muscle spasms and active trig-ger points in the neck muscles, specifically in the sterno-cleidomastoid muscles, have also been suggested in the etiology of proprioceptive cervicogenic dizziness.9,11,17

2

The sensory mismatch discussed above may result in a conscious awareness of balance and thereby a feeling of dysequilibrium.6 It is this proprioceptive cervicogenic dizziness, defined by Furman and Cass18 as a nonspecific sensation of altered orientation in space and dysequilib-rium originating from abnormal afferent activity from the neck, that is the topic of this monograph.

Cervicogenic DizzinessThe rationale for implicating aberrant information from

cervical mechanoreceptors in the etiology of cervicogenic dizziness is based on the anatomical connections between the cervical spine and the balance control systems, on studies on experimentally induced cervicogenic dizzi-ness, and on proposed clinical evidence.10 We described above the anatomical connections and their possible etiologic role in producing cervicogenic dizziness.

There is also research evidence linking the upper cervical region to a patient report of dizziness. Injection of a local anesthetic agent in the upper cervical spine of humans created a strong sensation of imbalance and of being pulled to the same side as the injection, as well as a postinjection gait ataxia.19 Similar experiments have produced transient increased ipsilateral and decreased contralateral extensor muscle tone, a tendency to fall, gait deviation, and past pointing toward the injected side.10 Application of a unilateral electrical or vibratory stimulus to neck muscles resulted in a modification of the visual vertical orientation as perceived by the test subjects.10

These experiments would seem to support a role for aber-rant afferent proprioceptive cervical information in the etiology of cervicogenic dizziness.

There is also some clinical support for this proposed proprioceptive cervicogenic dizziness. Dizziness, vertigo, and dysequilibrium are symptoms in 20% to 58% of indi-viduals that have sustained a whiplash-type injury of the cervical spine or a closed head injury.17 Between 40% and 70% of patients with chronic whiplash-associated disorder (WAD) complain of dizziness and unsteadiness often resulting in loss of balance and falls.20 Treleaven et al20 reported significantly greater cervical joint reposi-tioning errors in subjects with WAD when compared to asymptomatic controls. These authors also found a signifi-cantly greater joint repositioning errors in right rotation (P = 0.006) and a near-significant difference in left rota-tion (P = 0.06) when comparing subjects with WAD and complaints of dizziness to those not reporting dizziness. They implicated cervical mechanoreceptor dysfunction as the likely cause for cervicogenic dizziness. Heikkilä and Wenngren21 also reported significantly greater cervical joint repositioning errors in patients with WAD as com-pared to healthy controls. They also found significantly greater cervical joint repositioning errors in patients with WAD and dizziness as compared to those patients with WAD who did not report dizziness. They also noted a significant correlation between joint repositioning errors and abnormalities in smooth pursuit and saccadic eye movements, and suggested that restricted cervical range

of motion and altered proprioceptive afferent input might affect oculomotor function. Abnormal visual as well as proprioceptive input would seem to have an even greater potential to produce a sensory mismatch, as discussed above, and subsequent complaints of dizziness. Ernst et al22 reported dizziness, tinnitus, and hearing loss in pa-tients with neck and closed head injury. Information on the prevalence of dizziness in patients with other types of neck dysfunction is limited to case reports.17

However, we have to question the value of these clinical findings in linking dizziness after neck trauma to cervical proprioceptive dysfunction. Head trauma and whiplash injury can, of course, also affect structures other than the cervical spine including the brain, the brainstem and the cranial nerve nuclei located there, and the peripheral vestibular apparatus.10,22 In their case series of patients with dizziness after neck and closed head injury, Ernst et al22 reported both peripheral and central vestibular dysfunction. Grimm23 described either a damaged peripheral labyrinth or cochlea in 90% and both in 69% of a cohort of 227 patients with whiplash presenting for a neurology evaluation. Of these patients, 92% met the diagnostic criteria for inner ear contusion. Of this subgroup, 63% were diagnosed with benign paroxysmal positional vertigo (BPPV), 64% with second-ary endolymphatic hydrops, and 21% with unilateral or bilateral perilymphatic fistulae. Oostendorp et al24 reported a 25% prevalence of BPPV in 273 consecutive patients with rear-end impact whiplash injury without head injury. Cervical joint repositioning errors as tested by Treleaven et al20 and Heikkilä et al21 might, of course, also have been affected by injuries to structures other than the cervical mechanoreceptors. Other studies have reported abnormalities in saccadic and smooth pursuit eye movements in patients with chronic WAD but have either linked these oculomotor abnormalities to prefron-tal cortical dysfunction25 or have found no relationship with cervical positioning, making a proprioceptive origin for these oculomotor abnormalities less likely.26

Diagnostic Criteria and Differential DiagnosisThere is no gold standard test for cervicogenic dizzi-

ness, making it a diagnosis of exclusion.6 As discussed above, a clinician might suspect cervicogenic dizziness if the patient history includes a report of cervical whiplash trauma, spondylosis, disk herniations, head trauma, or cervical traction treatment.

Signs and symptoms proposed as indicative of cervi-cogenic dizziness include1,3,10,17:• Cervical region pain or discomfort, especially follow-

ing trauma• Dizziness described as lightheadedness or floating

unsteadiness• Dizziness provoked by certain head positions or

movements• Dizziness of short duration and decreasing intensity• Persistent occipital headache• Limited cervical range of motion

3

• Temporomandibular pain• Radicular symptoms in the arm• Episodic or persistent slight ataxia of stance and gait• Hearing loss associated with neck pain• Earache

Although seemingly the most relevant, dizziness provoked by certain head positions or movements has only limited value as a diagnostic criterion specific for cervicogenic dizziness. The cervical spine contains structures providing afferent input to the balance control system (cervical joint and muscle mechanoreceptors) but also structures that are part of the output portion of this system (spinal cord, nerve roots, and muscles). The neck also has structures relevant to cardiovascular control (carotid barosensors) and vascular structures (carotid and vertebral arteries). In addition, neck movements invari-ably produce head movements, thereby involving the vestibular and visual systems.10

The clinician should also consider that dizziness has a high prevalence. Dizziness accounts for 7% of physician visits for patients over the age of 45;27 for adults over 65, it is the number one reason to visit a physician.28 Diz-ziness is more common in women than in men,29 and the prevalence of dizziness increases with increasing age.30 However, only some of the 15% to 30% of people experiencing dizziness will seek medical attention.30 The complaint of dizziness that brought the patient to seek treatment after a recent trauma or other etiology linked to cervicogenic dizziness may have been, at least to some extent, preexisting but not previously reported and related to another pathology capable of causing dizziness.

To further complicate matters, patients reporting diz-ziness may mean lightheadedness, blurry vision, loss of balance, or a feeling of weakness in the legs. Dizziness is also used for various sensations of body orientation and position that are often difficult for patients to describe.31

In summary, there are no history items or physical ex-amination tests and measures specific for the diagnosis of cervicogenic dizziness. Neck movements have an effect not only on cervical joint and muscle systems but also on the vestibular, visual, vascular, and cardiovascular systems.10 Dizziness is highly prevalent among the gen-eral population and may be, to some extent, a preexist-ing complaint that, therefore, may have a multifactorial etiology that needs to be explored during the differential diagnostic process. Finally, most patients have great dif-ficulty expressing their problem in terms helpful to the clinician’s effort at differential diagnosis. This indicates the need for a comprehensive differential diagnostic process for every patient presenting with a complaint of dizziness.

Physical Therapy Management of Cervicogenic Dizziness

Historically, physical therapy interventions for patients with cervicogenic dizziness have included thrust and nonthrust manipulation, mechanical traction, physical modalities, posture reeducation, active range-of-motion

(AROM) exercises, massage, balance retraining, trig-ger point treatment, and the use of a soft collar during the acute phase.17 However, perhaps as a result of the absence of specific diagnostic criteria for cervicogenic dizziness, the research on the physical therapy manage-ment is limited.

Karlberg et al32 reported on 17 patients with suspected cervicogenic dizziness. Noncervical causes of dizziness had been excluded in all patients. Patients were random-ized into 2 groups: immediate and delayed (2 months) treatment. Outcome measures included body sway mea-sured by way of posturography, neck pain and dizziness intensity, and dizziness frequency. There were no pretest between-group differences and all patients demonstrated significantly poorer postural control as compared to a healthy population (P < 0.05). Treatment consisted of soft tissue and joint manipulation, cervical spine stabilization exercises, relaxation techniques, home exercises, and ergonomic changes at work. Treatment significantly im-proved postural performance (P < 0.05) and significantly reduced neck pain intensity and dizziness intensity and frequency (P < 0.01).

Galm et al33 reported on 50 patients with cervicogenic dizziness. The diagnosis was established by exclusion of otorhinolaryngologic and otoneurologic pathology. Of these patients, 31 had cervical segmental restrictions and were treated with manipulation and unspecified physi-cal therapy; 19 patients had no evidence of segmental dysfunction and received only physical therapy. A signifi-cantly greater number of the patients in the manipulation group reported improvement in dizziness symptoms (P = 0.0005).

Bracher et al34 reported on 15 patients with cervico-genic dizziness. A negative otorhinolaryngologic and otoneurologic medical examination, the presence of a rotary cervical nystagmus, and the presence of signs and symptoms suggestive of cervical dysfunction were used to establish the diagnosis. Treatment consisted of soft tis-sue and joint manipulation, electrical modalities for pain control, labyrinth-sedating medication, biofeedback, and upper quadrant range-of-motion exercises. After a mean number of 5 visits (range 3 to 10) over a median of 41 days (range 15 to 77 days), 9 patients reported complete resolution, 3 reported consistent improvement, and 3 reported no change.

Reid and Rivett35 performed a systematic review of the literature on the outcomes with manual therapy treatment of patients with cervicogenic dizziness. They identified 1 randomized clinical trial and 8 nonrandomized clinical trial studies including the 3 studies above. They noted that all studies of manual therapy intervention in patients complaining of cervicogenic dizziness resulted in signifi-cant posttreatment improvements in signs and symptoms of dizziness. However, they also noted that all studies reviewed were of low methodological quality.

Exercises to strengthen the upper cervical deep flexor muscles may be indicated for the treatment of patients with cervicogenic headache.36-38 Jull et al37 demon-

4

strated consistently poor endurance of these muscles in patients with cervicogenic headache. In these patients, this decreased deep flexor muscular endurance was often associated with increased upper trapezius, leva-tor scapulae, and scalenes recruitment.37,38 Jull39 also showed this decreased activity of the deep neck flexors and increased activity in more global neck flexors such as the sternocleidomastoid in patients with WAD. A study comparing various combinations of orthopaedic manual physical therapy and an exercise program consisting of deep cervical flexor endurance training, scapular retrac-tion exercises, postural education, and low-load cervical flexion and extension resistive exercises in 200 patients with cervicogenic headache showed that the 3 active treatments (orthopaedic manual physical therapy, exer-cise therapy, and orthopaedic manual physical therapy combined with exercise) reduced headache frequency and intensity more than the control therapy immediately

after intervention and after 12 months.36 The combined treatment showed clinically but not statistically relevant increased effect sizes over the other 2 treatment groups at 12 months.

The research above36-39 involved patients with cervico-genic headache. However, deep cervical flexor exercises may also be indicated for patients with cervicogenic dizziness. Hypertonicity of the sternocleidomastoid and upper trapezius muscles has been implicated in the etiol-ogy of cervicogenic dizziness.6,17 By way of reciprocal inhibition, deep cervical flexor exercises may play a role in decreasing this global neck flexor and suboc-cipital muscle hypertonicity. In addition, these exercises involve voluntary contraction and holding of the deep neck flexors that are heavily lined with mechanorecep-tors. This may improve mechanoreceptor function and thereby positively affect the complaints of proprioceptive dysfunction hypothesized to be the cause of cervicogenic dizziness. However, it should be noted that, at this time, the appropriateness of cervical spine stabilization exer-cises for patients with cervicogenic dizziness is based solely on a pathophysiologic rationale.

Treatment for cervicogenic dizziness may also need to include kinesthetic exercises for the cervical spine. We discussed the greater cervical joint repositioning errors in subjects with WAD when compared to asymptomatic controls and also in subjects with WAD and complaints of dizziness as compared to those with WAD not reporting dizziness.20 This finding contrasts with the nonsignificant differences found40 between patients with nontraumatic cervical pain and asymptomatic controls, and would seem to indicate the need for a different management for patients with cervicogenic dizziness of traumatic and nontraumatic origin.

Based on a pathophysiologic rationale, the clinician could choose interventions to affect cervical range of motion, upper quadrant muscle length and tone, and posture. One could consider soft tissue and joint manipu-lation, trigger point techniques, exercise interventions, modalities, ergonomic advice and modification, and pa-

tient education. Some authors1,17 have also suggested that a combination of these treatment options with vestibular rehabilitation techniques would provide for a superior outcome. However, it is clear that the research basis for management of patients with cervicogenic dizziness is at present very limited and that the clinician still has to heavily depend upon a pathophysiologic rationale when it comes to treatment of these patients.

DIAGNOSTIC CLASSIFICATION SYSTEMWe explained above the need for a comprehensive

differential diagnosis for every patient presenting with a complaint of dizziness. To enable the clinician to per-form this necessary differential diagnostic process, we need to discuss in detail not only the history and physical examination for a patient presenting with dizziness with an interpretation of the findings on all our tests and mea-sures, but we also need to review in sufficient detail the pathologies that may be responsible for a patient report of dizziness. Dizziness can have an extremely varied etiology. The consistent use of a diagnostic classifica-tion system may serve to minimize confusion regarding a patient’s dizziness symptoms and possible causative pathologies. Patients with complaints of dizziness can be classified into 4 subtypes: vertigo, presyncope, dysequi-librium, and other dizziness.31,41

VertigoVertigo is a false sensation of movement of either the

body or the environment, usually described as spinning, which suggests vestibular system dysfunction.29,30,42,43 It is usually episodic with an abrupt onset and often associ-ated with nausea or vomiting.41 The causative dysfunc-tion can be located in the peripheral or central vestibular system.42,44 Peripheral vestibulopathies account for about 35% to 55% of all cases of dizziness.30 Central vestibular disorders are less frequent and are responsible for only about 5% of cases of dizziness.30

PresyncopePresyncope is described as a sensation of an impend-

ing faint or loss of consciousness and is not associated with an illusion of movement.29,41,43 It may begin with diminished vision or a roaring sensation in the ears.41 This subtype of dizziness results from conditions that compro-mise the brain’s supply of blood, oxygen, or glucose.43 The frequency reported for presyncopal dizziness varied from 2% in a dizziness clinic to 16% in an emergency room.45,46 This type of dizziness may be accompanied by transient neurological signs (eg, dysarthria, visual distur-bances, and extremity weakness).47,48

DysequilibriumDysequilibrium is a sense of imbalance without ver-

tigo that is generally attributed to neuromuscular prob-lems.29 This condition is also characterized by the feeling that a fall is imminent.41 The unsteadiness or imbalance occurs only when erect and disappears when lying or

5

sitting.41 This subtype of dizziness may result from visual impairment, peripheral neuropathy, and musculoskel-etal disturbances, and may include ataxia. Prevalence of dysequilibrium among patients complaining of dizziness varies from 1% to 15%.29

Other DizzinessOther dizziness is dizziness described as a vague

or floating sensation with the patient having difficulty relating the specific feeling to the clinician.29 It includes descriptions of vague lightheadedness, heavy-headed-ness, or wooziness and cannot be classified as any of the 3 previous subtypes.41 Psychiatric disorders are the main cause for this subtype and account for about 10% to 25% of dizziness cases.29,31 Anxiety, depression, and hyperven-tilation are often at the root of this dizziness.29,49 Changes in vision and tilting of the environment are included in the subtype of other dizziness, as is psychogenic or psy-chosomatic dizziness due to panic disorder.29,50

Challenges to the Diagnostic Classification SystemThe classification of dizziness into these 4 subtypes

attempts to differentiate complaints of dizziness by symp-toms and pathophysiology. The clinician should note that this classification system is challenged when an individual complains about more than 1 subtype of dizziness. Diz-ziness may result from disorders in the musculoskeletal, vestibular, cardiovascular, neurological, and metabolic systems as well as from psychiatric disorders.30 The term geriatric syndrome was proposed to describe dizziness in older adults occurring as a result of multisystem impair-ment.51 The problem with this term, however, is that it suggests that dizziness is due to old age. In contrast, re-cent studies have demonstrated that dizziness is prevalent in all adult populations.29,31 The system is also challenged by symptoms of ataxia, a dyscoordination or clumsiness of movement not associated with muscular weakness. Ataxia can be the result of neuromuscular or peripheral proprioceptive disorders, but also of cerebellar and ves-tibular disorders with these latter 2 groups of disorders potentially occurring with or without symptoms of ver-

tigo.43 Using the above classification system, we will now define and discuss pathologies that may be responsible for a patient who reports dizziness.

VERTIGOAs previously noted, vertigo is the misperception of

movement of the body or of the environment.43 Vertigo is often accompanied by other signs and symptoms, includ-ing27,43:• Impulsion (ie, the sensation that the body is being

hurled or pulled in space)• Oscillopsia (ie, the visual illusion of moving back and

forth or up and down)• Nystagmus (ie, the rhythmic oscillation of the eye-

balls)• Gait ataxia (ie, dyscoordinated gait not resulting from

muscle weakness)• Nausea• Vomiting

Together, these symptoms are highly indicative of a peripheral or central vestibular dysfunction as discussed below. Table 1 summarizes the general differential diagnostic criteria for central and peripheral vestibular lesions.

Peripheral Vestibular DisordersBenign paroxysmal positional vertigo

Benign paroxysmal positional vertigo is considered the most common peripheral vestibular disorder.52,53 Annual incidence in the general US population has been estimated at 64 per 100 000. Benign paroxysmal positional vertigo accounts for 17% to 30% of all new patients presenting to vestibular clinics. It is generally seen in people over the age of 40 and is rare in people under 20.53 Idiopathic BPPV has a peak incidence of on-set in the sixth decade of life.54 Nonidiopathic BPPV has been associated with head trauma, insult to the labyrinth, surgical stapedectomy, chronic suppurative otitis media, and degeneration of the inner ear.52,53,55

Two pathophysiological theories have been proposed to explain the etiology of BPPV: cupulolithiasis and

Table 1. Differential Diagnostic Characteristics of Central Versus Peripheral Vertigo*

Central Lesions Peripheral Lesions

Vertigo • Often constant• Less severe

• Often intermittent• Severe

Nystagmus • Sometimes absent• Unidirectional or multidirectional• May be vertical

• Always present• Unidirectional• Never vertical

Hearing Loss or Tinnitus • Rarely present • Often present

Brainstem Signs† • Typically present • Never present

*Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.† Brainstem signs may include motor and sensory deficits, hyperreflexia, positive Babinski sign, dysarthria, and limb ataxia.

6

canalithiasis.53 The theory of cupulolithiasis proposes that sedimentous material, possibly macular otoconia, is released into the endolymphatic fluid in the SCCs. This release of sedimentous material is hypothesized to result from trauma or degenerative changes. When the head is upright, this material will settle on the SCC cupula. Fixed deposits on the cupula increase the density of this struc-ture, making the cupula, which previously had the same density as the surrounding endolymphatic fluid, now sen-sitive to gravity and, therefore, head position. The theory of cupulolithiasis is based on dissection studies in which cupular deposits appear to be relatively common, but a correlation with clinical symptomatology is lacking.53

The canalithiasis theory proposes that BBPV is the result of free-floating endolymphatic densities in the SCCs.53 Changes in head position are hypothesized to produce movement of these particles, creating a current in the SCCs; the resultant hydrodynamic drag could then displace the cupula, stimulating the SCC hair cells. The canalithiasis theory provides a better explanation for the latency of vertigo observed in BPPV than does the cupulolithiasis theory. One could assume that it takes a few seconds for the endolymphatic densities to over-come the inertia of the endolymphatic fluid in the SCC before they are able to create sufficient hydrodynamic drag to move the cupula. Fatigability or habituation of the vertigo response with repeated provocative head move-ment could be explained by dissolution of the clumped endolymphatic material. Free-floating particulate matter has been observed in SCC endolymphatic fluid during surgery.53

Canalithiasis and cupulolithiasis may well represent 2 stages of the same pathological process. All etiological factors for BPPV may result in endolymphatic densities, which may be free floating or adhered to the cupula.53 Infections (eg, acute labyrinthitis and chronic suppura-tive otitis media) result in white blood cells, phagocytes, and endothelial fragments floating in the endolymphatic fluid. Head trauma or stapedectomy may result in red blood cells in the endolymphatic fluid, and age-related degeneration may release cellular debris and macular otoconia.53

The name BPPV implies that this type of vertigo is po-sitional in nature. However, it may be more correct to call BPPV a positioning-type vertigo. In posterior SCC BPPV, vertiginous symptoms occur when a patient transfers quickly into a supine position, especially when the head is turned to the affected side, extending the head on the neck.52 Symptom onset occurs within 1 to 5 seconds upon a change in position.52,53 Symptom duration is brief (30 to 60 seconds); hence, it is a positioning-type vertigo rather than a positional-type vertigo as occurs in vertebrobasilar insufficiency (VBI). A horizontal-rotary nystagmus is the hallmark of BPPV originating in the posterior SCC.52,55 Excitation of neurons innervating the ipsilateral supe-rior oblique muscle and the contralateral inferior rectus muscle is responsible for the horizontal-rotary direction.52 Symptoms of dysequilibrium and nausea may also occur,

with a rare occurrence of vomiting.52,55 Most commonly the posterior SCC is involved in BPPV.52,55 However, BPPV may also involve the horizontal SCC.56 Rolling the head in the plane of the horizontal SCC while in a supine position usually induces the horizontal SCC variant of BPPV. Other provocations include flexion and extension of the head or shifting from supine to upright.56 An accompanying monograph has discussed BPPV in more detail.

Ménière diseaseMénière disease is characterized by paroxysmal ver-

tigo lasting minutes to days accompanied by tinnitus, fluctuating low-frequency hearing loss, and a sensation of fullness in the ear.41,43 Sensorineural hearing loss (a hear-ing loss caused by lesions in the cochlea or the cochlear nerve43) is progressive over multiple episodes, whereas the vertigo tends to become less severe.43 Before the first acute attack, patients frequently note an insidious onset of tinnitus, hearing loss, and the sensation of fullness in the ear.43 Subsequent attacks typically occur suddenly with incapacitating vertigo, roaring unilateral tinnitus, and ipsilateral hearing loss.41 Attacks are often associated with nausea and vomiting.41,43 Age of onset is usually between the ages of 20 and 50, and men are more often affected than women.43 Up to 20% of patients have a family history of Ménière disease.41 During an acute episode, spontane-ous horizontal or rotary nystagmus may be present, which may change direction.43 The underlying cause is thought to be an increase in the volume of the endolymphatic fluid in the membranous labyrinth.43 This endolymphatic hydrops results in excessive amounts of endolymphatic fluid, which displaces the inner ear structures with resul-tant signs and symptoms.41

Acute peripheral vestibulopathySudden onset vertigo, nausea, and vomiting lasting up

to 2 weeks characterize acute peripheral vestibulopathy. This diagnosis includes diagnoses of acute labyrinthitis and vestibular neuronitis. Simon et al43 noted that these 2 diagnoses are based on unverifiable inferences regard-ing pathophysiology and location of disease. Eaton and Roland41 mentioned acute labyrinthitis as a separate diagnosis characterized by acute onset of severe vertigo, nausea, vomiting, and diaphoresis lasting 1 to 5 days with subsequent resolution of complaints over a period of 2 to 3 weeks. A viral origin is likely. Approximately 50% of patients have an associated upper respiratory infection.41 Simon et al43 noted that acute vestibular neuropathy is not accompanied by hearing loss. The disease may be recurrent and some degree of vestibulopathy may be permanent.43 Differential diagnosis from central disorders characterized by acute vertigo is imperative.43

OtosclerosisThe pathophysiology mechanism behind otosclerosis

is immobility of the stapes. The stapes normally transmits sound-induced vibration of the tympanic membrane to the inner ear. Otosclerosis is characterized by conductive

7

hearing loss (a hearing loss resulting from disorders in the external or middle ear),43 but sensorineural hearing loss and vertigo also occur. Vertigo is recurrent and episodic, with or without positional vertigo, but may also be more constant. Nystagmus can be spontaneous or positional. Hearing loss has an age of onset before 30, and a positive family history is common.43

Head traumaWe discussed head trauma in the etiology of BPPV.

Head trauma may result in labyrinthine damage and subsequent vertigo. Undiagnosed skull fractures (petrosal bone) may damage the vestibulocochlear nerve with resultant vertigo and hearing loss. Otorrhea (discharge of cerebrospinal fluid from the ear) may be present.43

Cerebellopontine angle tumorA benign acoustic neuroma, a tumor of the Schwann

cells covering the vestibular portion of the vestibulo-cochlear nerve in the internal auditory canal, and me-ningiomas of the cerebellopontine angle can produce insidious unilateral sensorineural hearing loss.43,57 Ver-tigo, tinnitus, and a sensation of fullness in the ear are less common. Due to their anatomic relationship to the vestibulocochlear nerve, the trigeminal (cranial nerve V) and facial (cranial nerve VII) nerves are often affected. Patients may complain of headache, facial pain, or facial weakness.43 Vertigo develops in 20% to 30% of patients, but a nonspecific unsteadiness is more common.43 Age of onset is usually between 30 and 60. Acoustic neuromas are more common in neurofibromatosis patients. Café-au-lait spots on the skin and axillary or inguinal freckles may be external indicators to suspect neurofibromatosis 1 or Von Recklinghausen disease.43

Toxic vestibulopathiesIngested alcohol differentially distributes between

the cupula and the endolymphatic fluid. It initially dif-fuses preferentially into the cupula, decreasing its density relative to that of the endolymphatic fluid, thus rendering the peripheral vestibular apparatus unusually sensitive to gravity. With time, alcohol also diffuses the endolym-phatic fluid. As blood levels decrease, alcohol leaves the cupula before leaving the endolymphatic fluid again, causing temporary differences in sensitivity to gravity. Al-cohol-induced vertigo, therefore, consists of 2 symptom-atic phases separated by 1 to 2 hours. The whole episode lasts up to 12 hours. Vertigo and nystagmus are evident in the lateral recumbent position and are accentuated when the eyes are closed.43

Aminoglycosides are antibiotics that can cause both vestibular and auditory symptoms.43,57 Streptomycin, gentamicin, and tobramycin are likely to cause vestibular toxicity by destroying hair cells in the membranous laby-rinth. The use of amikacin, kanamycin, and tobramycin is associated with hearing loss. Vertigo, nausea, vomit-ing, and a spontaneous nystagmus may have an acute onset.43

Salicylates (aspirin and derivatives) can damage the vestibular and cochlear end organ resulting in vertigo, tin-nitus, and sensorineural hearing loss. Headache, nausea, vomiting, thirst, hyperventilation, and sometimes confu-sion may all indicate chronic salicylate overdosage.43

Quinine and quinidine can cause tinnitus, hearing loss, vertigo, vision deficits (including disorders of color vision), nausea, vomiting, abdominal pain, hot and flushed skin, and diaphoresis. Fever, encephalopathy, coma, and death can occur in severe cases. Symptoms can be the result of overdosage or may result from a single dose.43

The chemotherapeutic drug Cis-platinum causes oto-toxicity in about 50% of patients, with resultant reversible tinnitus, hearing loss, and vestibular dysfunction.43

Acoustic neuropathyBasilar meningitis from a bacterial, syphilitic, or

tuberculous infection or from sarcoidosis can lead to compression of the vestibulocochlear (acoustic) nerve. Hypothyroidism, diabetes mellitus, and Paget disease can also affect the vestibulocochlear nerve. Vertigo can occur, but hearing loss is more common. Other cranial nerves may also be affected.43

Perilymphatic fistulaA perilymphatic fistula is a rare cause of vertigo. An

opening develops between the middle and inner ear (oval or round window rupture). Head injury, barotrauma due to diving or flying, or a very forceful Valsalva maneuver are thought to induce the fistula.41 With rapid loss of perilym-phatic fluid, severe vertigo and hearing loss may develop. Low-volume leaks may only produce episodic vertigo or dysequilibrium and hearing loss may be absent.41

Autoimmune disease of the inner earThis diagnosis is associated with fluctuating deafness

and recurrent vertigo. Other autoimmune diseases (eg, rheumatoid arthritis, Crohn disease, or polyarteritis) are often concurrently present.57

Central Vestibular DisordersWe discussed above the differences between vertigo

of central and peripheral origin (Table 1). Some central vestibular disorders may occur without vertigo. All cer-ebellar disorders produce gait ataxia, inviting a misdiag-nosis of the dizziness subtype of dysequilibrium (Table 2). Central vestibular disorders can also be the result of ischemic processes. We will discuss vascular causes of central vestibular dysfunction (vertebrobasilar ischemia and infarction) under presyncope.

Drug intoxicationMany drug intoxication syndromes produce global

cerebellar dysfunction. Agents include43,57:• Alcohol• Sedative hypnotics: barbiturates, benzodiazepines,

meprobamate, ethchlorvynol, methaqualone• Anticonvulsants: phenytoin

8

• Hallucinogens: phencyclidine• Street drugs: heroin• Mercuric and organophosphoric compounds

Drug intoxication often also produces a confused state. Alcohol and sedatives tend to produce somnolence, and hallucinogens tend to cause agitation. The importance of taking a good history including medication or drug use is evident.

Wernicke encephalopathyThis acute disorder is comprised of the diagnostic triad

of ataxia, ophthalmoplegia (lateral rectus palsy), and con-fusion. It is caused by thiamine (vitamin B1) deficiency and is common in alcoholics but may also be caused by general malnutrition. Ataxia affects the arm in 10% of patients; the legs are involved in 20%. A horizontal or combined horizontal-vertical nystagmus is classically present.43

Inflammatory disordersViral cerebellar infections can occur in patients with

St Louis encephalitis, AIDS dementia complex, and me-ningoencephalitis associated with varicella, mumps, po-liomyelitis, infectious mononucleosis, and lymphocytic choriomeningitis. Bacterial infection of the cerebellum is rare; only 10% to 20% of brain abscesses are located

in the cerebellum. The cerebellum may be infected by bacteriae in Haemophilus Influenzae meningitis and Legionnaires disease.43 Some diseases are hypothesized to have an autoimmune origin. Acute cerebellar ataxia of childhood usually follows a viral infection or inocula-tion. Acute disseminated encephalomyelitis and a variant of Guillain-Barré syndrome also fall in this category.43

Multiple sclerosisVertigo is rarely the first symptom of multiple scle-

rosis but is common during the course of the disease. It may have an acute onset and can be positional. Gait ataxia is the presenting complaint in 10% to 15% of patients. Nystagmus is also a common sign in multiple sclerosis. A history of remitting and relapsing neurologic dysfunctions affecting multiple sites in the central neu-rologic system may be indicative of multiple sclerosis in undiagnosed patients.43

Alcoholic cerebellar degenerationAlcoholic cerebellar degeneration usually occurs

in patients with a history of 10 or more years of binge drinking. It usually has its onset between the ages of 40 and 60 and is more common in men. The onset is insidious and progression is gradual. As in Wernicke en-cephalopathy, this syndrome affects mainly the superior

Table 2. Signs and Symptoms of Cerebellar Disorders*

Location of Cerebellar Involvement

Signs Diagnoses

Midline • Nystagmus• Head and trunk oscillation (titubation)• Gait ataxia

• Tumor• Multiple sclerosis

Superior vermis • Gait ataxia • Wernicke encephalopathy• Alcoholic cerebellar degeneration• Tumor• Multiple sclerosis

Cerebellar hemisphere • Nystagmus• Ipsilateral gaze paralysis• Dysarthria• Ipsilateral hypotonia• Ipsilateral limb ataxia• Gait ataxia• Falling to the side of the lesion

• Infarction• Hemorrhage• Tumor• Multiple sclerosis

Global cerebellar • Nystagmus• Bilateral gaze paralysis• Dysarthria• Bilateral hypotonia• Bilateral limb ataxia• Gait ataxia

• Drug intoxication• Hypothyroidism• Hereditary cerebellar degeneration• Paraneoplastic cerebellar degeneration• Wilson disease• (Para) infectious encephalomyelitis• Creutzfeldt-Jakob disease• Multiple sclerosis

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

9

cerebellar vermis. Gait ataxia is the most common find-ing; nystagmus is a less frequent finding. Distal sensory deficits in the feet and absent ankle reflexes from diabetic polyneuropathy and signs of malnutrition may clue the clinician in to the diagnosis.43

Phenytoin-induced cerebellar degenerationPhenytoin is an anti-epileptic medication. Long-term

treatment with phenytoin may produce a global cerebel-lar degeneration.43

HypothyroidismHypothyroidism produces a global cerebellar dysfunc-

tion. The cerebellar syndrome associated with hypothy-roidism is usually subacute or chronically progressive in its onset. It is most common in middle-aged or elderly women. Gait ataxia is the prominent finding; nystagmus and dysarthria are less common. Other neurologic disor-ders associated with hypothyroidism include sensorineu-ral hearing loss, carpal tunnel syndrome, neuropathy, and myopathy; these signs and symptoms may raise suspicion of hypothyroidism in undiagnosed patients.43

Paraneoplastic cerebellar degenerationThe pathophysiological mechanism in paraneoplastic

cerebellar degeneration appears to involve antibodies to tumor cell antigens cross-reacting with cerebellar Purkinje cells. Patients with lung cancer, ovarian cancer, Hodgkin disease, and breast cancer are most at risk of developing this type of global cerebellar degeneration. Onset can be before or after the diagnosis of cancer; progression oc-curs over the course of months. Gait and limb ataxia and dysarthria occur in most cases; nystagmus is rare.43

Hereditary spinocerebellar degenerationsThere are 7 autosomal dominant spinocerebellar

ataxias characterized by adult-onset, slowly progressive cerebellar ataxia that affects gait early and severely. Fried-reich ataxia is an autosomal recessive spinocerebellar disease with an onset in childhood. Progressive gait ataxia is the first symptom, followed by ataxia of all limbs within 2 years. Decreased tendon reflexes in the legs, dysarthria, impairments of proprioceptive and vibration sense, and weakness in the legs are common, as are nystagmus, vertigo, and hearing loss.43

Ataxia-telangiectasiaThis syndrome is an autosomal recessive disorder with

an onset before age 4 and global cerebellar involvement producing nystagmus, dysarthria, and gait, limb, and trunk ataxia. Loss of vibration and position sense in the legs further adds to gait ataxia. Vascular lesions are present on the skin and the eyes, especially on the ears, nose, face, and antecubital and popliteal fossae.43

Wilson diseaseWilson disease is a disorder of the copper metabolism

with copper deposition in multiple body tissues. A rusty-

brown ring around the cornea is indicative of this disease and may indicate the origin of the cerebellar symptoms that are associated with this disorder.43

Creutzfeldt-Jakob diseaseThis disease is characterized by dementia, cerebellar

signs in 60% of patients, and gait ataxia in 10%. The ataxia is usually accompanied in 50% of patients thus affected with nystagmus, dysarthria, and trunk and limb ataxia. The disease involves progressive dementia, (extra) pyramidal dysfunction, and myoclonus, with death within a year of onset.43

Posterior fossa tumorsCerebellar tumors frequently present with headache

due to increased intracranial pressure or with ataxia. Nausea, vomiting, vertigo, and cranial nerve palsies are also common. Most common in adults are secondary tumors metastasized from primary tumors in the breast or lung. Primary tumors are more frequent in children and include astrocytomas and medullablastomas. Headache and vomiting are frequently presenting symptoms; ataxia and visual dysfunction are also a common first symptom with medullablastomas in children.43

Posterior fossa malformationsCongenital anomalies may cause vestibular or cer-

ebellar symptoms in adulthood.43,57 Type I Arnold-Chiari malformation involves downward displacement of the cerebellar tonsils through the foramen magnum, caus-ing symptoms of cerebellar involvement and brainstem compression. Ataxia in this malformation affects gait and is bilateral. Hydrocephalus may cause headache and vomiting. Brainstem compression can be associated with vertigo, nystagmus, and cranial nerve palsies.43 Other symptoms demonstrated in patients with compression at the level of the foramen magnum include suboccipital pain or neck pain described as a tight collar (65%), often exacerbated by neck movement; pain in the hand (59%) or arm (55%), especially burning along the ulnar border of the contralateral arm in unilateral lesions; pain in the leg (26%) and face (7%); weak arm (40%) or leg (30%); hand clumsiness (27%); bladder dysfunction (22%); dysphagia (13%); dysarthria (3%); and paresthesia along the spine with trunk and neck flexion (L’ Hermitte sign) (3%). Signs of foramen magnum compression include hyperreflexia and limb weakness (70%); a positive Babinski sign (60%); paraplegia with arms affected more than legs; wasting of the hand muscles (13%); disproportionate weakness of the sternocleidomastoid and trapezius as a result of compression of the spinal accessory nerve (30%); disso-ciated sensory loss, papilledema (7%); Horner syndrome (4%); and hiccups (2%). In patients with unilateral compression, paralysis may present in a clock-face way with ipsilateral arm, then leg, then contralateral leg, and finally contralateral arm weakness. Intracranial extension of the compressive lesion may result in a down-beating nystagmus (25%) and cruciate hemiplegia (ipsilateral lower

10

limb and contralateral upper limb weakness caused by a lesion at the motor decussation in the medulla).58

Familial paroxysmal ataxiaThis hereditary recurrent ataxia is associated with

nystagmus and dysarthria. Other symptoms may include vertigo, tinnitus, diplopia, oscillopsia, facial palsy, head-ache, and fever. Attacks last from 15 minutes to several hours and may be triggered by physical exercise, caffeine, alcohol, or sudden movements.57

PRESYNCOPEAs discussed earlier, presyncope is a sensation of an

impending faint or loss of consciousness that is not associ-ated with an illusion of movement. Presyncope results from conditions that compromise the brain’s supply of blood, oxygen, or glucose. This can compromise the function of the cerebral hemispheres or the brainstem. Different conditions can cause either a pancerebral hypoperfusion or a selective hypoperfusion of the brainstem.43

Pancerebral HypoperfusionCauses for presyncope due to pancerebral hypoperfu-

sion can be classified into 4 categories43:• Vasovagal presyncope• Cardiovascular presyncope• Cerebrovascular presyncope: migraine, benign parox-

ysmal vertigo of childhood, Takayasu disease, carotid sinus syncope

• Miscellaneous causes of presyncope: orthostatic hy-potension, hyperventilation syncope, cough syncope, micturition syncope, glossopharyngeal neuralgiaInsufficient supply of glucose and subsequent com-

promised pancerebral function can also result in presyn-cope.

Vasovagal presyncopeWith a vasovagal presyncope, parasympathetic hy-

peractivity causes a decrease in cardiac output with a subsequent decrease in cerebral blood flow.41 Precipitat-ing factors include emotional stimulation, pain, the sight of blood, fatigue, medical instrumentation, blood loss, or prolonged motionless standing. Vasovagal presyncope occurs in all age groups and affects men and women equally. Short prodromes (10 seconds to a few minutes) will precede syncope and include lightheadedness, nau-sea, pallor, salivation, blurred vision, and tachycardia.41,43 Vasovagal presyncope mainly occurs with the patient in a sitting or standing position; it is rare with a patient in the recumbent position.43

Cardiovascular presyncopeA cardiovascular syncope should be suspected when

syncope occurs with the patient in a recumbent position, during or after physical activity, or in a patient with a known medical history of heart disease. Table 3 provides an overview of cardiac causes of syncope. Associated symptoms may include chest pain or discomfort, neck or

arm pain and discomfort, palpitation, dyspnea, fatigue, cough, cyanosis, edema, and claudication.59

MigraineMigraine is generally characterized by headache that

is usually unilateral and of a pulsatile quality. Nausea, photophobia, phonophobia, vomiting, and lassitude are frequently associated with migraine. Migraine can occur without or with an aura. Visual or other neurological au-ras occur in 10% of patients. The International Headache Society has provided diagnostic criteria for both types of migraine (Table 4).60 Also, in about 10% of patients, migraine may be associated with presyncope. Syncope will occur during the migraine attack, often when the patent quickly rises to a standing position, suggesting a component of orthostatic hypotension. A family history of migraine is usually present. Migraine is more common in women with an onset early in life.43

Table 3. Causes of Cardiovascular Syncope*

Cardiac arrestCardiac inflow obstruction

• Left atrial myxoma or thrombus• Tight mitral stenosis• Constrictive pericarditis• Cardiac tamponade• Restrictive cardiomyopathies• Tension pneumothorax

Cardiac outflow obstruction• Aortic stenosis• Pulmonary stenosis• Hypertrophic obstructive cardiomyopathy

Dissecting aortic aneurysmSevere pulmonary-vascular disease

• Pulmonary hypertension• Acute pulmonary embolus

Cardiac dysrhythmias• Tachyarrhythmias: paroxysmal atrial

tachycardia, atrial filter, atrial fibrillation, accelerated junctional tachycardia, ventricular tachycardia, ventricular fibrillation

• Bradyarrhythmias: sinus bradycardia, sinus arrest, second or third degree heart block, implanted pacemaker failure

• Mitral valve prolapse• Prolonged Q-T interval syndromes• Sick sinus syndrome• Drug toxicity: digitalis, quinidine,

procainamide, propranolol, phenothiazines, tricyclic antidepressants, potassium

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

11

Benign paroxysmal vertigo of childhoodThis condition is a childhood periodic syndrome that

is a common precursor of migraine in later life, and it is, therefore, because of proposed shared pathophysiology, classified with migraine as a form of cerebrovascular presyncope.60 Benign paroxysmal vertigo of childhood is characterized by brief, recurrent attacks of vertigo that occur without warning and resolve spontaneously in otherwise healthy children. It is often associated with nystagmus and vomiting. Unilateral throbbing headache occurs at times. The International Headache Society has provided diagnostic criteria (Table 5).60

Takayasu diseaseTakayasu disease is most common in women of Asian

descent. Presyncope can occur after exercise, standing, or head movement and is associated with impaired vision and confusion. The disease is also known as pulseless disease because brachial artery pulsations are absent or decreased.43

Carotid sinus syndromeCarotid sinus syndrome is relatively rare. It occurs in

men twice as frequently as in women. Patients are usually over the age of 60. Propranolol, digitalis, and methyldopa seem to predispose patients to this syndrome. Pressure on the carotid sinus due to a tight collar or local neck tumor will cause vagal stimulation leading to bradycardia and subsequent syncope.43

Orthostatic hypotensionOrthostatic hypotension may occur in teenagers, but

it is most common in the sixth and seventh decades of

life. It occurs more often in men than in women. Syncope and presyncope happen when rapidly rising to a standing position, standing motionless for prolonged periods, and standing after prolonged recumbency. The pathophysiol-ogy of orthostatic hypotension usually involves reduced blood volume or autonomic nervous system dysfunc-tion.41,43 Table 6 lists causes of orthostatic hypotension.

HyperventilationHypocapnia is the pathophysiological cause for pre-

syncope in patients with hyperventilation. It induces ce-rebral vasoconstriction resulting in central nervous system hypoperfusion. Patients are usually women between the ages of 20 and 40. Other symptoms include lightheaded-ness, shortness of breath, perioral numbness and pares-thesia, and muscular twitching. Hyperventilation-induced presyncope commonly occurs when supine and can be brought on by asking the patient to hyperventilate.43

Cough-related syncopeCough syncope is immediately preceded by coughing,

which need not be prolonged. It occurs mainly in middle-aged men with a history of chronic obstructive pulmonary disease. There are no prodromal symptoms. Syncope (and presyncope) may be caused by an increase in intracranial pressure due to coughing with resultant cerebral hypoper-fusion. Cough-induced presyncope may occur when the patient is supine and may be reproduced by asking the patient to cough.43

Micturition syncopeMicturition-induced presyncope occurs almost exclu-

sively in men; episodes occur mainly at night and they oc-

Table 4. Diagnostic Criteria for Migraine Without and With Aura60

Migraine Without Aura Migraine With Aura

A. At least 5 attacks fulfilling criteria B and DB. Headache attacks lasting 4 to 72 hours (untreated or

unsuccessfully treated)C. Headache has at least 2 of the following

characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, aggravation by or causing avoidance of routine physical activity

D. During headache, at least 1 of the following: nausea or vomiting, photophobia, phonophobia

E. Not attributed to another disorder

A. At least 2 attacks fulfilling criteria BB. Migraine aura with criteria with regard

to symptoms and time of occurrence and duration specific to 6 subforms

C. Headache may or may not satisfy criteria B, C, and D from “migraine without aura” column; typical aura without headache not associated with headache

D. Not attributed to another disorder

Table 5. Diagnostic Criteria for Benign Paroxysmal Vertigo of Childhood60

A. At least 5 attacks fulfilling criterion BB. Multiple attacks of severe vertigo, occurring without warning and resolving spontaneously after minutes to

hoursC. Normal neurologic examination and audiometric and vestibular function between attacksD. Normal electro-encephalogram

12

cur before, during, or after micturition. Peripheral blood pooling, vagus-induced bradycardia, and prolonged recumbency are likely responsible.43

Glossopharyngeal neuralgiaSyncope in glossopharyngeal neuralgia is the result of

a glossopharyngeal-vagal reflex circuit causing transient bradyarrhythmia that results in cerebral hypoperfusion. Ventricular asystole, sinus bradycardia, and atrioven-tricular block correlated with swallowing have all been described. This syndrome is also known as deglutition syncope, swallow syncope, or syncopal dysphagia.61 Glossopharyngeal neuralgia is rare; symptoms include paroxysmal pain in the tonsillar pillar or the external ear canal during swallowing, talking, or coughing.43 Dizzi-ness, lightheadedness, confusion, or fainting on swal-lowing can also occur. Medications that increase atrio-ventricular block (eg, digoxin, calcium channel blockers, and beta-blockers) may increase symptoms. Many pa-tients with glossopharyngeal neuralgia have identifiable

esophageal lesions (diffuse esophageal spasm, achalasia, hiatal hernia, diverticula, and stricture).61

HypoglycemiaPresyncopal dizziness may also be the result of a

hypoglycemic reaction. Asking the patient whether the dizziness occurs mainly when he or she has not eaten may clue in the clinician to hypoglycemia as a cause for dizziness. Polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), weight loss, and fatigue may be diagnostic indicators for patients with undiagnosed diabetes.62

Brainstem HypoperfusionSelective hypoperfusion of the brainstem is the result

of compromise or disease processes in the vertebrobasilar system.

Vertebrobasilar insufficiencyVertebrobasilar insufficiency is characterized by diz-

ziness symptoms associated with focal neurologic abnor-malities of sudden onset and brief duration (seconds to minutes) that relate to the specific areas supplied by the vertebrobasilar vessels.44,53,63 Terrett64 provided us with a useful mnemonic for signs and symptoms associated with VBI (Table 7). Van der Velde53 suggested classifying dizziness caused by VBI as a positional-type dizziness to distinguish it from the positioning-type dizziness pro-duced by BPPV and cervicogenic dizziness. Dizziness, and other symptoms, will increase in patients with VBI when maintaining the head in the provocative position in contrast to the latter 2 pathologies where symptoms are provoked by positioning but adapt when the head is maintained in the provocative position. Table 8 provides characteristics helpful for the differential diagnosis of these 3 conditions.

Vertebrobasilar insufficiency may be caused by intrin-sic or extrinsic mechanical disorders.63 Atherosclerosis, thromboembolic events, and arterial dissections are examples of intrinsic mechanical disorders.63-65 Anoma-

Table 6. Causes of Orthostatic Hypotension*

Hypovolemia or hemorrhageAddison diseaseDrug-induced hypotension

• Antidepressants• Antihypertensives• Bromocriptine• Diuretics• Levodopa• Monoamine oxidase (MOA) inhibitors• Nitroglycerin• Phenothiazines

Polyneuropathies• Myeloid neuropathy• Diabetic neuropathy• Guillain-Barré syndrome• Porphyric neuropathy• Vincristine neuropathy

Other neurologic disorders• Idiopathic orthostatic hypotension• Multiple sclerosis• Parkinsonism• Posterior fossa tumor• Shy-Drager syndrome• Spinal cord injury with paraplegia• Surgical sympathectomy• Syringomyelia• Syringobulbia• Tabes dorsales (syphilis)• Wernicke encephalopathy

Cardiovascular disordersProlonged bed rest or immobilization

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

Table 7. Five D’s and Three N’s*

DizzinessDrop attacksDiplopiaDysarthriaDysphagiaAtaxia of gaitNauseaNumbnessNystagmus

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

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lous soft tissue structures, such as bands of the deep cervical fascia, or compression of the vertebral artery between the longus colli and anterior scalene muscles are examples of extrinsic mechanical disorders.63 Osteo-phytes laterally projecting from the uncinate processes and backward bending of the upper cervical spine in the forward head posture may also cause mechanical compression.65 Additionally, vertebral artery occlusion may result following acute cervical spine trauma, caus-ing fracture and dislocation.66

The nystagmus in patients with VBI may be vertical, implicating the central vestibular structures affected by this ischemic process.67 When syncope occurs, recovery is frequently prolonged (30 to 60 minutes or longer).43 Patients may report symptoms following cervical ma-nipulation, but symptoms have also been reported after activities such as a shampoo treatment at the hair salon, yoga exercises, painting a ceiling or wall, changing a light bulb, turning the head when backing up the car, giving birth, having surgery, hanging the wash, archery, swimming, Tai Chi, sexual intercourse, and wrestling.64,68 Terrett64 provided a comprehensive overview of all reported nonmanipulative causes of VBI. A position of rotation or extension is frequently implicated in causing VBI. However, even in a patient with mechanical disor-ders of the vertebral artery, this position need not result in symptoms due to compensation by the collateral circulation, namely the opposite vertebral artery and the carotid arteries.63 Symptoms of VBI are more likely to occur when the collateral circulation is concurrently compromised.63 The previous monograph has discussed

in more detail the role of the vertebral artery in producing dizziness.

Vertebrobasilar infarctionRecurrent vertebrobasilar ischemic attacks lead to

stroke in 20% of patients.43 Stroke can develop acutely or subacutely after arterial wall damage due to a combina-tion of vasospasm, thrombus formation, thromboemboli-zation, and the formation of a dissecting aneurysm.64 Due to its association with cervical manipulation and other nontraumatic causes, but also because of the contrain-dication to further manipulative treatment and the need for medical referral, knowledge of signs and symptoms of a dissecting aneurysm is important. A sudden onset of severe neck and occipital pain is the hallmark of dis-section of the vertebral artery.69,70 Vertigo, unilateral facial paresthesia, cerebellar signs, and visual field defects may also be present.69 It is sobering to realize that the sudden onset of neck and occipital pain may, in fact, be the com-plaint for which a patient with arterial dissection seeks physical therapy intervention.

Vertebrobasilar infarction will produce signs and symptoms based on the area cut off from its vascular sup-ply. Presyncopal dizziness in an acute cerebellar infarc-tion is accompanied by unilateral sensorineural hearing loss and nystagmus with occlusion of a branch from either the basilar artery or the anterior inferior cerebellar artery, called the internal auditory artery, which supplies the vestibulocochlear nerve.43 Acute proximal vertebral artery occlusion may result in Wallenberg syndrome, combining presyncopal dizziness with vertigo, vomiting,

Table 8. Differential Diagnostic Characteristics of Cervicogenic Dizziness, Benign Paroxysmal Positional Vertigo, and Vertebrobasilar Insufficiency8,53,64*

Vertigo Type Nystagmus Characteristics Associated Signs and Symptoms

Cervicogenic Dizziness

Positioning-type • No latency period• Brief duration• Fatigable with repeated motion

• Nystagmus• Neck pain • Suboccipital headaches• Cervical motion

abnormality

Benign Paroxysmal Positional Vertigo

Positioning-type • Short latency: 1 to 5 seconds• Brief duration: less than 30

seconds• Fatigable with repeated motion

• Nystagmus

Vertebrobasilar Insufficiency

Positional-type • Long latency: 55 ± 18 seconds8

• Increasing symptomatology with maintained head position

• Not fatigable with repeated motion

• Dizziness• Drop attacks• Diplopia• Dysarthria• Dysphagia• Ataxia of gait• Nausea• Numbness• Nystagmus

*Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

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nausea, dysphagia, hoarseness, nystagmus, ipsilateral Horner syndrome, sensation loss in the face, limb ataxia, and loss of light touch and position sense in the limbs. Cerebellar infarction due to occlusion of the anterior inferior cerebellar artery, posterior inferior cerebellar ar-tery, or superior cerebellar artery all result in ipsilateral limb ataxia and hypotonia. Other symptoms and signs include headache, nausea, vomiting, vertigo, nystagmus, dysarthria, ocular or gaze palsies, facial weakness or sensory loss, contralateral hemiparesis, and hemisensory deficit.43

Basilar-type migraineBasilar-type migraine is a subtype of migraine with

an aura that indicates involvement of the brainstem or both hemispheres simultaneously. Average duration of symptoms is 20 to 30 minutes and symptoms can be relieved by sleep. The most common symptoms include bilateral visual and sensory disturbances, changes in consciousness and mood, and vertigo.71 As basilar artery involvement is uncertain, the International Headache So-ciety has suggested using the name basilar-type migraine rather than basilar or basilar artery migraine. It is distinct from vertebrobasilar migraine (discussed below) by its absence of motor deficits. Basilar-type migraine most commonly occurs in young adults. Many patients also report migraine episodes with a more typical aura. The International Headache Society has provided diagnostic criteria for basilar-type migraine (Table 9).60 It is suggested that in the presence of motor symptoms, patients should be classified under sporadic or familial hemiplegic mi-graine.60

Vertebrobasilar migraineThis pathology usually affects young women with

prolonged attacks (up to 72 hours) consisting of intense vertigo, vomiting, dysarthria, and limb and perioral paresthesia. Transient quadriplegia, fainting, confusion, and stupor for a period of hours can occur during an attack but are rare. A visual aura may occur preceding the attack, and an attack may be followed by an occipi-tal-region headache. A family history of migraine and a correlation of attacks with the menstrual period are diag-nostic indicators.57 This type of migraine is not part of the International Headache Society classification, and due to

the duration of symptoms, it would not seem to fit any of the diagnostic categories.60

Vestibular migraineDieterich and Brandt72 reported on 90 patients with

episodic vertigo for whom they were able to substantiate a diagnosis of migraine. The disease was characterized by rotational or translational vertigo lasting from a few seconds to several hours or even days. Duration of a few minutes or several hours was most common. Most patients (78%) only noted vertigo; 16% also had auditory symptoms. In 32% of patients there was no headache. In the symptom-free intervals, 66% of patients showed oculomotor abnormalities including dysfunction in verti-cal or horizontal saccadic pursuit and gaze-evoked, po-sitional, and spontaneous nystagmus. Initial presentation could occur at any age. Prevalence in men was highest in the fourth decade and in women from the third to the fifth decade. Because of the duration of symptoms and predominantly monosymptomatic aura, most patients did not fit the International Headache Society criteria, leading the authors to propose a diagnostic entity of vestibular migraine. Lempert and Neuhauser73 have suggested the name migraine-associated vertigo based on the presence of signs and symptoms indicative of an underlying causative migraine disorder.

Subclavian steal syndromeThis syndrome results from retrograde flow in the

vertebral artery and subsequent brainstem hypoperfusion due to subclavian or innominate artery stenosis.43 In the subclavian steal syndrome, blood passes from the verte-bral artery into the distal subclavian artery with physical activity of the ipsilateral arm.74 Symptoms include ver-tigo, diplopia, limb paresis, arm fatigue, paresthesia, and ataxia, all of which are more common than presyncope.43 Symptoms are brought on by arm exertion, not head or neck movements, allowing for differential diagnosis with, for example, VBI.74

DYSEQUILIBRIUMAs discussed earlier when we introduced the 4-cat-

egory diagnostic classification system for the diagnosis of patients complaining of dizziness, dysequilibrium is a sense of imbalance without associated vertigo.

Table 9. Diagnostic Criteria for Basilar-type Migraine60

A. At least 2 attacks fulfilling criteria B, C, and DB. Aura consisting of at least 2 of the following fully reversible symptoms but no motor weakness: dysarthria, vertigo,

tinnitus, hypacusia, diplopia, visual symptoms simultaneously in both temporal and nasal fields of both eyes, ataxia, decreased level of consciousness, simultaneous bilateral paresthesia

C. At least 1 of the following: at least 1 aura symptom develops gradually over ≥5 minutes, different aura symptoms occur in succession over ≥5 minutes, or both; each aura symptom lasts ≥5 and ≤60 minutes

D. Headache fulfilling criteria B, C, and D from “migraine without aura” column (Table 4) that begins during the aura or follows the aura within 60 minutes

E. Not attributed to another disorder

15

Visual ImpairmentWe already discussed the gaze-related palsies and

decreased gaze fixation related to vestibular, cerebellar, and brainstem lesions. More germane changes, such as decreased visual field, visual acuity, and depth percep-tion, may also produce dysequilibrium and subsequent complaints of dizziness.75

Somatosensory ImpairmentSomatosensory deficits result from pathologies that

cause sensory ataxia. These pathologies can be classified as polyneuropathies, myelopathies, or a combination of both. Table 10 reviews causes of sensory ataxia. My-elopathy and cervicogenic dizziness are most relevant to orthopaedic physical therapy practice. Mal de debarque-ment syndrome is another pathological entity that may fall into this category. We discussed cervicogenic dizzi-ness in detail in the beginning of this monograph.

MyelopathyTable 10 also provides an overview of pathologies

associated with spinal cord compression. Cord compres-sion can occur in the cervical, thoracic, and high lumbar regions of the spine. With obvious variations in presen-

tation depending on the segmental level of spinal cord compromise and the amount of compromise, spinal cord compression may result in76-78:• Variable upper limb, lower limb, neck, and trunk

pain • Sensory impairment of the upper and lower limbs not

limited to a single dermatome• Nonmyotomal arm or leg weakness• Velocity-dependent limb hypertonia• Upper motor neuron signs in the extremities: hyper-

reflexia, positive Babinski sign and Hoffman reflex, gait ataxia, and spastic bladderAtrophy of the intrinsic hand muscles is the result

of segmental necrosis of anterior horn cells in patients with cervical myelopathy.76,78 Anterior horn cell necrosis usually occurs at the level of compression. Myelopathic hands result from compression of the C8-T1 nerve levels at the C6-C7 spinal level because of the oblique course of the cervical nerve roots. Cord compression can also result from interactions with the musculoskeletal system. This indicates a possible need for range-of-motion and provocative (ie, spinal arthrogenic instability) testing; the cervical spine has especially been implicated due to a combination of degenerative stenosis, instability, and a physiological narrowing of canal diameters in backward bending.79

Landsickness and mal de debarquement syndromeMotion sickness is common and likely the result of a

mismatch between visual, vestibular, and somatosensory afferent input during exposure to motion. Landsickness or post-motion vertigo refers to inappropriate sensations of movement after exposure to motion. An incidence of landsickness of 73% has been reported in healthy crewmen of seagoing vessels. The duration of symptoms ranged from 1 minute to 2 days, with 88% of subjects noting symptoms for less than 6 hours.80

Mal de debarquement syndrome is defined as land-sickness lasting greater than 1 month.80 Information on mal de debarquement syndrome is limited, but it seems to occur predominantly in middle-aged women after a sea voyage or air or train travel. Symptoms are mostly constant but can be intermittent and include a rocking or swaying sensation and imbalance. A sensation of tilt-ing and ear symptoms including a sensation of fullness, tinnitus, hyperacusis, ear pain, and decreased hearing occur in about half of patients. Nausea and headache are less common and vertigo is rare. Provoking factors include further motion exposure, anxiety and stress, rapid head movement, and positional changes. Symp-toms of headache, tilting, and ear symptoms were nega-tively related to the duration of mal de debarquement syndrome (ie, were less frequent with longer duration). Otolith dysfunction and a persistent adaptation of the central nervous system to altered afferent input have been suggested in the etiology of mal de debarquement syndrome.80 Limited evidence exists of a moderate effect of physical therapy consisting of vestibular habituation

Table 10. Causes of Sensory Ataxia*

Polyneuropathy or Myelopathy• Friedreich ataxia• Neurosyphilis (tabes dorsalis)• Nitrous oxide• Vitamin B12 deficiency• Vitamin E deficiency

Polyneuropathy• Autosomal-dominant sensory ataxic

neuropathy• Cis-platinum use• Dejerine-Sottas disease• Diabetes• Diphtheria• Hypothyroidism• Immune-mediated neuropathies• Isoniazid• Paraneoplastic sensory neuronopathy• Pyridoxine• Refsum disease• Taxol

Myelopathy• Acute transverse myelitis• AIDS (vacuolar myelopathy)• Multiple sclerosis• Tumor or cord compression• Vascular malformations

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

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and postural control exercises.81 A link with Ménière disease, psychological abnormalities, and migraine has not been established.80

Musculoskeletal ImpairmentThe musculoskeletal system is the effector organ of

the balance control systems. Decreased muscle strength and endurance, decreased joint range of motion and sta-bility, increased through-range resistance of joints, and posture negatively affecting the location of the center of gravity in relation to the base of support can all have a negative effect on balance and may contribute to a sense of dysequilibrium for which the patient will seek our assistance. This provides the indication for a com-prehensive evaluation of musculoskeletal impairment in the differential diagnostic process of patients complain-ing of dizziness.

Basal Ganglia ImpairmentParkinsonism is common, especially in older

adults.41,43 It occurs in all ethnic groups with an ap-proximately equal distribution among men and women. Clinical findings include tremor, rigidity, hypokinesia, and gait and postural abnormalities.43 The characteristic forward bent posture negatively affects the location of the center of gravity in relation to the base of support. The characteristic festinating gait with short, shuffling steps that become successively more rapid can further contribute to a sense of imbalance.41 Phenothiazines, butyrophenones, metoclopramide, reserpine, and tet-rabenazine are drugs associated with a reversible par-kinsonian syndrome. Manganese dust, carbon disulfide, and carbon dioxide poisoning can also result in Parkin-sonism. Use of the illicit meperedine-analog Angel Dust can also cause Parkinsonism.43 We earlier mentioned parkinsonism as a cause for presyncopal dizziness due to orthostatic hypotension (Table 6).

OTHER DIZZINESSAs discussed above, other dizziness is dizziness de-

scribed as a vague or floating sensation with the patient having difficulty describing the sensation.31 Other diz-ziness may be associated with anxiety and depression. In fact, psychiatric disorders are considered the primary cause of this subtype of dizziness, accounting for about 10% to 25% of all dizziness cases.31 Yardley et al82 found a significantly higher rate of psychiatric disorders in primary care patients who complained of dizziness as compared to age-matched controls who did not com-plain of dizziness. In older adults, anxiety, depression, and adjustment reactions were factors contributing to dizziness.83 Tilting of the environment also falls under the other dizziness subtype.

Psychogenic DizzinessWe will discuss 2 types of psychiatric disorders fre-

quently associated with dizziness: panic disorder and phobic postural vertigo.

Panic disorderPanic disorder is a chronic illness characterized by so-

matic and psychological complaints (Table 11).50,84 This disorder occurs in 1 of 75 persons worldwide and can be either inherited (incomplete autosomal dominance) or acquired.50 It accounts for 15% of all medical visits and has been reported to average 10 different physician evaluations before it is correctly diagnosed.50 Patients with panic disorder are thus 7 more times likely to be high users of health care.50 Work disability is also com-mon in panic disorder.50 Additionally, panic disorder is associated with significantly increased risk of suicide, increased cardiovascular morbidity, and, if left untreated, increased occurrence of stroke.85 Patients who suffer from panic disorder usually have an abrupt onset of fear or discomfort that peaks in approximately 10 minutes.50 It is accompanied by at least 4 of the signs and symptoms listed in Table 11. Correct diagnosis also requires that panic attacks either recur unexpectedly every 2 weeks or that a single attack be followed by at least 1 month of the following symptoms50:• Persistent concern about future attacks• Worry that attacks will cause physical illness or insan-

ity• Significant changes in behavior related to the attacks

Phobic postural vertigoPhobic postural vertigo may be the second most com-

mon cause of patient complaints of dizziness after BPPV, and it seems to be associated with somatization as well

Table 11. Diagnosis of Panic Disorder*

Signs and symptoms (diagnosis requires 4):• Sweating• Rapid heart rate, palpitations, pounding heart• Tremor• Shortness of breath• Feeling of choking• Chest pain• Nausea or abdominal distress• Dizziness• Lightheadedness• Feeling of unreality• Fear of losing control• Fear of dying• Paresthesia• Hot flashes

Associated signs and symptoms• Anxiety• Depression• Insomnia• Chronic fatigue• Gastroesophageal reflux

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

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as compulsive, depressive, and anxiety disorders.86 The diagnostic criteria for phobic postural vertigo consist of86:• Vertigo and subjective complaints of dysequilibrium

in the absence of findings from neurologic or balance examination

• Description of fluctuating dysequilibrium with stand-ing or walking and paroxysmal fear of falling without actual falls

• Description of feelings of anxiety and sympathetic symptoms during or shortly after attacks or vertigo without accompanying anxiety

• Provocation of dizziness in situations commonly implicated in other phobic syndromes (eg, crossing bridges, driving a vehicle, being in empty spaces or among large numbers of people)

• Premorbid compulsive personality traits and depressive characteristics

• Initial onset of symptoms related to vestibulopathy or external stressors

Tilting of the EnvironmentTilting of the environment is a rare form of dizziness at-

tributed to otolith dysfunction. The function of the otoliths (utricle and saccule) is to provide sensory information on linear motion and acceleration in the horizontal and verti-cal directions, respectively. They also provide information on static head tilt due to the presence of the otoconia. Tilting of the environment is probably caused by an imbal-ance of otolith signals due to unilateral vestibular loss and is enhanced when rapid perturbations of posture make somatosensory cues difficult to interpret.87 This asym-metry in otolith input to the vestibular nuclei causes the individual to sense a tilt of the environment to the side of the involved inner ear.87,88 As the symptom is tilting of the environment, and not spinning or rotating, this asymmetry of otolith input is not classified under vertigo, despite it being a vestibular disorder. Tilting of the environment leading to a sudden fall has also been referred to as a drop attack.89 Drop attacks associated with vestibular disorders usually occur in the later stages of Ménière disease and are called otolithic crises of Tumarkin.89,90 An increase in endolymphatic pressure causes physical distention and mechanical disruption of the otolith organs, causing a sudden sense of tilting or falling.89 Otolithic crises of Tu-markin occur without warning and are not associated with vertigo, loss of consciousness, numbness, or paralysis.89 We previously discussed drop attacks associated with VBI (Table 7).

The symptom of tilting of the environment may be rare due to central compensation and substitution from the visual and somatosensory systems.91 Additionally, roll tilt illusion and linear acceleration perception deficit due to unilateral vestibular loss are generally experienced only within the first few hours or up to 1 week following onset.91

Tilting of the environment is another form of dizziness that tends to challenge the diagnostic classification system introduced in this monograph. Ischemia or infarction in

the vertebrobasilar system and its branches unilaterally affecting the vestibular nuclei, the medial longitudinal fascicle, other nuclei involved in the vestibular mecha-nism, or the thalamus can also result in a patient report-ing a subjective tilt of the visual vertical axis in a frontal plane.92

PHYSICAL THERAPY VERSUS MEDICAL DIFFERENTIAL DIAGNOSIS

We discussed above a 4-category diagnostic clas-sification system to facilitate the differential diagnosis of patients with a complaint of dizziness. It should be obvious that many of the pathologies discussed above require medical evaluation and management rather than, or in addition to, physical therapy evaluation and man-agement. Also, many tests and measures that are needed for a full differential diagnostic work-up of patients pre-senting with dizziness are clearly outside of the physical therapy scope of practice. It is the role of the physician to play the lead role in this comprehensive medical dif-ferential diagnostic process.

However, there is mounting evidence that conserva-tive measures as provided by the physical therapist may be beneficial for a select subset of patients with dizzi-ness. Repositioning maneuvers may decrease symptoms in patients with BPPV involving the posterior, horizontal, and anterior SCCs.93-97 Manual physical therapy inter-ventions may positively affect cervicogenic dizziness.35 Musculoskeletal impairments, such as decreased muscle strength and endurance, joint stability and mobility, and posture, which are implicated in patients with the dys-equilibrium subtype of dizziness, are dysfunctions tra-ditionally addressed by physical therapists.6 Habituation exercises have proven beneficial for patients with acute unilateral vestibular loss, and adaptation and balance ex-ercises have produced positive outcomes in patients with chronic bilateral vestibular deficits.95 Limited evidence also exists of a moderate effect of vestibular habituation and postural control exercises in patients with mal de de-barquement syndrome.81 For the latter 3 patient groups, physical therapy management is preceded by a medical differential diagnostic work-up. An isolated otolith dys-function may theoretically also be amenable to conserva-tive management, but as no clinical tests exist to identify this dysfunction, we cannot make any evidence-based recommendations at this time. Table 12 provides signs and symptoms indicative of the pathologies amenable to sole physical therapy management.

The greatest danger for patients complaining of dizzi-ness (and for the therapist managing such patients) is that the therapist may fail to recognize signs and symptoms that are indicative of a pathology requiring urgent medi-cal or surgical management but that resemble pathology amenable to sole physical therapy management.93 A delayed medical diagnosis and delayed subsequent ap-propriate medical or surgical management may prove harmful in these cases.93 Therefore, the foremost goal of physical therapy differential diagnosis for previously

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Table 12. Signs and Symptoms Indicative of Pathologies Amenable to Sole Physical Therapy Management*

Benign Paroxysmal Positional Vertigo (BPPV)

• Intermittent, severe positioning-type dizziness• Precipitated by positioning, movement, or other stimuli (see below)• Short latency: 1 to 5 seconds • Brief duration: less than 30 seconds• Fatigable with repeated motion• Associated signs and symptoms: nystagmus, nausea, and at times vomiting• Occurs in people over age 40 with peak incidence of onset in the sixth decade• Rare in people under 20• Medical history of head trauma, labyrinthine infection, surgical stapedectomy, chronic

suppurative otitis media, and degenerative changes to the inner ear may indicate nonidiopathic BPPV

Posterior Semicircular Canal BPPV

• Patients complain of dizziness when they quickly transfer to a supine position, especially when the head is turned to the affected side

• Positive response of vertigo and apogeotropic torsional nystagmus on ipsilateral Hallpike-Dix maneuver

Anterior Semicircular Canal BPPV

• Patients also complain of dizziness when they quickly transfer to a supine position, especially when the head is turned to the affected side, but there is less specificity as to the direction of head rotation

• Bilateral positive response on Hallpike-Dix maneuver with vertigo and geotropic torsional nystagmus on ipsilateral test

• Hallpike-Dix maneuver may also cause down-beating vertical nystagmus• Positive response on straight head-hanging test

Horizontal Semicircular Canal BPPV

• Dizziness is brought on when rolling over in supine but can also occur with flexion and extension of the head or when transferring from supine to upright

• A bilaterally positive test with a purely horizontal nystagmus on Hallpike-Dix maneuver; the nystagmus will be geotropic beating in the direction of the face turn or downside ear; nystagmus will occur in both directions but is generally stronger when the head is turned toward the affected side

• Positive roll test• Positive walk-rotate-walk test to affected side

Cervicogenic Dizziness

• Intermittent positioning-type dizziness• Precipitated by head and neck movement• No latency period: onset of symptoms is immediate upon assuming the provoking position• Brief duration but may last minutes to hours• Fatigable with repeated motion• Associated signs and symptoms: nystagmus, neck pain, suboccipital headaches, sometimes

paresthesia in the trigeminal nerve distribution• Possible lateral head tilt due to tightness of the sternocleidomastoid or upper trapezius• Possible forward head posture• Medical history of cervical spine trauma and degeneration• Motion dysfunction in the upper cervical segments on active range-of-motion and passive

intervertebral motion testing• Positive neck torsion test: nystagmus with reproduction of dizziness

Musculoskeletal Impairments

• Subjective complaints of weakness, unsteadiness• Insidious onset• Postural deviations negatively affecting the location of the center of gravity in relation to the

base of support: trunk flexion, hip flexion, knee flexion, and ankle plantarflexion contractures• Decreased trunk extension, hip extension, knee extension, and ankle dorsiflexion on range-of-

motion testing• Loss of strength and endurance in antigravity muscles• Impaired joint position sense lower extremity

* Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and Manipulative Therapy.

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undiagnosed patients complaining of dizziness should be to distinguish between 2 groups of patients:• Patients that may respond to conservative interven-

tions within the physical therapy scope of practice, specifically patients with BPPV, cervicogenic dizzi-ness, and musculoskeletal impairments leading to dysequilibrium

• Patients that require referral for medical differential diagnosis and medical or surgical comanagementBelow we will provide a template for the history

(Tables 13 and 14) and physical examination (Table 15) relevant to the physical therapy differential diagnosis of previously undiagnosed patients with a main complaint of dizziness. Consistent with the foremost goal of this physical therapy differential diagnostic process as iden-tified above, we have provided in the text and tables indications for when to refer the patient for medical or surgical evaluation. In keeping with the evidence-based practice paradigm, we have attempted to provide, where available, data on reliability and validity of history items and physical tests by way of a Medline search over the period 1995 to April 2006 of English-language articles with a title containing search terms relevant to these tests and items. The complete list of search terms is available upon request from the authors. In addition, we performed a hand search of articles in our personal libraries. Our recommendations for referral throughout the text are based to the maximum extent possible on psychometric properties of the tests and measures. However, data on diagnostic accuracy of the history items and physical tests are often absent, contradictory, or insufficient for confident diagnostic decision making.

The therapist should also be guided by an analysis of the risk of harm to the patient should the therapist decide not to refer. At times, it is better to refer the patient and have the patient found normal than to not refer and do potential harm. Considering the patholo-gies possibly responsible for complaints of dizziness, the potential for harm is real and present when working with this population. Clearly documenting the reason for a medical or surgical referral based on the infor-mation presented in this article will clarify the need for referral and allow for better communication with our medical colleagues. Any uncertainty regarding the proper diagnosis should result in referral. But even if the signs and symptoms appear to fit with a diagnosis amenable to sole physical therapy management, the patient’s failure to respond to seemingly appropriate conservative measures also indicates the need for a medical second opinion.95

In summary, the decision to refer the patient for a medical or surgical evaluation is based on our findings, the interpretation of such findings in light of data on diagnostic accuracy of history items and physical tests, an analysis of the risk of harm to the patient, and the response to seemingly appropriate intervention.

HISTORYOur literature search located no studies that dis-

cussed the reliability or validity of history items. History taking with patients complaining of dizziness is com-plex. Table 13 provides a suggested patient self-report intake questionnaire and Table 14 contains a template for a structured interview.

Table 13. Patient Self-report Intake Questionnaire*

Patient Name_________________________________________ Age__________ Gender M/F

MEDICAL HISTORYHave you in the past been diagnosed with or do you currently have (check all that apply):m Head traumam Neck traumam Inner or middle ear infectionm Middle ear surgerym Inner ear degenerationm Recent upper respiratory infectionm Recent bacterial infectionm Syphilism Tuberculosism Rheumatoid arthritism Crohn diseasem Polyarteritis (autoimmune disease affecting the arteries)m AIDSm Recent chicken poxm Recent mumpsm Recent poliomyelitism Mononucleosis (Epstein-Barr, mono)

m Recent viral infectionm Recent inoculationm Multiple sclerosism Lung cancerm Ovarian cancerm Hodgkin disease (lymphatic cancer)m Breast cancerm Heart diseasem Chronic obstructive lung diseasem Atherosclerosis (hardening arteries)m Thromboembolic disease (blood clots)m Neck degenerationm Recurrent episodes of vertebrobasilar ischemia (limited blood supply to the brain)m Visual impairmentsm Migraine or migraine-related disordersm Joint replacement in the legm Other orthopaedic surgical procedure

20

SymptomsSymptom description

A description of dizziness symptoms may be help-ful for initial classification into 1 of the 4 dizziness subtypes of vertigo, presyncope, dysequilibrium, and other dizziness. Vertigo is often described as a spinning or rotating sensation, a sensation of self-movement or of the environment moving, whereas patients with presyn-copal dizziness complain of lightheadedness, a sense of impending fainting, or tiredness. Patients with dysequi-librium may complain of unsteadiness and weakness. Patients who fall into the subtype of other dizziness may report anxiety, depression, or fatigue. However, patients commonly have difficulty describing their symptoms. The above classification system is also challenged when an individual complains of symptoms fitting more than 1 subtype, as may be the case in older adults with mul-tisystem impairment.51 However, symptom description

indicating presyncopal and other dizziness may indicate the need for referral.

VertigoAn illusion of rotary movement implicates the SCC.67

Rotary vertigo is a symptom in most peripheral ves-tibulopathies. An illusion of linear movement, arguably not true vertigo, indicates a lesion involving the otolith organs but can also occur in patients with a perilym-phatic fistula.67 Vertigo as a result of peripheral lesions is often severe, intermittent in nature, and of a shorter duration than vertigo due to a central lesion. A central lesion often produces constant but less severe vertigo.43 Vertigo is a symptom in patients with BPPV, Ménière disease, acute peripheral vestibulopathy, otosclerosis, toxic vestibulopathies, and autoimmune disease of the inner ear.43,57 It is less common in patients with cerebel-lopontine angle tumors or acoustic neuropathy.43 Vertigo

Have you recently:m Been in contact with rodents (mice, guinea pigs, hamsters)m Gone divingm Gone for a long train ridem Had your neck manipulated

Has a member of your family ever been diagnosed with or does a family member currently have (check all that apply):m Familial paroxysmal ataxiam Ménière diseasem Otosclerosism Migrainem Vertebrobasilar migraine

Have you used or are you currently using (check all that apply):m Alcoholm Amikacinm Angel dustm Antidepressantsm Antihypertensivesm Aspirinm Barbituratesm Benzodiazepinesm Bromocriptinem Butyrophenonesm Cis-platinumm Digitalism Diureticsm Ethchlorvynol

How many different medications are you using in total on a daily basis? ____________Are you taking the medication as prescribed? Y/N

* Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and Manipulative Therapy.

m Gentamicinm Heroinm Isoniazidm Kanamycinm Levodopam Meprobamatem Methaqualonem Methyldopam Metoclopramidem Monoamine oxidase (MOA) inhibitorsm Nitroglycerinm Phencyclidinem Phenothiazines

Table 13. Continued.

m Phenytoinm Potassiumm Procainamidem Propranololm Pyridoxinem Quinidine m Quininem Reserpinem Streptomycinm Taxolm Tetrabenazinem Tobramycinm Tricyclic antidepressants

m Gone flyingm Coughed, sneezed, or strained forcefullym Lifted very heavy itemsm Gone on a boat trip

m Coronary artery diseasem Peripheral vascular diseasem Spinocerebellar ataxiam Friedreich ataxiam Ataxia-telangiectasia

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Patient Name__________________________________________________________ Date______________________

Symptom description _______________________________________________________________________________________________________________________________________________________________________________ m Vertigo m Presyncopal dizziness

Symptom onset m Sudden m Insidious_________________________________________________________________________________________________________________________________________________________________Precipitating factors m Constant m Intermittent m Episodic_______________________________________________________________________________________________________________________________________________ m Transfer sitting to supine position m Rolling over in supine m Head flexion and extension m Transfer supine to sitting position m Any head movement m Caffeine m Exercise m Alcohol m Emotional stimuli m Pain m Fatigue m Fear

Prodromal symptoms Y/N Duration__________________________________________________________________ m Lightheadedness m Pallor m Salivation m Blurred vision

Symptom latency Y/N Duration_____________________________________________________________________Symptom duration m 30-60 sec____________________________________________________________________Symptom fatigability Y/N__________________________________________________________________________Associated symptoms m Ataxia_____________________________________________________________________________________ m Hearing loss: m Sudden onset m Fluctuating m Progressive m Left m Right m Both____________________ m Tinnitus: m Left m Right m Both _____________________________________________________________ m Sensation of fullness in the ear: m Left m Right m Both____________________________________________ m Nausea____________________________________________________________________________________ m Vomiting___________________________________________________________________________________ m Dysarthria__________________________________________________________________________________ m Pain_______________________________________________________________________________________ m Headache in combination with neck pain m Unilateral and pulsating headache m Sudden onset neck and occipital pain m Chest, neck, and arm pain m Sensory abnormalities_______________________________________________________________________ m Perioral numbness and paresthesia m Unilateral facial paresthesia m Strength___________________________________________________________________________________ m Facial weakness m General fatigue m Chronic fatigue

m Dysequilibriumm Other dizziness

m Prolonged standingm While recumbent and motionlessm Wearing tight collarm Hyperventilationm Coughingm Urinationm Rapid rising from sittingm Prolonged neck extension-rotationm Menstrual periodm Arm activitym Anxiety

m Tachycardiam Visual auram Other neurological aura

m Tonsillar pillar or external ear pain with swallowing, talking, or coughing

m Abdominal pain

m Quadrilateral paresthesiam Trigeminal distribution paresthesia

m Transient quadriplegiam Arm fatigue-paralysism Generalized arm and leg weakness

Table 14. Patient History Form*†

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m Visual abnormalities___________________________________________________________________________ m Loss of color vision m Visual field deficits m Constant diplopia m Tilt illusion m Mental and psychological status_________________________________________________________________ m Decreased cognition m Acute confusion m Memory deficits m Other________________________________________________________________________________________ m Diaphoresis m Hot flushed skin m Myoclonus m Muscular twitching m Spastic bladder m Discharge from the ear m Thirst m Polyuria m Polyphagia m Unexplained weight loss m Palpitations m Shortness of breath

Current history___________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________Diagnostic tests______________________________________________________________________________________________________________________________________________________________________________________Occupation________________________________________________________________________________________Leisure time________________________________________________________________________________________Social history N/A __________________________________________________________________________________General health Unexplained weight loss +/- Night pain +/- Consistent pattern of night pain +/- Loss of appetite +/- Other_____________________________________________________________________________________________

* Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and Manipulative Therapy.

†Reason for referral indicated in italics.

m Blurry visionm Diplopia with head movementm Photophobia

m Stuporm Anxietym Depression

m Coughingm Cyanosism Edema legsm Claudicationm Feeling of chokingm Feeling of unrealitym Fear of losing controlm Fear of dyingm Insomniam Gastroesophageal refluxm Drop attacksm Remitting-relapsing neurological dysfunction

Table 14. Continued.

may only be episodic in patients with a perilymphatic fistula in case of a low-volume leak but can be severe in patients with a large fistula.41 Vertigo also occurs in the diseases causing brainstem hypoperfusion (eg, VBI, vertebrobasilar infarction, basilar-type migraine, verte-brobasilar migraine, vestibular migraine, and subclavian steal syndrome).43,57,60,64,69,71,72 Any complaint of vertigo other than intermittent, severe, rotary, short-lasting ver-tigo likely indicates a need for referral.

AtaxiaAtaxia is a dyscoordination or clumsiness of movement

not associated with muscular weakness.43 It is a symptom in patients with cerebellar tumors and subclavian steal

syndrome.43 Ataxia may affect gait in patients with hy-pothyroidism, paraneoplastic cerebellar degeneration, ataxia-telangiectasia, Arnold-Chiari malformation, VBI, and myelopathy.43,64,76-78 Gait ataxia is the presenting symptom in all patients with hereditary spinocerebellar degenerations. It is also the most common finding in patients with alcoholic cerebellar degeneration and the presenting complaint in 10% to 15% of patients with multiple sclerosis. Trunk ataxia is a symptom in patients with ataxia-telangiectasia and Creutzfeldt-Jakob disease; these 2 diseases also produce limb ataxia, as does para-neoplastic cerebellar degeneration.43 In addition, 10% of patients with Wernicke encephalopathy present with ataxia of the arms while 20% present with ataxia affect-

23

Patient Name___________________________________________________________ Date___________________

OBSERVATIONSkin m Red spider veins on ears and cheeks m Dry skin m Brittle hair m Lemon-yellow discoloration skin m Papilledema m Clubbing fingernails m Trophic changes skin m Peripheral edemaPosture m Increased kyphoscoliosis m Craniocervical junction abnormalities m Lateral head tilt m Forward head postureEyes m Pigmented corneal rings m Red spider veins corner of the eyes m Vertical misalignment L high m Vertical misalignment R high m Horizontal misalignment m Horner syndrome m Corrective lateral head tilt when covering one eye in case of vertical misalignmentOther________________________________________________________________________________________

VITAL SIGNSBlood pressure m Arm systolic difference (≥45 mm Hg) +/-_______________________________________Heart rate m Palpitations +/-______________________________________________________________Sit-to-stand test m Blood pressure (decrease ≥20 mm Hg) +/- m Heart rate (increase ≥20 bpm) +/- m Lightheadedness____________________________________________________________Auscultation m Carotid bruit +/- m Cardiac abnormalities +/-____________________________________

GAIT ASSESSMENT_________________________________________________________________________________________________________________________________________________________________________m Wide-based gaitm Titubationm Unilateral deviation when walking a straight linem Unable to walk tandem gait

VESTIBULOSPINAL EXAMINATIONSingle-leg stance m L ______sec m R ____sec_______________________________________________Romberg m Eyes open________________________ m Eyes closed ______________________Sharpened Romberg m Eyes open________________________ m Eyes closed ______________________CTSIB m Level, eyes open___________________ m Level, eyes closed_________________ m Foam, eyes open___________________ m Foam, eyes closed_________________Fukuda step test m Rotate >30° +/- m Rotate L/R m Forward displacement >50 cm +/-

CRANIAL NERVE EXAMINATION_______________________________________________________________

Cranial nerve Test L/RI. Olfactory Identify different odors + -II. Optic Test visual fields (confrontation method) + -III. Oculomotor Upward, downward, and medial gaze + -IV. Trochlear Downward and lateral gaze + -V. Trigeminal Corneal reflex, face sensation, clench teeth + -VI. Abducens Lateral gaze + -VII. Facial Close eyes tight, smile, whistle, puff cheeks + -VIII. Vestibulocochlear Hear watch ticking, hearing tests, balance tests + -IX. Glossopharyngeal Gag reflex, ability to swallow + -X. Vagus Gag reflex, ability to swallow, say “ahhh” + -XI. Accessory Resisted shoulder shrug + -XII. Hypoglossal Tongue protrusion (observe for deviation) + -

m Steppage gaitm Improved gait with assistive devicem Difficulty with concurrent head rotationm Wildly lurching without loss of balance

Table 15. Patient Physical Examination Form*†‡

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OCULOMOTOR EXAMINATIONSpontaneous nystagmus central gaze +/-________________________________________________________m Jerkm Pendularm Horizontal m L m Rm Vertical m Up-beating m Down-beatingm TorsionalSpontaneous nystagmus eccentric gaze +/-________________________________________________m Increased with looking towards fast phasem Horizontal nystagmusSaccadic eye movements +/-______________________________________________________________m Hypometriam Hypermetriam Horizontal saccades with vertical testSmooth pursuit testing +/-________________________________________________________________

HEARING EXAMINATIONWeber test m Midline m L m RRinne test m Bone conduction > air conduction m Bone conduction ≤ air conduction

ACTIVE RANGE-OF-MOTION EXAMINATION Asterixis +/- Myoclonus +/- Chorea +/-________________________________________________________________________________________________________________________________________________________________________________________________________________________

LIMB ATAXIA EXAMINATIONFinger-to-nose test m Intention tremor L+/R+/- m Overshooting L+/R+/-Finger-to-finger-test m Horizontal overshooting L+/R+/- m Vertical overshooting L+/R+/-Heel-to-shin test m Intention tremor L+/R+/- m Overshooting L+/R+/-Toe-to-finger test m Intention tremor L+/R+/- m Overshooting L+/R+/-Dysdiadochokinesia m Finger tapping +/- m Pronation-supination +/- m Toe tapping +/-Barre test L+/R+/-________________________________________________________________________________

PASSIVE RANGE-OF-MOTION EXAMINATION Hypotonia +/- Rigidity +/- Spasticity +/- Clonus +/-______________________________________________________________________________________________________________________________________________________________________________________________Stability tests____________________________________________________________________________________PPIVM/PAIVM__________________________________________________________________________________

STRENGTH EXAMINATION ____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

REFLEX EXAMINATION Hoffman reflex L+/R+/- Babinski sign L+/R+/- DTR_____________________________________________________________________________________________________________________________

SENSATION TESTS______________________________________________________________________________m Joint position sense__________________________________________________________________________m Vibration sense_____________________________________________________________________________

VERTEBROBASILAR EXAMINATIONDe Kleyn-Nieuwenhuyse test L+/R+/-______________________________________________________m Latency 0 _____sec m >60 secm Duration 0 ____ sec m Nonaccommodatingm Fatigable Y/Nm Horizontal nystagmusm Torsional nystagmus

m Skewm Alternating m Periodic m Irregularm Suppressed with visual fixation m Yes m Nom Suppressed by convergencem Increased by fixation

m Provoked on lateral or upward gazem Small, unsustained eye movements at end range

m Saccades during fixation on targetm Oscillating horizontal saccades with gaze shift

m Vertical down-beating nystagmusm Other nystagmusm Geotropicm Apogeotropic

Table 15. Continued.

25

Sustained cervical rotation test L+/R+/-___________________________________________________________m Latency 0 _____sec m >60 secm Duration 0 ____ sec m Nonaccommodatingm Fatigable Y/Nm Horizontal nystagmusm Torsional nystagmusHautant test m Midrange +/- m Extension-rotation L+/R+/- m Latency with + extension-rotation position Y/N

VESTIBULO-OCULAR EXAMINATIONDynamic visual acuity Decrease by ≥2 lines on Snellen chart +/-____________________________________Autorotation test Inability to continue for 60 sec +/- <100 oscillations in 60 sec +/-____________________Doll’s head test Catch-up saccades toward fixation target +/-________________________________________Head-shaking nystagmus test +/ - m Nystagmus toward side of lesion m Nystagmus away from side of lesion m Nonhorizontal nystagmusHead thrust test +/- m Corrective saccade on head moving right m Corrective saccade on head moving left

BPPV EXAMINATIONHallpike-Dix L+/R+/-___________________________________________________________________________m Positive bilateral m L < R m L > Rm Latency 0 _____sec m >60 secm Duration 0 ____ sec m Nonaccommodatingm Fatigable Y/Nm Horizontal nystagmusStraight head-hanging test +/-___________________________________________________________________m Latency m _____sec m >60 secm Duration m ____ sec m Nonaccommodatingm Fatigable Y/Nm Horizontal nystagmusRoll test +/-_________________________________________________________________________________m L < Rm L > Rm Latency 0 _____secm Duration 0 ____ secm Fatigable Y/Nm Horizontal nystagmusWalk-rotate-walk test L+/R+/-_________________________________________________________________

CERVICOGENIC DIZZINESS EXAMINATIONNeck torsion test L+/R+/-________________________________________________________________m Latency m Immediate m_____secm Duration m ____ secm Fatigable Y/Nm Horizontal nystagmus

BREATHING-RELATED TESTSHyperventilation test m Dizziness +/- m Nystagmus +/- m Minimal latency +/- Latency _____secValsalva test m Dizziness +/- m Nystagmus +/- m Minimal latency +/- Latency _____secCough test m Dizziness +/-

* Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and Manipulative Therapy.

†Reason for referral indicated in italics.‡ CTSIB indicates Clinical Test of Sensory Integration of Balance; PPIVM, passive physiological intervertebral motion; PAIVM, passive accessory intervertebral motion; and BPPV, benign paroxysmal positional vertigo.

m Vertical down-beating nystagmusm Other nystagmusm Geotropicm Apogeotropic

m Torsional nystagmusm Vertical down-beating nystagmusm Other nystagmusm Geotropicm Apogeotropic

m Torsional nystagmusm Vertical down-beating nystagmusm Other nystagmus

m Torsional nystagmusm Vertical down-beating nystagmusm Other nystagmusm Geotropicm Apogeotropic

m Torsional nystagmusm Vertical down-beating nystagmusm Other nystagmus

Table 15. Continued.

26

ing the legs.43 A patient report of ataxia confirmed by physical tests indicates a need for referral.

Hearing lossA sudden onset of unilateral deafness may be due

to labyrinthine artery infarction, possibly indicating an infarction in the vertebrobasilar system.42 A rapid loss of perilymphatic fluid due to a perilymphatic fistula will produce hearing loss, but hearing may be normal in the case of a low-volume leak.41 Ménière disease produces a fluctuating low-frequency hearing loss, which is progres-sive over multiple episodes.43,98 Autoimmune disease of the inner ear also produces a fluctuating hearing loss.57 Progressive unilateral hearing loss is also a typical pre-sentation of patients with acoustic neuromas.99 Hearing loss is also a symptom in patients with acute labyrinthi-tis, quinine or quinidine toxicity, salicylate overdosage, Friedreich ataxia, otosclerosis, vestibulocochlear nerve compression due to bacterial, syphilitic, or tuberculous infection or due to sarcoidosis, Paget disease, diabetes mellitus, hypothyroidism, and in 50% of patients treated with the chemotherapeutic drug Cis-platinum.43,98 Any previously undiagnosed complaint of hearing loss, espe-cially when confirmed by physical tests, indicates a need for referral.

TinnitusTinnitus may occur in patients with Ménière disease

as does a feeling of fullness of the ear.41,43,98 Tinnitus also occurs in patients with Cis-platinum and salicy-late toxicity and in patients with familial paroxysmal ataxia.43,57 Tinnitus can also be more benign, resulting from increased tone in the tensor tympani muscle due to trigeminal hyperactivity associated with an upper cervi-cal injury.100 A complaint of tinnitus combined with aural fullness, a positive medication history, or a family history positive for familial paroxysmal ataxia indicates a need for referral.

NauseaNausea is common in patients with BPPV, Ménière

disease, acute peripheral vestibulopathy, salicylate overdosage, quinine or quinidine overdosage, cerebel-lar tumors, Arnold-Chiari malformation, migraine, or VBI.41,43,52,64 It can also be indicative of panic disorder.50,84 A positive family history for Ménière disease or a positive medication history in combination with nausea indicates a likely need for referral.

VomitingVomiting may be a symptom for patients with Mé-

nière disease, acute peripheral vestibulopathy, salicylate overdosage, quinine or quinidine overdosage, cerebellar tumors, Arnold-Chiari malformation, and vertebrobasilar migraine.41,43,57 The occurrence of vomiting in patients with BPPV is rare.52,55 Vomiting, headache, ataxia, and visual dysfunction are often the presenting symptoms in children with primary cerebellar tumors and a clear

indication for referral.43 A complaint of vomiting with dizziness may indicate a need to refer in adults and constitutes a clear reason for referral in children.

DysarthriaDysarthria can be a symptom in patients with hy-

pothyroidism, paraneoplastic cerebellar degeneration, Friedreich ataxia, ataxia-telangiectasia, Creutzfeldt-Jakob disease, familial paroxysmal ataxia, VBI, Arnold-Chiari malformation, and vertebrobasilar migraine.43,57,58,64 A complaint of dysarthria indicates the need for referral.

PainHeadache is a symptom in patients with cerebel-

lopontine angle and cerebellar tumors, salicylate over-dosage, Arnold-Chiari malformation, familial paroxys-mal ataxia, and cervicogenic dizziness.17,43,57 In fact, a correlation between neck pain and dizziness is one of the diagnostic criteria for cervicogenic dizziness.17 Suboccipital and neck pain described as a tight collar and aggravated by neck movements and burning pain along the ulnar arm may indicate posterior fossa mal-formation with compression at the foramen magnum.58 A unilateral pulsatile headache may be indicative of migraine.43,60 A sudden-onset neck and occipital pain is the hallmark symptom of vertebral artery dissection.69,70 Occipital headache is a symptom of vertebrobasilar mi-graine.57 Chest, neck, and arm pain or discomfort may be symptoms implicating a cardiovascular etiology for patients complaining of presyncopal dizziness.59 Chest pain may also occur in patients with panic disorder.50,84 Paroxysmal pain in the tonsillar pillar or external ear with swallowing, talking, or coughing implicates glos-sopharyngeal neuralgia as a cause for presyncopal dizziness.43,98 Variable patterns of arm, leg, and trunk pain can be a symptom in patients with myelopathy.76-78 Abdominal pain may occur due to quinine or quinidine toxicity.43 In the context of evaluating patients with diz-ziness, any pain pattern other than those indicative of cervicogenic dizziness-related neck pain and musculo-skeletal pain possibly associated with musculoskeletal impairments causing dysequilibrium indicates a need for referral.

Sensory abnormalitiesPerioral numbness and paresthesia are symptoms in

patients with hyperventilation but also occur in patients with VBI.43,64 Limb paresthesia is also a symptom for pa-tients with vertebrobasilar migraine.57 Bilateral or quad-rilateral limb paresthesia, either constant or reproduced or aggravated by neck movements, may indicate VBI.4 Arm paresthesia is common in patients with subclavian steal syndrome.43 Nondermatomal sensory impairments are indicative of myelopathy.76-78 Paresthesia along the spine that occurs with neck and trunk flexion may indi-cate a compressive lesion at the foramen magnum.58 Pe-ripheral neuropathy in the lower extremities commonly occurs in persons with diabetes, resulting in impaired

27

somatosensory function.101 Paresthesia in the trigeminal nerve distribution may occur with cervicogenic dizzi-ness, indicating involvement of the trigemino-cervical nucleus.63 Trigeminal distribution (facial) and nonder-matomal patterns of paresthesia indicate the need for careful evaluation and possible referral.

Strength and enduranceFacial weakness is a symptom in patients with cer-

ebellopontine angle tumor and familial paroxysmal ataxia.43,57 General fatigue occurs in patients with dia-betes or cardiovascular etiologies for presyncopal dizzi-ness complaints.59,62 Chronic fatigue is also a symptom of panic disorder.50,84 Transient quadriplegia is a rare symptom in patients with vertebrobasilar migraine.57 Ipsilateral arm fatigue or even paresis is indicative of subclavian steal syndrome.43 Nonmyotomal weakness in the legs and arms may indicate myelopathy; generally, complaints of weakness may focus the clinician on a musculoskeletal impairment as causative or contributory to the patient’s complaint of dizziness or dysequilibrium. Any weakness not directly related to a discrete musculo-skeletal problem indicates a need for referral.

Visual abnormalitiesQuinine and quinidine toxicity may cause vision

deficits, including the loss of color vision.43 Visual dysfunction is often one of the presenting symptoms in children with primary cerebellar tumors.43 Visual field deficits may indicate vertebrobasilar infarction.69 Blurred vision may be a prodromal symptom for vasovagal syncope.41,43 Visual instability with head movement or oscillopsia suggests an impaired vestibulo-ocular reflex and is indicative of vestibular system involvement.102 A tilt illusion or deviation of the subjective visual vertical axis may indicate otolith dysfunction; however, it can also be caused by ischemia or infarction in the vertebro-basilar system and its branches, unilaterally affecting the vestibular nuclei, the medial longitudinal fascicle, and other nuclei involved in the vestibular mechanism, or the thalamus.92 Nonvestibular disorders can also cause a tilt illusion; third and fourth cranial nerve palsies may be responsible for monocular tilts of the subjective visual vertical.103 In general, nonvestibular causes for a tilt of the subjective visual vertical result in minor and unpre-dictable changes as compared to vestibular disorders.103 Otolith dysfunction or pathological processes in the oto-lith-ocular reflex pathways involving central processes can result in patients complaining of vertical diplopia or sometimes diplopia, where one image is tilted in relation to another.67 Diplopia is also a symptom in patients with paroxysmal familial ataxia, VBI, and subclavian steal syndrome.43,57,64 Visual auras can precede vertebrobasi-lar migraine; 10% of patients with migraine experience a visual or other neurological aura.43,57 Photophobia is another symptom in patients with migraine.43 Any report of visual abnormality, with the possible exception of oscillopsia, indicates a need for referral.

Mental and psychological statusChanges in mental and psychological status may be

noted by the patient or by people close to the patient. Dementia is a state in which there is a significant loss of intellectual capacity and cognitive functioning, lead-ing to impairment in social or occupational functioning or both.104 Wilson disease, Creutzfeldt-Jakob disease, hypothyroidism, paraneoplastic syndromes, and some spinocerebellar degenerations may cause dementia in association with ataxia. Dementia with sensory ataxia may indicate neurosyphilis or vitamin B12 deficiency. An acute confusional state with ataxia may occur with alcohol, sedative, salicylate, or hallucinogen intoxica-tion, or in patients with Wernicke encephalopathy. Korsakoff anamnestic syndrome and cerebellar ataxia are associated with chronic alcohol abuse. Lassitude is common in patients with migraine.43 Confusion and stupor can result from vertebrobasilar migraine.57 Anxiety and depression may be indicative of dizziness due to panic disorder.50,84 In one study, depression and panic disorder were present in 50% of patients with initially organic vestibular hypofunction 3 to 5 years after onset, leading Tusa105 to suggest that psychological disturbances that develop due to vestibular disorders may become the primary cause of dizziness, replacing the initial organic cause. Eckhardt-Henn et al86 reported that 15.8% of 190 patients complaining of dizziness fell into this category of psychosomatic dizziness. Standardized measures with established reliability and validity, such as the Mini-Men-tal State Examination106 and the Beck Depression Inven-tory107 may facilitate communication with a physician when referring a patient for further medical evaluation. Any noted mental or psychological abnormality indicates the need for referral.

Other symptomsDiaphoresis is a symptom in patients with acute

labyrinthitis, quinine or quinidine toxicity, and panic dis-order.41,43,50,84 Patients with quinine or quinidine toxicity may indicate hot and flushed skin.43 Fever is a symptom of familial paroxysmal ataxia.57 Myoclonus may occur in patients with Creutzfeldt-Jakob disease; hyperventila-tion is associated with muscular twitching.43 A spastic bladder can be caused by myelopathy.76-78 Patients with undiagnosed skull fractures may note discharge from the ear.43 Extrapyramidal signs and symptoms may occur in Creutzfeldt-Jakob disease.43 Carpal tunnel syndrome, myelopathy, and neuropathy may raise suspicion of hypothyroidism in undiagnosed patients.43 The clinician may suspect multiple sclerosis with a history of remitting and relapsing dysfunctions in multiple locations in the nervous system.43 Salicylate toxicity and diabetes melli-tus may cause excessive thirst.43,62 The clinician may also suspect undiagnosed diabetes in cases of polyuria, poly-phagia, and unexplained weight loss.62 Palpitation and shortness of breath are symptoms in both patients with cardiovascular disease and panic disorder.50,59,84 Patients with cardiovascular disease may also note coughing,

28

cyanosis, edema in the legs, and claudication,59 whereas patients with panic disorder may complain of a feeling of choking, a feeling of unreality, fear of losing control or dying, insomnia, and gastroesophageal reflux.50,84 Unremitting hiccups may indicate a posterior fossa mal-formation.58

Pettman4 noted that drop attacks, defined as buckling of the legs in response to neck movements without loss of consciousness, may indicate VBI. Due to the ischemic etiology of VBI, the authors would expect true vertebro-basilar compromise due to neck movement to have a slow onset that is progressive with sustained neck position and that causes presyncopal dizziness or actually results in loss of consciousness. In the authors’ clinical experience, a drop attack may occur with neck motion in patients with traumatic, degenerative, or disease-related upper cervical instability. Although the resultant shear forces certainly would seem to have the potential of mechani-cally compromising the vertebral artery, the typical drop attack seems more likely related to cord compromise in this region. With a patient report indicative of drop attacks, we also need to consider a vestibular etiology as discussed above. Vestibular drop attacks or otolithic crises of Tumarkin occur without warning and are not as-sociated with vertigo, loss of consciousness, numbness, or paralysis.89 A patient report of any of the symptoms above indicates the need for referral.

Symptom behaviorSymptom onset

The initial episode of Ménière disease has an insidious onset, with the patient first noticing tinnitus, hearing loss, and a sensation of fullness in the ear.43 Most symptoms in patients with central vestibular disorders are the result of slowly progressive pathologies and thus have an insidious onset. The onset of symptoms in patients complaining of dysequilibrium is also generally insidious. The onset of dizziness and other symptoms is sudden in patients with acute peripheral vestibulopathy, aminoglycoside toxicity, labyrinthine damage due to head trauma, and large perilymphatic fistulae, and in pa-tients suffering subsequent attacks of Ménière disease.41,43 Presyncopal dizziness usually is sudden in onset when precipitating activities are performed. Landsickness and mal de debarquement syndrome are often brought on by sea, air, or train travel.80 An abrupt onset is also charac-teristic of patients with symptoms due to panic disorder.50 An insidious onset of vertiginous dizziness and an abrupt onset of presyncopal or other dizziness indicate a need for referral.

Precipitating factorsDizziness is often constant in patients with central and

bilateral peripheral vestibular lesions.43,67 Other forms of dizziness are intermittent and precipitated by positioning, movement, or other stimuli. Patients with posterior SCC BPPV complain of dizziness when they quickly transfer to a supine position, especially when the head is turned

to the affected side.52 This also occurs in patients where the anterior SCC is involved, but there is less specific-ity as to the direction of head rotation.108 Dizziness is brought on in patients with horizontal SCC BPPV when rolling over in supine, but it can also occur with flexion and extension of the head or when transferring from supine to upright.56 Head movement may also provoke symptoms in patients with cervicogenic dizziness.17

Dizziness in patients with otosclerosis may be po-sitional but can also be constant.43 Attacks of familial paroxysmal ataxia can be triggered by exercise, caffeine, alcohol, or sudden movements.57 A vasovagal presyn-cope can be brought on by emotional stimuli, pain, the sight of blood, fatigue, medical instruments, blood loss, or prolonged motionless standing,41,43 and it usually oc-curs when the patient is in a sitting or standing position; only very rarely is the patient recumbent.43,98 A patient complaining of presyncopal dizziness while recumbent or after physical exercise should be screened for a car-diovascular etiology.43 Carotid sinus syndrome has been related to wearing collars that are too tight or may be due to local tumors in the neck pressing on the carotid sinus.43,98 In patients with Takayasu disease, exercise, standing, or head movements may bring on dizziness.43 Hyperventilation and coughing may bring on hyperven-tilation and cough presyncope, respectively.43 Dizziness due to micturition syncope may occur before, during, or after micturition.43 Orthostatic hypotension-related diz-ziness occurs when rapidly rising from a sitting position, when standing up after prolonged recumbency, or after prolonged motionless standing.41,43 A position of cervical extension and rotation is often implicated as a trigger for VBI.63 Neck manipulation has been associated with cervical artery dissection (adjusted odds ratio 3.8; 95% confidence interval 1.3-11).5 Vertebrobasilar migraine occurs frequently during the menstrual period.57 Subcla-vian steal syndrome produces symptoms with physical activity of the ipsilateral arm.74 Stress, hyperventilation, and anxiety can all produce the symptoms of dizziness associated with panic disorder.50,84 Situations commonly associated with other phobic syndromes (eg, large crowds, open spaces, driving, or crossing a bridge) can precipitate an attack of phobic postural vertigo.86 Dizzi-ness described as tilting of the environment is aggravated by rapid postural changes.87 Constant vertiginous dizzi-ness or dizziness brought on by factors other than neck or head movement indicate a likely need for referral.

Prodromal symptomsSome pathology is characterized by prodromal symp-

toms, which occur after encountering the precipitating stimulus but before the symptoms of dizziness. Prodromes lasting 10 seconds to a few minutes and consisting of lightheadedness, pallor, salivation, blurred vision, and tachycardia often precede a vasovagal syncope.41,43 A visual aura may precede migraine, basilar-type migraine, and vertebrobasilar migraine;57,71 10% of patients with migraine report a visual or other neurological aura.43

29

Any report of prodromal symptoms indicates a need for referral.

Symptom latencySymptom latency refers to the time lapsed between

exposure to the precipitating stimulus and the onset of symptoms. Symptoms in patients with BPPV occur after a latency period of 1 to 5 seconds.52,53 The latency pe-riod in patients with VBI is long; Oostendorp8 reported a latency period of 55 ± 18 seconds after assuming the De Kleyn-Nieuwenhuyse test position. One could assume that patients with subclavian steal syndrome also have a longer latency period; sufficient ischemia needs to develop before symptoms occur. Depending on the eti-ology, a vertebrobasilar infarction may be rapidly or very slowly progressive.64 Onset of symptoms is immediate in patients with cervicogenic dizziness upon assuming the provoking position.53 A prolonged latency period (more than 60 seconds) indicates a likely need for referral.

Symptom durationAs noted before, dizziness symptoms in patients with

central vestibulopathies are generally less severe but constant and prolonged; symptoms with peripheral ves-tibulopathies are often severe but intermittent.43 Symp-toms in patients with BPPV generally last less than 30 seconds but may occur for up to 60 seconds.53 Vertigo may last from minutes to days in patients with Ménière disease.41,43,98 In patients with acute peripheral vestibu-lopathy, vertigo may be constant for up to 2 weeks.43 Symptoms in patients with familial paroxysmal ataxia last from 15 minutes to several hours.57 The average symptom duration for patients with basilar-type migraine is 20 to 30 minutes.71 Symptoms last for up to 72 hours in patients with vertebrobasilar migraine.57 On average, vertigo and auditory symptoms last from a few minutes to several hours in patients with vestibular migraine.72 Symptoms in patients with VBI and subclavian steal syn-drome are progressive and nonaccommodating until the precipitating postures or activities are discontinued.53,74 One could assume that, based on the pathophysiology, the other types of presyncopal dizziness will behave similarly. The duration of symptoms in patients with cervicogenic dizziness is usually brief after assuming the provoking position, although symptoms have been reported as lasting minutes to hours.17,53 Dizziness and other symptoms in patients with panic disorder have an abrupt onset and peak in about 10 minutes.50 Symptom duration of longer than 60 seconds and nonaccommo-dating forms of dizziness indicate the need for referral.

Symptom frequencyDizziness associated with precipitating factors is,

of course, recurrent in nature depending on exposure to those factors, as discussed above. Dizziness and other symptoms are episodic in patients with Ménière disease, otosclerosis, perilymphatic fistulae with low-volume leaks, migraine, vertebrobasilar migraine, panic

disorder, and phobic postural vertigo.41,43,50,86,98 We have already discussed the constant symptoms in patients with central vestibular lesions.6,43 Episodic bouts of dizziness indicate a likely need for referral.

Symptom fatigabilityFatigability of symptoms refers to the decrease in symp-

toms of vertigo and nystagmus with repeated position-ing.108 It is characteristic for cervicogenic dizziness and BPPV.53 Nonfatigable dizziness indicates a likely need for referral, even though few patients will willingly provoke dizziness repeatedly to find out about this characteristic.

Pertinent Past and Present Medical HistoryPatient demographics

Ataxia-telangiectasia has its onset before the age of 4.43 Friedreich ataxia also starts in childhood.43 Migraine and vertebrobasilar migraine also usually have their onset early in life.43,57 Prevalence of vestibular migraine is highest in the fourth decade in men and from the third to the fifth decade in women; initial presentation can occur at any age.72 Cervical artery dissection is most prevalent in sub-jects below the age of 45.5 Takayasu disease affects mainly women between the ages of 15 and 30.109 Panic disorder often first occurs in young adulthood.50 Hyperventilation most commonly affects patients between ages 20 and 40.43 The age of onset in Ménière disease is usually between 20 and 50.43 Hearing loss associated with otosclerosis generally starts before age 30.43 Cerebellopontine angle tumors have an age of onset between 30 and 60.43 The age of onset for alcoholic cerebellar degeneration is 40 to 60.43 Cough syncope is most prevalent in middle-aged men.43 Hypothyroidism is most common in middle-aged or elderly women.43 Benign paroxysmal positional vertigo generally occurs in people over age 40, and it rarely occurs in people under 20; however, peak incidence of onset for BPPV is in the sixth decade of life.54 Orthostatic hypotension is most common in people in the sixth and seventh decades.41,43 Parkinsonism is most prevalent in older adults.41,43 Vasovagal syncope as a cause of dizzi-ness can occur in all age groups.41,43 Onset of dizziness and ataxia in childhood is a strong indicator for referral.

Men are more often affected by Ménière disease, al-coholic cerebellar degeneration, orthostatic hypotension, carotid sinus syndrome, and cough syncope.41,43 Women are more often affected by hypothyroidism, migraine, vertebrobasilar migraine, and hyperventilation-induced presyncope.43,57 Mal de debarquement syndrome is most prevalent in middle-aged women.80 Takayasu disease affects only women, while micturition syncope occurs almost exclusively in men.43 Takayasu disease only affects women of Asian descent. Parkinsonism affects all ethnic groups equally.43

Medical historyPast and concurrent medical history may provide di-

agnostic or screening clues in patients with complaints of dizziness. A medical history of head trauma, labyrinthine

30

infection, surgical stapedectomy, chronic suppurative otitis media, and degenerative changes to the inner ear may indicate nonidiopathic BPPV.52,53,55 An upper-respi-ratory infection precedes acute peripheral vestibulopathy in 50% of patients.41 Acoustic neuromas are more com-mon in patients with neurofibromatosis.43 Vestibuloco-chlear nerve compression can be the result of bacterial, syphilitic, and tuberculous infection or sarcoidosis.41 Barotrauma due to diving or flying, a forceful Valsalva maneuver, or head trauma can produce a perilymphatic fistula.41,98 Head trauma can also cause occult skull fractures; a petrosal bone fracture can cause vertigo and hearing loss.43 Autoimmune diseases such as rheumatoid arthritis, Crohn disease, and polyarteritis are often con-currently present in patients with autoimmune disease of the inner ear.57 Varicella, AIDS, mumps, poliomyelitis, infectious mononucleosis, and lymphocytic choriomen-ingitis (a virus borne by rodents) can all provide the viral agent responsible for viral cerebellar infections.43 Acute cerebellar ataxia of childhood is often preceded by a viral infection or inoculation.43 Vertigo is a common symptom in patients with multiple sclerosis, albeit not often the presenting symptom.43 Epilepsy in the medical history should prompt questions about phenytoin; long-term treatment with phenytoin may produce cerebellar degeneration.43 Patients with lung cancer, ovarian can-cer, Hodgkin disease, and breast cancer are at risk for paraneoplastic cerebellar degeneration.43 Breast and lung cancer are also apt to metastasize to the posterior fossa in adults.43 A medical history positive for heart disease could imply a cardiovascular origin for presyncopal dizziness complaints.59 Chronic obstructive pulmonary disease is frequent in patients with cough-related presyncopal diz-ziness.43 Atherosclerosis, thromboembolic disease, and cervical spine trauma and degeneration have been sug-gested to predispose patients to VBI.55,65,66 However, Ru-binstein et al5 noted no correlation for cervical artery dis-section and atherosclerosis risk factors, such as cigarette smoking, oral contraceptive use, diabetes, hypertension. They noted this might have been related to comparison in their systematic review with studies on patients with ischemic stroke not related to arterial dissection. A medi-cal history of migraine did show a strong association with cervical artery dissection (adjusted odds ratio 3.6; 95% confidence interval 1.5-8.6).5 Atherosclerosis can also lead to subclavian steal syndrome.11 Recurrent episodes of VBI predispose patients to vertebrobasilar infarction.43 Cervical spine trauma and degeneration may also be the basis for cervicogenic dizziness.16,17 A recent optometry or ophthalmology report may reveal the visual impair-ments associated with complaints of dysequilibrium.75 A recent lower extremity joint replacement or other orthopaedic surgery may be the cause for dysequilibrium in the elderly patient. A history of migraine or migraine-related disorders has been associated with vestibular dysfunction.110,111 In fact, vertigo is 3 times more com-mon in patients with migraine, and there is a 30% to 50% prevalence of migraine in patients with vertigo.112

With the exception of neck trauma and degeneration and recent lower extremity joint replacement or other orthopaedic procedures, a positive medical history in the absence of signs and symptoms indicative of the 3 con-ditions amenable to sole physical therapy management discussed above may indicate the need for referral.

Family historyFamilial paroxysmal ataxia is a hereditary recurrent

form of ataxia.57 Also, 20% of patients with Ménière disease have a positive family history.41 Patients with otosclerosis, migraine, and vertebrobasilar migraine also commonly have a positive family history.43,57 Coronary artery disease and peripheral vascular disease with a possible role in producing presyncopal dizziness have a strong family history.113 Some of the spinocerebellar atax-ias are hereditary autosomal dominant diseases, while Friedreich ataxia and ataxia-telangiectasia are autosomal recessive diseases.43 A positive family history linked to relevant pathognomonic signs and symptoms constitutes a reason for referral.

Medication historyTable 16 lists prescription, over-the-counter, and

recreational drugs associated with the various subtypes of dizziness, allowing the therapist to establish whether symptom description matches the possibly causative medication use reported. A strong relationship has been established between the number of medications taken (more than 5) and dizziness symptoms.51 Careful ques-tioning may implicate such overmedication as a cause of dizziness. Noncompliance with medication may also be an issue (eg, the failure to take antidepressants in a patient with panic disorder). Additionally, the use of a particular medication may signal to the therapist a medical condition that the patient failed to report. A positive medication history with symptoms indicative of a relevant dizziness subtype (Table 16), polypharmacy, and noncompliance with prescribed medication may all constitute reason for referral.

PHYSICAL EXAMINATIONPhysical examination with the aim of differential di-

agnosis in patients complaining of dizziness requires a multitude of tests. Table 15 provides a suggested format for the physical examination. The proposed order of examination in this format is intended to safeguard previ-ously undiagnosed patients from unnecessary and poten-tially harmful physical tests by establishing the need for referral and obviating the need for further testing in case of a positive response to an earlier physical test.

ObservationSkin

Children with ataxia-telangiectasia have tiny, red spi-der veins on the ears and cheeks. Dry skin with brittle hair may indicate hypothyroidism. Vitamin B12 deficiency can cause a lemon-yellow skin discoloration. Papilledema

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due to increased intracranial pressure occurring together with dysequilibrium is indicative of an intracranial mass lesion, usually in the posterior fossa.43,58 Clubbing of the fingernails, cyanosis of lips, trophic changes of the skin, and peripheral edema could suggest a cardiovascular disorder.104,113 All abnormalities above in combination with relevant symptoms noted in the history may indicate the need for referral.

PosturePostural deviations negatively affecting the location of

the center of gravity in relation to the base of support may result in patients complaining of the dysequilibrium type of dizziness. These deviations also prompt further muscu-loskeletal examination to determine cause and potential management strategies. Postural deviations may also indicate possible pathology. Friedreich ataxia typically causes an increased kyphoscoliosis. Neurosyphilis fre-quently leads to hypertrophic or hypermobile joints with subsequent effects on posture. Craniocervical junction abnormalities can occur with Arnold-Chiari malforma-tion.43 A lateral head tilt might indicate an otolith prob-lem (tilting of the environment) or just tightness of the sternocleidomastoid or upper trapezius commonly seen

in cervicogenic dizziness,17,29 but it may also be caused by ischemia or infarction in the vertebrobasilar system.92 A forward head posture, with the head backward bent on the upper cervical spine, may cause external mechani-cal compression of the vertebral artery, thus potentially producing symptoms of VBI,63 but it may also lead to hypomobility of soft tissue and joint structures especially in the upper cervical spine, an area implicated in cervi-cogenic dizziness. We should interpret findings from a visual posture assessment with caution: Fedorak et al114 noted fair mean intrarater reliability (κ = 0.50) and poor mean interrater reliability (κ = 0.16) for visual posture evaluation using a 3-point rating scale. Craniocervical junction abnormalities and lateral head tilt may indicate the need for referral.

EyesPigmented corneal Kayser-Fleischer rings are due to

copper deposition in the cornea in patients with Wilson disease.43 Children with ataxia-telangiectasia also have spider veins in the corners of the eyes. Vertical and horizontal misalignments of the eyes may be caused by cranial nerve palsies. A skew deviation is a vertical misalignment of the eyes that is not the result of ocular

Table 16. Medications Associated With Subtypes of Dizziness*

Vertigo Presyncope Dysequilibrium Other Dizziness

AlcoholAminoglycoside antibiotics

• Streptomycin• Gentamicin• Tobramycin• Amikacin• Kanamycin

Salicylates Quinine and quinidine Cis-platinumSedative hypnotics

• Barbiturates• Benzodiazepines• Meprobamate• Ethchlorvynol• Methaqualone

Anticonvulsants• Phenytoin

Hallucinogens• Phencyclidine

Street drugs• Heroin

Mercuric and organophosphoric compounds

DigitalisQuinidineProcainamidePropranololPhenothiazinesTricyclic antidepressantsPotassiumMethyldopaAntidepressantsAntihypertensivesBromocriptineDiureticsLevodopaMonoamine oxidase (MOA)

inhibitorsNitroglycerinPhenothiazines

PhenothiazinesButyrophenonesMetoclopramideReserpine TetrabenazineAngel dust Cis-platinumIsoniazidPyridoxineTaxol

AlcoholAminoglycoside antibiot-

ics• Streptomycin• Gentamicin• Tobramycin• Amikacin• Kanamycin

Salicylates Quinine and quinidine Cis-platinum

* Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and Manipulative Therapy.

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muscle palsy.67 Skew deviation is best detected by alter-nately covering the eyes; patients with skew deviation make a vertical corrective movement in the sense of a lateral head tilt when switching the cover from the unaf-fected to the affected side. Skew deviation, head tilt, and ocular counter-rolling constitute the ocular tilt reaction.67 Unilateral lesions of the vestibular nucleus, the medial longitudinal fascicle, and other vestibular centers due to vertebrobasilar infarction can produce a full ocular tilt re-action.92 A unilateral thalamus lesion or a benign otolith dysfunction can produce a partial ocular tilt reaction.92 In patients with peripheral or vestibular nucleus lesions, the lower eye indicates the side of the lesion; lesions above the level of the vestibular nucleus present with the higher eye on the side of the lesion.67 Horner syndrome occurs in some patients with foramen magnum compressive le-sions.58 Any of these abnormalities indicates a need for referral.

Vital SignsBlood pressure

In patients with subclavian steal syndrome, a differ-ence in blood pressure between the affected and unaf-fected arm is virtually always present. On average, systolic blood pressure is 45 mm Hg lower in the arm supplied by the stenotic blood vessel.43 Symptoms indicative of subclavian steal syndrome in combination with at least 45 mm Hg lower systolic blood pressure in the symp-tomatic arm is a reason for referral. Hypertension and hypotension can contribute to dizziness symptoms.104 Monitoring the patient’s blood pressure response when transferring from a lying to a standing position is used as a diagnostic test for orthostatic hypotension. A drop in systolic blood pressure of at least 30 mm Hg or a drop of 10 mm Hg in diastolic blood pressure is indicative of orthostatic hypotension.43 Eaton and Roland41 considered a drop of 20 mm Hg in systolic or 10 mm Hg in diastolic blood pressure 2 minutes after standing indicative of orthostatic hypotension, but they also warned that blood pressure readings in elderly patients might not precisely meet those criteria. Witting and Gallagher115 established normative values; in 176 healthy subjects, systolic blood pressure decreased by 1.2 ± 9.8 mm Hg after 1 minute of standing preceded by 5 minutes of sitting. A drop in systolic blood pressure of at least 20 mm Hg had a speci-ficity of 0.97 for detecting orthostatic hypotension.115 Combined with a complaint of presyncopal dizziness, this finding warrants referral.

Heart ratePalpation of pulses may be useful in detecting a cardio-

vascular disorder. Palpitations, the presence of an irregular heartbeat, may indicate a disturbance in the heart’s abil-ity to normally conduct electrical impulses104 and may be benign or quite dangerous. Palpitations lasting for hours or irregular heartbeats accompanied by pain, shortness of breath, or lightheadedness require referral to a physician for medical evaluation.104 Similarly, tachycardia (greater

than 100 beats per minute) and bradycardia (less than 60 beats per minute) may indicate relatively benign condi-tions, such as mitral valve prolapse and athlete’s heart but may also occur in more serious conditions such as coronary artery disease and aneurysm.104,113 Monitoring pulse rate during a sit-to-stand test may also be helpful for diagnosing orthostatic hypotension. Witting and Gal-lagher115 established a normative value of a pulse rate increase of 5.3 ± 6.6 beats per minute in normal subjects and suggested an increase of at least 20 beats per minute as a positive test for orthostatic hypotension based on a sensitivity of 0.98. Combined with a complaint of presyn-copal dizziness, this finding warrants referral.

AuscultationAuscultation tests can provide information on a pos-

sible cardiovascular disorder responsible for a patient complaint of presyncopal dizziness. Lok et al116 found poor accuracy and interrater agreement for identification of some cardiac auscultation parameters. Listening for carotid bruits has been suggested as a screening tool for the likelihood of a vertebrobasilar incident with cervical manipulation.64 We earlier discussed the role of collateral (carotid) circulation in the occurrence of VBI. Terrett64 noted that the validity of carotid bruits in the diagnosis of carotid stenosis or prediction of a vertebrobasilar inci-dent is questionable. Negative auscultation results would seem to provide the therapist with a false sense of doing a relevant vertebrobasilar screening.64 In contrast, Magyar et al117 reported 56% sensitivity and 91% specificity for detection of a 70% to 99% carotid stenosis when com-pared with color duplex ultrasound. They also reported a positive predictive value of 27% of a bruit found and a 97% negative predictive value for a normal ausculta-tion. They concluded that carotid auscultation is a useful screening procedure for carotid occlusion or stenosis. In light of the possible contradictory interpretation of these values for diagnostic test accuracy for auscultation of carotid bruits and the poor values for accuracy of cardiac auscultation, positive auscultation findings indicate the need for cautious continued examination.

Gait AssessmentPatients with cerebellar ataxia have a wide-based

staggering gait, sometimes with titubation (staggering or stumbling gait) or oscillation of head and trunk.43 Uni-lateral cerebellar lesions result in a deviation toward the side of the lesion when the patient attempts to walk in a straight line. Patients with cerebellar ataxia are unable to walk in a tandem gait. In patients with sensory ataxia, gait is also wide based. Impaired proprioception may cause steppage gait. The patient lifts the feet excessively high off the ground and slaps them down rather heavily. Us-ing a cane or a railing often dramatically improves gait.43 Difficulty walking with concurrent rotation of the head in the horizontal plane may indicate a peripheral vestibular deficit. Gait unsteadiness may also be a complaint in patients with psychiatric or factitious disorders. Simon

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et al43 noted that wildly reeling or lurching movements from which the patient is able to recover without loss of balance may be indicative of conversion disorder or malingering. Recovery of balance from self-imposed extreme positions and movements, in fact, demonstrates well-developed balance function. Gait assessment can also be done quantitatively with measures such as the Tinetti Balance Scale and the Berg Balance Scale, both with established predictive validity with regard to fall risk. The former has been reported to identify 7 out 10 fallers with 70% sensitivity and 52% specificity,118 whereas the latter was able to correctly identify fallers from nonfallers with 91% sensitivity and 82% specific-ity.119 A score on either measure indicative of a low fall risk despite a complaint of dizziness and dysequilibrium may indicate kinesiophobia or movement-related fear, which can be classified under other dizziness and may indicate the need for referral. Titubation, oscillation of head and trunk, unilateral deviation when attempting to walk in a straight line, and wild reeling or lurching mo-tions without loss of balance are less likely indicators of musculoskeletal impairments and, therefore, indicators for referral.

Vestibulospinal ExaminationThe vestibulospinal reflex stabilizes the body dur-

ing head movement; thus, it is responsible for postural control. The vestibulospinal tests, in general, have poor or untested diagnostic accuracy but can serve to guide further examination by indicating the presence of pos-tural instability and by implicating the vestibular versus somatosensory system. In isolation, these tests do not affect a decision to refer or treat.

Single-leg stanceSingle-leg stance, with eyes open or closed, can be

used to screen for decreased postural control. In the acute stage of vestibular loss, a patient will be unable to perform this test; however, patients who have a compen-sated vestibular loss may test normal.120 This screening test is not specific to vestibular loss, as patients with other balance disorders may have difficulty perform-ing single-leg stance.120 A normal single-leg stance test (especially with eyes closed) precludes further vestibu-lospinal testing.

Romberg and sharpened RombergThe Romberg test (Figure 1A) challenges balance by

decreasing the base of support. Patients with sensory or vestibular dysfunction may be able to stand in a Romberg stance, but closing the eyes takes away the visual cues used to maintain balance, causing them to fall (ie, have a positive Romberg sign).43 Patients with a vestibular le-sion tend to fall in the direction of the lesion.43 Patients with cerebellar ataxia are unable to use visual cues to compensate and are unable to maintain their balance in a Romberg stance whether their eyes are open or closed.43 A normal performance on the Romberg test for

a young adult is 30 seconds, and a low normal score is 6 seconds.121 The Romberg test has predictive validity with regard to recurrent falls over a 6-month period in patients with Parkinson disease (sensitivity was 65% and specificity greater than 90%).122

A sharpened Romberg test (Figure 1B) involves stand-ing with a decreased base of support as compared to the Romberg test. The ataxic patient will prefer to stand with a wider base of support and will show reluctance when asked to stand with the feet close together. Patients with sensory ataxia are usually able to stand with the feet close together, as are some patients with vestibular lesions. These patients will compensate for the loss of somatosensory and labyrinthine input, respectively, with an increased reliance on visual input.

Figure 1. (A) Romberg test and (B) sharpened Romberg test.

A B

Modified Clinical Test of Sensory Integration of BalanceThe modified Clinical Test of Sensory Integration of

Balance assesses the contribution of the visual, vestibu-lar, and somatosensory systems to postural control. The test has 4 components: the patient standing on a level surface with the eyes open (Figure 2A), on a level sur-face with eyes closed (Figure 2B), on foam with the eyes open (Figure 2C), and on foam with eyes closed (Figure 2D). Initially, a patient will have available all sensory systems to maintain balance. The eyes-closed condition will eliminate visual contribution, putting increased demand on the somatosensory and vestibular systems. Standing on a foam surface with eyes closed alters the somatosensory input and eliminates visual input; thus, the patient has to rely mostly on vestibular input. Patients with vestibulopathy will have difficulty maintaining an upright posture.120 Platform posturography is a computer-ized version of this test with greater than 90% specificity but very low sensitivity for the diagnosis of patients with peripheral vestibular deficits. Posturography in combina-tion with other vestibular function tests has been shown to increase sensitivity to 61% to 89%.123

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Fukuda step testThe Fukuda step test (Figure 3) assesses stability

during self-initiated movement by asking the patient to march 50 or 100 steps in place with the arms raised in front to 90° and with the eyes closed. A patient with a unilateral vestibular lesion will tend to rotate greater than 30° toward the involved side.120 Forward displacement of more than 50 centimeters is also considered positive.124 These unilateral lesions include infarctions in the distri-bution of the anterior and posterior inferior cerebellar arteries.92 Bonanni and Newton125 found higher reliability for the 50-step than the 100-step protocol. Herdman and Whitney120 noted that there are many false positives and negatives. Fell124 noted that the Fukuda step test is not a test specific to vestibular lesions.

Cranial Nerve ExaminationCranial nerve palsies may be present with central

vestibular disorders and some peripheral vestibular dis-orders. A cranial nerve examination may also serve as a nonprovocative test for suspected ischemic conditions

affecting the brainstem. Obviously, the vestibulocochlear nerve can be involved in patients complaining of dizzi-ness as well as the anatomically closely related trigeminal and facial nerves.43 Optic neuropathy can be the result of multiple sclerosis, neurosyphilis, and vitamin B12 defi-ciency. A depressed corneal reflex or a facial nerve palsy on the same side as the ataxia can result from a cerebello-pontine angle tumor. Lower brainstem disease can cause tongue or palate weakness, hoarseness, and dysphagia.30 Some pathologies cause dizziness in combination with hearing loss. Table 15 contains a sample cranial nerve examination.126 Visual field confrontation testing (cranial nerve II) had low sensitivity but high specificity (97%) and positive predictive value (96%) when compared to automated perimetry,127 indicating that a confrontation-method visual field test may only have diagnostic value if positive. We found no further data on reliability and validity of the cranial nerve examination. Abnormal find-ings on the cranial nerve examination constitute a reason for referral.

Oculomotor ExaminationTo some extent, observation and the cranial nerve

examination already test oculomotor function. They also allow clinicians to note static abnormalities (strabismus) and ensure full range of movement for each eye before

Figure 3. Fukuda step test.

Figures 2A to D. Modified Clinical Test of Sensory Inte-gration of Balance.

A B

DC

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doing the oculomotor tests. No data on reliability and validity of the oculomotor examination were found.

Observation for spontaneous nystagmusNystagmus can be defined as repetitive, back-and-

forth, involuntary eye movements initiated by slow drifts away from the visual target.128 It can be classified as a pendular nystagmus, consisting of slow sinusoidal oscillations, or as a jerk nystagmus, characterized by an alternating slow drift and a quick corrective phase. In the latter type, a slow phase takes the eye away and a quick corrective phase brings it back to the target.128

The clinician first observes for spontaneous nystagmus by asking the patient to fix on a stationary target at a dis-tance of more than 2 meters.128 A spontaneous nystagmus may imply an acute peripheral vestibular lesion and, in this case, occurs due to an imbalance in the tonic firing rate of the vestibular neurons.129 The spontaneous nystag-mus following a lesion of the peripheral vestibular system is a jerk nystagmus with the quick phase indicating the unaffected side. In fact, the detectable eye movement during spontaneous nystagmus is the quick phase toward the unaffected ear.128,130 In the acute phase, patients will have difficulty reading and watching television. After the acute episode, a patient can suppress the nystagmus with visual fixation, making it difficult for the examiner to observe eye movements.129 A spontaneous nystagmus may also occur in the symptom-free interval in patients with vestibular migraine.72 Preventing visual fixation by using Frenzel glasses facilitates observation of a spon-taneous nystagmus. These glasses prevent light from activating the smooth pursuit system, which can cancel out the imbalance of the tonic firing rate produced by a peripheral vestibular lesion.130 A purely vertical (upbeat or downbeat) or torsional spontaneous nystagmus is indicative of a central vestibular lesion.67,128 Nystagmus due to a central lesion usually cannot be suppressed with visual fixation.128,131 A positional down-beating vertical nystagmus occurs particularly in posterior fossa lesions with Arnold-Chiari malformation as its most common cause.132,133 It may also indicate an intracranial exten-sion of this or another compressive lesion at the foramen magnum.58 Nystagmus with one eye beating down and the other up (skew nystagmus) has only been reported in patients with Arnold-Chiari malformation.133 A few minutes of observation are required to identify periodic alternating nystagmus, a horizontal jerk nystagmus that changes direction about every 2 minutes and that is indicative of midline cerebellar lesions.128 Spontaneous nystagmus may also be congenital. This variant is gener-ally horizontal, may alternate directions but not at regular intervals, increases with attention, fixation, and anxiety, and decreases with convergence.128 Pendular nystagmus occurs most commonly in patients with multiple sclerosis and brainstem stroke.128 The presence of a pendular, a vertical or torsional jerk, skew, or a periodic alternating horizontal jerk spontaneous nystagmus indicates the need for referral. In fact, any spontaneous nystagmus requires

referral with the exception of the congenital variant noted above.

The clinician then observes for spontaneous nystagmus in eccentric positions.128 Deviation of the eye in the direc-tion of the quick phase will increase the frequency and velocity of the nystagmus (Alexander’s law) in patients with a unilateral peripheral vestibular lesion, and it may still produce a positional nystagmus in accommodated patients.67 A gaze-evoked nystagmus may also occur in the symptom-free interval in patients with vestibular migraine.72 Detection of gaze-evoked nystagmus on lat-eral or upward gaze suggests a central lesion.120 In fact, a gaze-evoked horizontal nystagmus implies lesions in the cerebellar flocculus and the medial vestibular nucleus-nucleus prepositus hypoglossus complex, but it can also be the effect of medications, such as hypnotics, sedatives, and anxiolytics or alcohol intoxication.67,128 Gaze-evoked nystagmus may also be the result of extra-ocular muscle weakness as in myasthenia gravis.128 Unsustained eye movements of low frequency and amplitude are indicative of end-point nystagmus, a nonpathological variant in nor-mal subjects.128 The presence of gaze-evoked nystagmus (with the exception of end-point nystagmus) indicates the need for referral.

Saccadic eye movementsHaving the patient look back and forth between 2

targets tests saccadic eye movements. Abnormalities of horizontal or vertical saccadic eye movements may occur in the symptom-free interval in patients with vestibular migraine.72 Overshooting of the target (saccade overshoot dysmetria) may be observed in cerebellar disorders, such as Friedreich ataxia.134 Undershooting of the target, or hy-pometria, can occur in patients with Parkinson disease.134 Vertical saccadic eye movements in patients with Wal-lenberg syndrome as a result of vertebrobasilar infarction may result in eye lateropulsion requiring a corrective horizontal saccade.67 Uncalled-for saccades during gaze fixation on one of the targets can occur in patients with viral cerebellar infection, paraneoplastic syndrome, and Friedreich ataxia.67 Macrosaccadic oscillations, which are horizontal saccades occurring in waxing and waning bursts with 200-millisecond saccadic intervals induced by a gaze shift, are indicative of midline cerebellar disease, spinocerebellar degenerations, and pontine lesions.128 Although saccadic eye movement abnormalities using electro-oculography have been reported in patients with dizziness due to chronic WAD,21,25,26 they are not likely to be noted in the clinical examination described here. Abnormalities identified during saccadic eye movement tests indicate the need for referral.

Smooth pursuit testingHaving the patient follow a slowly moving target (ie, no

faster than 20° per second) tests smooth pursuit. A marked deficit in smooth pursuit is indicative of a degenerative cerebellar process.67 Small bilateral saccades in the same direction in both eyes during smooth pursuit testing are

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indicative of spinocerebellar lesions, especially Friedreich ataxia.128 Smooth pursuit testing may also be positive in pa-tients with a severe acute peripheral vestibular lesion due to superposition of an intense spontaneous nystagmus.67 Although smooth pursuit eye movement abnormalities using electro-oculography have been reported in patients with dizziness due to chronic WAD,21,26 they are not likely to be noted in the clinical examination described here. Abnormal findings on smooth pursuit testing indicate the need for referral.

Hearing ExaminationThe cranial nerve examination may indicate hearing

loss. A conductive hearing loss results from disorders in the external or middle ear; lesions in the cochlea or the cochlear nerve43 cause a sensorineural hearing loss. A sensorineural loss is a symptom of salicylate overdose.43 Ménière disease produces a sensorineural loss that is pro-gressive over multiple episodes.43,98 Progressive unilateral sensorineural hearing loss is also a typical presentation of patients with acoustic neuromas.92 Otosclerosis can pro-duce both a conductive and a sensorineural hearing loss.43 It is the authors’ experience that many elderly patients complaining of dizziness present with an undiagnosed but unrelated conductive hearing loss. Even without as-sociated symptoms, this constitutes a reason for referral to an audiologist. The presence of symptoms implicating hearing loss as part of a pathology causing complaints of dizziness indicates the definite need for medical referral.

Weber testWith the Weber test,43 the therapist places a tuning fork

[256 or 512 hertz (Hz)] on the top of the patient’s skull. With unilateral sensorineural hearing loss, the patient will perceive the sound as coming from the normal ear. With a conductive disorder, the patient perceives the sound as coming from the abnormal ear. Midline is the normal response for this test.124 A non-midline response indicates the need for referral.

Rinne testThe Rinne test43 allows the therapist to distinguish

between a sensorineural and a conductive deficit in the affected ear. Normally, air conduction of the sound of a vibrating tuning fork (256 or 512 Hz) is perceived as loud-er than bone conduction. Holding the tuning fork next to the external auditory canal produces a louder sound than placing the base of the tuning fork on the mastoid bone in patients with normal hearing. The same is true in patients with sensorineural hearing loss. However, in patients with conductive deficits, bone conduction will appear louder than air conduction on the affected side. Burkey et al135 reported that the sensitivity of the Rinne test was sufficient to be used as part of a screening protocol in the hands of an experienced examiner and when interpreting equivo-cal results as indicative of a conductive loss. The finding of bone greater than air conduction indicates the need for referral.

Active Range-of-motion TestsMusculoskeletal impairments (ie, decreased muscle

strength and endurance, joint stability and mobility, and posture) are implicated in patients with the dysequilib-rium subtype of dizziness and may be amenable to sole physical therapy management. Range-of-motion limita-tions, specifically trunk, hip, and knee flexion and ankle plantarflexion contractures, will adversely influence the location of the center of gravity in relation to the base of support. Active range-of-motion testing should, therefore, concentrate on assessing trunk, hip, and knee extension and ankle dorsiflexion. Assessing neck motions allows the clinician to observe possible adverse responses in the sense of ischemic reactions during patient-controlled AROM. It also serves to see if patients will be able to assume the test positions needed in further tests. Cervical AROM tests may also reveal upper cervical hypomobility implicated in cervicogenic dizziness.32,33

Active range-of-motion tests also provide indica-tions on strength and coordination deficits in the form of ataxia or abnormal involuntary motions. Asterixis is an episodic cessation of muscular activity in patients with hepatic encephalopathy, hepatocerebral degenera-tion, and other metabolic encephalopathies.43 Episodic cessation of extensor muscle activity occurs when the patient holds the arms outstretched with wrists and fingers extended causing the hands to fall into flexion followed by a return to the extended position.43 Myoc-lonus is a rapid, twitch-like muscle contraction. It can result from the same conditions causing asterixis or with Creutzfeldt-Jakob disease.43 Chorea can occur in patients with Wilson disease, acquired hepatocerebral degenera-tion, and ataxia-telangiectasia.43 Chorea is characterized by rapid, irregular muscle jerks, occurring unpredictably and involuntarily in different body parts.43 An ischemic response during cervical AROM testing or the presence of abnormal involuntary motions during AROM testing of the limbs indicates the need for referral.

Limb Ataxia TestsThese tests serve to confirm possible limb ataxia ob-

served during AROM testing. During the finger-to-nose test, the quality of arm motion is observed as the patient moves the index finger to the tip of the nose or the chin. Closing the eyes eliminates visual substitution. Mild cere-bellar ataxia results in an intention tremor near the begin-ning and end of the movement with possible overshooting of the target.43 With the finger-to-finger test, the patient attempts to touch his or her finger to the therapist’s finger. Horizontal overshooting implicates a unilateral labyrin-thine lesion; vertical overshooting occurs in patients with midline lesions to the medulla oblongata or the bilateral cerebellar flocculus.92 Having the supine patient track the heel of the foot smoothly up and down the contralateral shin tests for leg ataxia. Having the seated patient touch the great toe to the examiner’s finger is another test for leg ataxia.136 Dysdiadochokinesia is the inability to perform rapidly alternating movements, and in adults it is usually

37

caused by multiple sclerosis; in children, it frequently results from cerebellar tumors. Patients with other move-ment disorders such as Parkinson disease also may have difficulty with rapidly alternating movements, but this is due to akinesia or rigidity rather than true dysdiadocho-kinesia.137 Dysdiadochokinesia can be tested with rapid alternating finger tapping, forearm pronation-supination, and toe-tapping movements, for example.136,137 With the Barre test, the standing or sitting patient holds the hands outstretched with the forearms supinated and eyes closed. Sinking of 1 arm with simultaneous pronation may indicate a central neurological, likely cerebellar, dysfunction.138

The finger-to-nose test has poor test-retest and inter-rater reliability for dysmetria and tremor but excellent reliability for time of execution.139 Swaine et al140,141 reported mean reliability coefficients of 0.77-0.82 for time of execution of 5 repetitions of the finger-to-nose test, indicating clinically sufficient test-retest reliability in healthy adults and also established norms for healthy subjects aged 15 to 34. Simon et al43 reported a posi-tive heel-to-shin test in 80% of patients with alcoholic cerebellar degeneration. We found no further data on reliability and validity for these ataxia tests. Positive limb ataxia tests (including seeming dysdiadochokinesia due to akinesia or rigidity) indicate the need for referral.

Passive Range-of-motion TestsPassive range-of-motion (PROM) testing includes

passive physiological motion, passive accessory motion, and instability tests. In the spine, they include passive physiological intervertebral motion (PPIVM), passive accessory intervertebral motion (PAIVM), and segmental stability tests. Upper cervical segmental motion abnor-malities may be the cause for cervicogenic dizziness. In the case of a hypomobility found on AROM testing, PROM tests may determine cause and subsequent inter-vention.

Instability tests of the upper cervical spine are espe-cially relevant prior to tests involving regional passive rotation of the neck or PPIVM and PAIVM testing. As discussed above, inadvertent shear forces produced during these tests due to ligamentous insufficiency may damage the cord and vertebral arteries.4 The therapist may want to postpone PPIVM and PAIVM tests to the cervical spine until both the segmental stability tests and the VBI tests have provided a negative response.

Intrarater reliability of PPIVM and PAIVM tests has consistently been shown to be greater than interrater re-liability, with the latter varying from generally poor to at times perfect.142 Jull et al143 examined construct validity and found 100% sensitivity and specificity when com-paring cervical PPIVM and PAIVM testing with single facet blocks. Cattryse et al144 found acceptable interrater reliability only for the supine upper cervical flexion in-stability test but not for the Sharp-Purser or atlas lateral displacement test. A positive finding on upper cervical segmental stability tests in combination with signs and

symptoms of cord or vertebral artery compromise indi-cates the need for referral.

Passive range-of-motion tests can also detect muscle tone abnormalities. Hypotonia is indicative of cerebellar disorders with unilateral cerebellar disorders producing ipsilateral limb hypotonia.43 Hypertonia or rigidity may oc-cur in patients with cerebellar ataxia due to Wilson disease, acquired hepatocerebral degeneration, Creutzfeldt-Jakob disease, and some olivopontocerebellar degenerations. Spasticity on PROM testing is common in patients with multiple sclerosis, posterior fossa tumors, Arnold-Chiari malformation, VBI or infarction, Friedreich ataxia and the other hereditary ataxias, olivopontocerebellar degenera-tion, Creutzfeldt-Jakob disease, neurosyphilis, and vitamin B12 deficiency.43 Prochazka et al145 showed poor reliability for a 5-point rating scale for rating rigidity in patients with Parkinson disease. Tone abnormalities on PROM testing indicate the need for referral in a previously undiagnosed patient.

Strength TestsThe musculoskeletal system is the effector organ of the

balance control system. Sufficient strength and endurance in the muscles involved in static and dynamic balance is an obvious prerequisite for optimal balance. Loss of strength and endurance in these muscles can be the cause of patient complaints of dizziness and dysequilibrium. The pattern of any weakness present may also provide diagnostic indicators for the underlying dysfunction or disease. Single or multiple muscle weakness can be the result of disuse atrophy, especially in the elderly. Weak-ness in a peripheral nerve distribution implies a peripheral neuropathy. Monosegmental myotomal weakness can im-plicate a nerve root problem. Multisegmental weakness can implicate a process affecting the cauda equina or the spinal cord. Distal neuropathic weakness can be the result of disorders producing sensory ataxia (eg, polyneuropa-thies). Multiple sclerosis, foramen magnum lesions, spinal cord tumors, and vitamin B12 deficiency can cause para-paresis.43 Paraparesis with the arms more affected than the legs is typical of foramen magnum compressive lesions. Compression of the spinal division of the accessory nerve can cause weakness specific to the sternocleidomastoid and trapezius in such lesions. Unilateral compression at the foramen magnum results in clock-face paralysis, first involving the ipsilateral arm, then the ipsilateral leg, then the contralateral leg, and finally the contralateral arm.58 Intracranial extension of such a compressive lesion may cause cruciate hemiplegia affecting the ipsilateral lower and contralateral upper limb.58 Ataxic quadriparesis, hemi-ataxia and contralateral hemiparesis, or ataxic hemiparesis are all diagnostic indicators of a brainstem lesion.43

We discussed the possible role of deep cervical flexor muscle dysfunction in the etiology and treatment of cervi-cogenic dizziness. Grimmer146 described a useful clinical test for determining the endurance of the deep cervical flexors. The patient is supine without a pillow and is asked to retract the neck and then lift the back of the head off the

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plinth to a height of 2 centimeters. Endurance is measured as the time from start of the test to the moment the chin begins to thrust forward. Chin thrust can be determined visually or by way of palpation. Grimmer146 reported high test-retest reliability with an ICC of 0.92 in women and 0.93 in men.

Knepler and Bohannon147 and Bohannon and Cor-rigan148 showed large interrater variability in the forces used to establish manual muscle testing grades of 3+, 4-, 4+, and 5. Herbison et al149 recommended the use of a handheld myometer over manual muscle testing to detect strength changes. Jepsen et al150 established interrater κ-values of 0.25 to 0.72 for upper extremity manual muscle testing when using a dichotomous rating scale, and they calculated an odds ratio of 2.5 to 7.7 for the presence of symptoms in the case of reduced strength on manual muscle testing, indicating that it may be an appropriate screening test. In contrast, Bohannon151 calculated a specificity of manual muscle testing of greater than 80% and a sensitivity to detect between-side differences or deficits relative to a grade of normal that did not exceed 75%; diagnostic accuracy was less than or equal to 78%, leading Bohannon151 to doubt the value of manual muscle testing as a screening tool. Multisegmental weakness, including paraparesis, quadriparesis, and hemiparesis but also progressive monosegmental paresis, indicates the need for referral.

Reflex TestsCerebellar disorders cause hypoactive deep tendon re-

flexes with unilateral cerebellar disorders resulting in ipsi-lateral hyporeflexia. Friedreich ataxia, neurosyphilis, and polyneuropathies cause leg hyporeflexia. Hyperreflexia is present in multiple sclerosis, vitamin B12 deficiency, focal brainstem lesions, and some spinocerebellar and olivo-pontocerebellar degenerations.43 A positive Babinski sign, Hoffman reflex, and ankle clonus may occur in patients with myelopathy, multiple sclerosis, vitamin B12 deficien-cy, focal brainstem lesions, and some spinocerebellar and olivopontocerebellar degenerations.6,67 Sung and Wang152 established 100% sensitivity for a positive Hoffman reflex for detecting patients with cervical cord compression confirmed on x-ray film or magnetic resonance imaging. We found no additional data on reliability and validity of reflex tests. Clearly, hypoactive or hyperactive deep ten-don reflexes may indicate a need for referral; the presence of pathological reflexes is a definite reason for referral.

Sensation TestsSensation testing may include tests for light touch per-

ception, sharp and dull discrimination, vibration sense, and propriocepsis.27 Sensation testing may reveal deficits in the distribution pattern of single or multiple peripheral nerves, a nerve root, or a multisegmental pattern, provid-ing diagnostic clues for underlying cause or contributing factors to the patient’s complaint of dizziness. Joint posi-tion sense can be tested by asking the patient to detect the presence and the direction of a passive movement in

the joints.43,51 Simon et al43 suggested beginning this type of testing distally and moving proximally to establish the upper level of deficit in each joint. Placing a joint in a position and having the patient reproduce this position with the contralateral joint can also be used as a test for abnormality of joint position sense;43 the patient’s eyes are closed during joint position testing to prevent visual compensation. Joint position sense in the legs is always impaired in patients with sensory ataxia; the arms may be affected depending on the type and extent of pathology responsible. Placing a 128 Hz tuning fork over a bony prominence may serve as a test of vibration sense. Suc-cessively more proximal sites can determine the upper level of deficit in limbs or even trunk. Sensory ataxia is often combined with a decrease in vibratory sensation.43

Using a 3-point rating scale, Jepsen et al153 reported median interrater κ-values of 0.69 for sensitivity to light touch, 0.48 for sensitivity to pin prick, and 0.58 for sen-sitivity to vibration using a 256 Hz tuning fork. Peters et al154 showed limited interrater reliability for a quantita-tive method of assessing vibration sense implying even less reliability for the tuning fork method. Jepsen et al155 reported a sensitivity of 0.73, a specificity of 0.86, a positive predictive value of 0.93, and a negative predic-tive value of 0.90 for a combination of manual muscle tests, sensation tests (light touch, pain, vibration), and sensitivity of nerve trunks to mechanical pressure when compared to patient report of pain, strength deficits, or paresthesia indicating the screening value of this test regimen. Okuda et al156 reported a positive correlation between the degree of knee joint position sense deficits and functional disability scores and electrophysiological findings in patients with compressive myelopathy. It is the authors’ experience that elderly patients frequently present with undiagnosed decreased proprioceptive acu-ity and vibration sense in the feet and ankles, which may contribute to dysequilibrium-type dizziness. Multiseg-mental deficits may indicate the need for referral.

Vertebrobasilar Insufficiency TestsDe Kleyn-Nieuwenhuyse test

Terrett64 noted that the original test description had postulated decreased or even absent vertebral artery blood flow based on cadaver perfusion studies in differ-ent head and neck positions. A long latency, progressive symptoms when held in the sustained test position of cervical extension and rotation, and a lack of habituation with repeated testing are indicative of VBI and not of cer-vicogenic dizziness or BPPV.53 Oostendorp8 reported a latency of 55 ± 18 seconds in these patients with positive findings on variations of the De Kleyn-Nieuwenhuyse test (Figure 4). He also reported a recovery time of 120 ± 40 seconds.8 A positive test may include symptoms of ver-tigo, nausea, diplopia, and dysphagia. Positive signs may include nystagmus and dysarthria,64 which may be noted by having the patient talk during the test hold. Pettman4 noted horizontal nystagmus but the authors have noted vertical and rotary nystagmus in symptomatic subjects.

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This test has been extensively studied with equivocal results. Some authors reported significant decreases in blood flow,157,158 whereas others reported no changes.159,160 Support for this test becomes even more problematic with case reports noting false negative results161,162 and case series noting 75% to 100% false positive results.160,163 Cote et al164 reported 0% sensitivity for detection of in-creased impedance to blood flow, 0% positive predictive value, and 63% to 97% negative predictive value. This test (and the cervical rotation test) is obviously a ques-tionable screening procedure for VBI. Vidal165 questioned its routine use, concluding that vertebral artery tests are not clinically useful screening tools for VBI. Rather, he suggested relying upon history suggestive of VBI, medical history (especially when indicative of ischemic processes, such as coronary artery disease, transient isch-emic attacks, or cerebrovascular accidents), and other relevant examination findings (eg, during cranial nerve and AROM tests). Due to the potential for harm with this test and its poor psychometric properties, it should not be done in patients with a positive medical history or a history strongly indicative of VBI.165 However, the test may serve as a screening tool in patients not fitting these categories. In those patients, a positive finding with clear central neurological signs of nystagmus and dysarthria on this test warrants referral.

Sustained cervical rotation testSustained supine cervical rotation may also test for

VBI. Symptom behavior can be expected to be similar to the extension-rotation test with regard to latency, nonaccommodation, and nonhabituation. However, findings on sustained cervical rotation alone are equally equivocal, with significant decreases in vertebral artery flow157-159,166,167 or no effect on blood flow168 or blood volume.169 Indications for this test and implications of a clearly central neurological involvement are as described for the extension-rotation test.

Hautant testThis test is used for differential diagnosis of vestibular,

cervicogenic, and ischemic dysfunction (Figures 5A and B). However, it is also a test with multiple descriptions in manual medical literature. Terrett64 described the test with the patient seated, the arms outstretched, and the forearms supinated. The therapist moves the patient’s head in an extension-rotation position with the patient’s eyes closed. Symptom reproduction and sinking of one hand into pronation implicates the vertebrobasilar sys-tem.64 Van der El138 described this test with the forearms pronated. Deviation of one of the arms with the head in midposition indicates vestibular dysfunction. A lateral deviation of the contralateral arm in the opposite direc-tion of the cervical extension-rotation implicates the neck. Immediate arm motion suggests a somatosensory dysfunction; a latency period indicates ischemic dysfunc-tion.138 No data on reliability or validity were found. A test indicating ischemic dysfunction suggests the need for referral.

Figure 4. De Kleyn-Nieuwenhuyse test.

A B

Figures 5A and B. Hautant test.

Vestibulo-ocular TestsThese tests examine the vestibulo-ocular reflex circuit

by inducing movements at an angular velocity that does not allow for compensation by the cervico-ocular reflex.

Dynamic visual acuityAfter establishing baseline visual acuity with a Snel-

len chart, this test measures visual acuity with concurrent head movement. The head is moved from side to side at a frequency of 1 Hz while the patient reads the Snel-len chart.108 A decrease by 2 lines is suspicious and by 3 or more is indicative of an abnormal vestibulo-ocular reflex.27,108 This test is not suited for detecting unilateral peripheral or central vestibular lesions but is indicated in case of suspected bilateral vestibular loss.108,170 Herdman et al95 reported poor reliability for this test.

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Autorotation testThe autorotation test is performed with the patient

sitting with an upright posture, holding gaze on a station-ary target, and performing small oscillations of the head side to side and up and down.102 The patient is instructed to move at 2 Hz (ie, 120 oscillations in 60 seconds). An abnormal response includes the inability to continue the test for 60 seconds due to dizziness, double vision, or blurry vision due to oscillopsia, or fewer than 100 oscillations in 60 seconds, and may indicate peripheral or central vestibular dysfunction.102 The autorotation test is easier to perform in the clinical setting than high-frequency range rotational chair testing, which requires specialized and powerful systems. However, test-retest reliability for the autorotation test is poor.171

Doll’s head testThe examiner faces the patient, who fixes the gaze

on the examiner’s nose. The examiner then oscillates the patient’s head 30° side to side at 0.5 to 1 Hz. Eye movements that are not smooth but interrupted by catch-up saccades toward the fixation target indicate bilateral vestibular lesions.108 We found no data on reliability and validity.

Head-shaking nystagmus testThe examiner vigorously moves the patient’s head

back and forth horizontally for about 30 seconds with the patient’s eyes closed. Upon opening the eyes, the nystagmus will beat away from the side of a unilateral peripheral vestibular lesion170 or toward the lesioned side in patients with Ménière disease.172 When compared to a caloric test, the head-shaking nystagmus test (with Frenzel glasses) had 66% sensitivity and 77% specificity for detecting canal paresis greater than 20%.173 Kamei and Iizuka172 reported on the possible prognostic value of a reversal of nystagmus direction toward the affected ear to predict an imminent recurrence of Ménière dis-ease. Wu et al174 reported head-shaking nystagmus when the degree of horizontal canal paresis exceeded 25%. Head-shaking nystagmus was also dependent on the stage of vestibular compensation. Monophasic nystag-mus occurred in patients with acute loss, while biphasic nystagmus occurred with development of vestibular compensation. Any result other than monophasic or biphasic horizontal nystagmus was suggested to indicate central abnormalities and, therefore, indicate a reason for medical referral.

Head-thrust testThe head-thrust test (Figures 6A and B) may also

detect an impaired vestibulo-ocular reflex.175 The patient fixates the gaze on the therapist’s nose. The therapist then moves the patient’s head in the horizontal plane in a rapid passive manner with unpredictable timing and direction (5° to 10° at 3000° to 4000° per second). A patient with vestibular loss will have difficulty maintain-ing gaze fixation, requiring a corrective saccade (fast

eye movement) to maintain gaze fixation on the nose.131 A corrective saccade following head thrust to the right indicates the vestibular loss is on the right; corrective saccades with head thrust to the left suggest an involved left side.176 Schubert et al177 reported a sensitivity of 71% and a specificity of 82% for the head-thrust test with the head tilted down 30° in the diagnosis of patients with unilateral vestibular loss and 84% sensitivity and 82% specificity for bilateral loss.

Benign Paroxysmal Positional Vertigo TestsThese tests look for canalithiasis or cupulolithiasis in

all SCCs. A positive response on these tests in combination with corroborating history findings and in the absence of findings indicative of other pathology implies that sole physical therapy management may be indicated.

Hallpike-Dix maneuverThis maneuver (Figures 7A and B) tests all SSCs.46 The

long-sitting patient turns the head 45° and is then assisted into supine with the rotated head 30° below horizontal. This position is maintained for at least 30 seconds. De-layed-onset, torsional, horizontal, or (less commonly) vertical nystagmus in combination with vertigo lasting less than 60 (canalithiasis) or more than 60 seconds (cu-

A B

Figures 6A and B. Head-thrust test.

Figures 7A and B. Hallpike-Dix maneuver.

A B

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pulolithiasis) that decreases with repeated testing consti-tutes a positive finding.108,132,178 Relevant for differential diagnosis with regard to which SCC is involved is the type of nystagmus and whether the test is unilaterally or bilaterally positive:• An ipsilateral maneuver positions the posterior SCC

of the down-side ear in the plane of the pull of gravity. Shifting of otoconia, whether free floating (canalithia-sis) or adhered to the cupula (cupulolithiasis), deflects the cupula and alters the posterior SCC neuronal firing rate.178 This results in an apogeotropic (beating away from the earth or down-side ear) torsional nys-tagmus.178

• A bilateral positive test implicates either the anterior or horizontal SCC.108,132 With anterior SCC BPPV, the ipsilateral test provokes a geotropic (beating toward the earth or the affected ear) torsional178 or a down-beating vertical nystagmus.132

• A bilaterally positive test with a purely horizontal geotropic (beating in the direction of the face turn or down-side ear) nystagmus implicates the horizontal SCC.108 Nystagmus will occur in both directions but will generally be stronger with the head turned toward the affected side.108

Positional nystagmus on this test has been shown to identify patients with posterior SCC BPPV with 78% sensitivity.179 Specificity as high as 88% has been re-ported.30

Straight head-hanging testIn the straight head-hanging test, the patient is as-

sisted into lying back from long sitting with the head extended but not rotated. This test may be more sensitive for anterior SCC BPPV. An additional 20° of extension as compared to the Hallpike-Dix maneuver causes the ampullary segment of the anterior SCC to approach a more vertical position.132 We found no data on reliability and validity.

Roll testThe roll test detects horizontal SCC BPPV. The thera-

pist quickly log rolls the supine patient with the head 30° flexed to one side, maintaining this position for at least 1 minute. Otoconia moving back and forth within the SCC with left and right rotation will cause the positive response of nystagmus and vertigo. Canalithiasis causes fatiguing geotropic (toward the earth) nystagmus and cupulolithiasis persistent apogeotropic (away from the earth) nystagmus. More severe and longer lasting symp-toms indicate the affected side.178 We found no data on reliability and validity.

Walk-rotate-walk testIn this test for the horizontal SCC,180 the patient

walks straight ahead at the patient-selected maximum tolerable speed in a room with ample space. The patient then rotates 180° on the axis of the rotation-direction foot, returning back in a continuous movement. The test

is performed to both sides. Staggering, side stepping, making corrective movements of the body or hands, discontinuing the rotation in one direction, or slowed and difficult rotation indicate a positive test. A positive response on rotation to the right implicates the right and a positive response on rotation to the left implicates the left SCC. The difference must persist over 3 repetitions. Rahko and Kotti180 found 100% predictive validity for this test in determining a positive response to a horizontal SCC BPPV treatment. The 180° turn in this test versus the 90° turn in the roll test may allow for higher otoconia ac-celeration and ampulla cell stimulation. Sensitivity was acceptable; some patients with acute vestibular neuritis tested positive on the walk-rotate-walk test.180

Cervicogenic Dizziness TestingThe neck torsion test (Figures 8A and B) is used to

detect cervicogenic dizziness.181,182 The head is held stationary during neck and trunk rotation. An alternate way of screening the cervical spine as the possible origin of dizziness symptoms is to have the patient sit and flex forward at the hips while simultaneously extending and rotating the neck (Figure 9).183 As both tests keep the in-ner ear stationary, the vestibular system is not stimulated. Nystagmus and dizziness with this test are, therefore, interpreted as cervicogenic. However, the therapist still needs to differentiate between vascular or somatosensory cervicogenic involvements.183 Diagnostic accuracy is questionable; 50% of subjects without cervical pathology tested positive for nystagmus,184 possibly a manifestation of the cervico-ocular reflex.17 Fitz-Ritson2 found that 47% of patients with cervical trauma demonstrated sub-jective symptoms of vertigo or postural instability during the neck torsion test; 90% improved following therapy. We found no additional data on reliability and validity. A positive response on these tests in combination with corroborating history findings in the absence of findings indicative of other pathology implies that sole physical therapy management may be indicated.

Figures 8A and B. Neck torsion test.

A B

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Breathing-related TestsHyperventilation test

The hyperventilation test requires patients to vol-untarily hyperventilate (ie, 30 breaths per minute for 3 minutes).109 It may be a useful and simple test for validat-ing a diagnosis of panic disorder or dizziness related to hyperventilation presyncope. In these patients, this test will produce dizziness but no nystagmus.67 Patients with demyelinating lesions of the vestibulocochlear nerve due to an acoustic neuroma, compression by a small blood vessel, or central demyelinating lesions (multiple sclerosis) may show nystagmus on the hyperventilation test.67 Hyperventilation may accentuate down-beating nystagmus in patients with Arnold-Chiari malformation and evoke a nystagmus toward the lesion in patients with vestibular schwannomas.170 Nardi et al185,186 found that the hyperventilation test produced significantly more symptoms in patients with panic disorder than in patients with obsessive-compulsive disorder or depression, or in normals, and they noted that it might be an easy test to validate panic disorder.186 Nakao et al187 reported 62% sensitivity and 100% specificity for this test in the diagno-sis of coronary spasm. The authors have noted clinically that near-immediate reproduction of symptoms may indi-

cate psychogenic contribution to dizziness complaints. A positive finding on these tests indicates the need for referral.

Valsalva testIn patients with Arnold-Chiari malformation, perilym-

phatic fistulae, and other abnormalities of the ossicles (eg, otosclerosis), oval window, and saccule, a Valsalva maneuver may produce nystagmus. Changes of middle ear pressure due to loud noises, application of positive and negative pressure to the tympanic membrane (Hen-nebert sign), and opening and closing the eustachian tube may have a similar effect.67 The cough test is a variant on the Valsalva test. Having the patient cough to increase intrathoracic pressure may be useful in detecting dizzi-ness due to cough presyncope.43 We found no data on reliability and validity. Positive tests indicate the need for referral.

HISTORY AND PHYSICAL EXAMINATIONAbout 50% of dizziness is vestibular and benign.30

More serious causes (eg, brain tumors and cerebrovas-cular disorders) account for about 1% and 5% of cases, respectively.30 Froehling et al188 studied diagnostic accu-racy of symptoms and signs in distinguishing benign from serious causes: • Vertigo or vomiting combined with a positive Hall-

pike-Dix test demonstrated 85% positive predictive value and a 7.6 positive likelihood ratio for a benign cause

• A negative Hallpike-Dix maneuver and the absence of vertigo or vomiting had a 68% negative predictive value for peripheral vertigo

• Age of 69 or less, the absence of neurological deficits, the presence of vertigo, or a combination of these factors has a negative predictive value of 88% with a negative likelihood ratio of 0.3 for a serious cause of dizziness

• Age greater than 69, the presence of neurological defi-cit, the absence of vertigo, or a combination of these factors carries a positive predictive value of 40% and a positive likelihood ratio of 1.5 for a serious cause of dizziness

CASE STUDIESCase Study 1Subjective information

The patient, a 75-year-old white man, is a retired Royal Canadian Navy fighter and helicopter pilot. Four years prior to this first physical therapy evaluation, he woke up severely perspiring in the middle of the night with paresthesia around the left eye. The next morning he noted severe and persistent dizziness, described as disorientation. His primary care physician subsequently referred the patient for a computerized tomography scan of the head. This scan revealed a sinus infection that was treated with antibiotics. The sinus infection was cured but symptoms of dizziness persisted unabated. Referral to a

Figure 9. Alternate neck torsion test.

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neurologist resulted in further testing. A magnetic reso-nance imaging scan of the brain, an ultrasound examina-tion of the carotid artery, a Holter monitor test, and lab tests all came back negative. An ophthalmologist found no abnormities implicating the visual system. A second neurological opinion resulted in a diagnosis of probable inner ear dysfunction with a suggested benign natural history. No further intervention was suggested. Symptoms indeed decreased some 2 years after the initial onset but returned 1 year ago for another 6 months after swimming and again 2 months ago after what was diagnosed by an emergency room physician as an anxiety attack, perhaps as an unusual side effect of taking the nonsteroidal anti-inflammatory medication Meloxicam for right medial compartment knee osteoarthritis.

The current complaint consists of episodes of constant dysequilibrium that are preceded by a feeling of fullness in the head. Symptoms remain at their worst intensity for about 3 to 4 hours. The patient can report no precipitating factors but has noted numbness around the left eye, some difficulty swallowing, and chest palpitations accompany-ing the feeling of unsteadiness. When severe, symptoms also include nausea, general fatigue, impatience, and irritability. Since this last onset, but not in previous epi-sodes, the patient also reports a weakness in the legs that fluctuates with other symptoms. The patient intake ques-tionnaire (Table 13) revealed a positive personal medical history of heart disease. Further questioning revealed a coronary artery bypass graft surgery 9 years previous. There were no further relevant check marks on the in-take questionnaire. Current medications taken included Simvastatin (hypercholesterolemia), aspirin (prevention of cardiovascular events), Xalitan eye drops, and Rivotril (anxiolytic). Anxiety had been suggested 3 years ago as a possible cause for the prolonged complaints of dizzi-ness. A history using the structured interview suggested in Table 14 revealed no further relevant information.

Objective findingsThe physical examination followed the proposed

examination template in Table 15. Postural observation revealed a forward head posture. The sit-to-stand test for orthostatic hypotension showed a normal blood pres-sure and heart rate response. Cranial nerve, oculomotor, hearing, and limb ataxia tests were all negative. Active range-of-motion testing revealed decreased left rotation and extension of the cervical spine. Passive range-of-motion testing of the arms and legs showed no muscle tone abnormalities. Upper cervical ligamentous stability tests were normal, and the sustained rotation test of the cervical spine produced no signs or symptoms indica-tive of VBI. Segmental motion testing of the cervical and thoracic spine revealed a decreased left C1-C2 rotation, left C3-C6 extension, and C7-T5 bilateral rotation and extension. The patient was unable to perform the cervical deep flexor endurance test without forward chin thrust. Pathological reflexes (Hoffman signs and Babinski reflex) were bilaterally absent and deep tendon reflexes in the

arms and legs were bilaterally normal. Vibration sense at bilateral ankles and big toes, tested with a 256 Hz tuning fork, was equal and normal. The vestibulo-ocular tests were all normal, with the exception of a horizontal biphasic nystagmus initially beating right and then left with the head-shaking nystagmus test. Tests for BPPV were negative, with the exception of consistent stag-gering and decreased speed of movement on the left walk-rotate-walk test. The neck torsion test for detection of cervicogenic dizziness was negative and so were the Valsalva, cough, and hyperventilation tests.

Physical therapy diagnosisThe history and physical examination seemed to indi-

cate a physical therapy diagnosis of:• Decreased or absent function of the left horizontal

SCC• Decreased segmental mobility in the cervical and up-

per thoracic spine• Decreased endurance of the deep cervical flexor

muscles• Cervicogenic dizziness• Lack of knowledge with regard to diagnosis and prog-

nosis of current complaintThe therapist was confident that previous medical ex-

aminations and the results of the current physical therapy examination excluded a central vestibular or other central neurologic, cardiovascular, and metabolic etiology for the current complaint of dizziness. However, the report of palpitations, nausea, generalized fatigue, irritability, and impatience, as well as the prescription for anxiolytic medication did not exclude a psychogenic contribution to the current complaint of dizziness.6 Positive findings on the left walk-rotate-walk test implicated the left horizontal SCC.180 A biphasic horizontal nystagmus initially beating right and then left with the head-shaking nystagmus test implicated a central adaptation to a left horizontal SCC hypofunction.174

The therapist entertained a working hypothesis of an initial onset of the complaints due to compression of the vestibulocochlear nerve in the internal auditory canal as a result of an inflammatory or infectious process. This would seem to explain the diaphoresis at initial onset and fit with the diagnosed sinus infection. The paresthesia reported at that time around the left eye and later the numbness may have been a misinterpretation of motor deficits from the facial nerve that might also have been compressed with the vestibulocochlear nerve as they both travel through the internal auditory canal.11 The horizontal canal paresis had a benign course as other afferent information com-pensated, most likely proprioceptive afferent information from the cervical spine.

Although the neck torsion test was negative, the seg-mental hypomobilities in the cervical spine and the de-creased deep cervical flexor muscle function implicated the cervical spine and resultant cervicogenic dizziness. Fighter pilots are subjected to excessive acceleration and deceleration and may be more prone to degenerative

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changes in the cervical spine. A preexisting horizontal SCC paresis and periodic aggravation of cervical dysfunctions with resultant alterations in cervical proprioceptive input to the central vestibular apparatus may have resulted in decompensation of vestibular adaptive mechanisms and the periodic described complaints of dizziness.

Guide to Physical Therapist Practice diagnosisThe diagnosis according to the Guide to Physical

Therapist Practice189 is:• Practice pattern 4C: impaired muscle performance• Practice pattern 4D: impaired joint mobility, motor

function, muscle performance, and range of motion associated with connective tissue dysfunction

• Practice pattern 5D: impaired motor function and sen-sory integrity associated with nonprogressive disorders of the central nervous system acquired in adolescence or adulthood

Physical therapy management and outcomesPhysical therapy management on the first visit con-

sisted of the examination described above followed by patient education on examination findings, diagnosis, prognosis, and proposed treatment plan. The goal of this education was twofold: to get informed consent for the suggested plan of care and to decrease any possible causative anxiety regarding the current complaints. The patient reported that the education had indeed put him at ease and expressed his eagerness to participate in the suggested plan of care.

Further treatment on the first visit included thrust trac-tion manipulation to the upper thoracic restricted motion segments, as thoracic thrust manipulation has not been associated with the same risk of adverse effects as cervical thrust manipulation and because preliminary evidence exists for its immediate efficacy with regard to reported mechanical neck pain.190 A cervical autorotation exercise in the horizontal plane was used as a home exercise. The patient was told to sit on a chair, focus on a fixed point, and rotate the head 45° side to side for 30 to 60 seconds 5 times per day, just below the level of producing diz-ziness. The intent of this exercise was to reintegrate the cervical afferent input and allow for partial substitution of the vestibulo-ocular reflex by the cervico-ocular reflex. The second home exercise was an active upper thoracic extension exercise to maintain post-thrust increase in range of motion.

On the second visit, 1 week later, the patient reported a decrease in the feeling of unsteadiness. However, AROM testing and segmental motion tests of the cervical spine still showed limitations as noted on the initial examina-tion. Even though atherosclerosis and atherosclerotic risk factors as present in this patient have not been im-plicated as a risk factors for adverse effects with cervical manipulation,5 after a risk-benefit analysis as part of an informed consent procedure, the therapist and patient decided not to use cervical thrust manipulation but rather nonthrust techniques. Soft tissue techniques to the cervi-

cal spine, including effleurage, petrissage, and inhibitory techniques, were followed up with grade IV-IV+ oscilla-tory mobilization into left C1-C2 rotation and left C3-C6 extension. Upper thoracic traction thrust manipulation was repeated because some segmental restrictions were still noted at C7-T5. The home program was expanded to include cervical autorotation techniques in standing first with a normal stance and progressing as tolerated to a narrow stance and heel-to-toe stance, stretching exercises for the cervical and pectoral muscles, and left rotation of the head and neck in flexion for self-mobilization of the C1-C2 restriction noted.

On the third visit, 3 weeks after the initial examina-tion, the patient reported only very minimal complaints of unsteadiness. Cervical and thoracic active and seg-mental motion were only minimally restricted. The walk-rotate-walk test to the left resulted in staggering on only 1 trial out of 3. The cervical nonthrust and thoracic thrust manipulations were repeated, as were the cervical soft tissue techniques described above. The patient was in-structed in a progression of deep cervical flexor muscle-strengthening exercises with specific written instructions. In an effort to ensure greater compliance, the home program was cut down to just this strengthening exercise, the autorotation exercise in heel-to-toe stance, and an exercise that involved a left 180° rotation while walking just below the rotational speed causing unsteadiness to integrate visual, somatosensory, and remaining vestibu-lar input in a motion with more relevance to functional situations that in the past may have caused complaints. The patient was discharged from physical therapy at this time. A follow-up phone call 1 month later revealed only minimal and occasional complaints of unsteadiness as reported during the initial examination.

Case Study 2Subjective information

The primary care physician referred this patient, a 45-year-old white woman, to physical therapy with a diagnosis of acute cervical strain. The patient works as a computer programmer, which requires her to sit in front of a computer throughout the day. She is also an avid recreational soccer player. Five days prior to referral to physical therapy, the patient, in the midst of playing in a soccer game, was struck on the right side of the back of her head by a soccer ball. No loss of consciousness occurred. After 2 days of self-management, which in-cluded rest, ice, and over-the-counter anti-inflammatory medication, the patient did not experience any decrease in neck pain. The patient was subsequently examined by her primary care physician and was prescribed Skelaxin to help decrease muscle spasm and pain, and referred to physical therapy with the diagnosis noted above. Diagnostic tests including plain film radiographs of her cervical spine were not ordered.

The patient’s chief complaint is of constant right-sided cervical pain, but with variable intensity. Pain assessment via a visual analog scale (0 = no pain, 10 = worst pain

45

imaginable) demonstrates the patient’s worst pain at 8 out of 10 and best pain at 4 out of 10. Pain is worst at the end of the workday and is aggravated by cervical flexion and left rotation. Neck pain improves with Skelaxin (800 mil-ligrams) and the application of a heating pad to the painful area for 20 minutes. The patient denies any upper extrem-ity or lower extremity symptoms, but she complains of a recent onset of intermittent dizziness that began the day after her physician examined her. The patient’s dizziness symptom is described as spinning and lightheadedness, most notably when rolling onto her right side and when bending over to tie her shoes. She feels that the spinning lasts about 30 seconds, but the lightheadedness may last for a few hours. The lightheadedness seems to be worst at the end of the workday when her neck pain is also at its worst. The patient’s lightheadedness also seems to worsen about 1 hour after taking the Skelaxin for her neck pain. The patient denies other associated or prodomal symp-toms. The patient’s medical intake questionnaire did not reveal any past medical or surgical history. Skelaxin was the only current medication.

Objective findingsPostural observation revealed a forward head posture,

rounded shoulders, and increased thoracic kyphosis. Blood pressure and heart rate measurements were normal in sitting and standing. The patient’s gait pat-tern was normal except when performing concurrent head rotation, which produced a decrease in cadence and mild deviation to the right from a straight line. The Romberg test was essentially unremarkable, producing only a mild anterior to posterior sway with eyes closed. Cranial nerve, oculomotor, and limb ataxia tests and measures did not produce any significant findings. Visual assessment of AROM revealed decreased left rotation, left side bending, and flexion of the cervical spine. Pain and lightheadedness were reproduced with all of these motions at end range. A mild feeling of spinning was produced with cervical flexion and right rotation. Upper cervical stability tests were normal. The vertebral artery test was not performed for reasons noted by Vidal.165 Passive mobility testing revealed restricted left rotation at C1-C2, decreased forward nodding at Occ-C1 right, and restricted bilateral rotation at C7-T3. Palpation revealed a hypertonic right sternocleidomastoid muscle and pro-duced mild lightheadedness. Decreased endurance was detected in the cranial flexors during the cervical deep flexor endurance test. Reflex testing was unremarkable. The vestibular system examination was normal except for a positive right Hallpike-Dix maneuver; this test pro-duced a delayed onset of up-beating horizontal-rotary nystagmus lasting less than 30 seconds. The roll test, left and right, for horizontal canal BPPV failed to reproduce nystagmus, but a sense of lightheadedness was experi-enced with the left roll test. The neck torsion test did not reproduce spinning but did reproduce a moderate sense of lightheadedness with the trunk rotating right.

Physical therapy diagnosisThe history and physical examination seemed to indi-

cate a physical therapy diagnosis of:• Decreased AROM of the cervical spine• Decreased segmental mobility in the upper cervical

spine and upper thoracic spine• Decreased endurance of the deep cervical flexor

muscles• Cervicogenic dizziness• Right posterior canal BPPV• Potential medication-related side effect of Skelaxin• Poor ergonomic and body mechanics awareness at

workBased on the history and physical examination find-

ings, the therapist was confident that the patient’s neck pain was musculoskeletal in origin and that the complaint of dizziness was peripheral, not central, in origin. The physical impairments detected in the cervical and tho-racic spines combined with the finding that the patient’s lightheadedness was worse when her neck pain was worse, the absence of red flag items for vertebrobasilar involvement (Table 7), an onset of neck pain related to physical trauma, a reproduction of dizziness symptoms with cervical AROM, and a positive neck torsion test led to the most likely diagnosis of cervicogenic dizziness. Al-though the diagnostic accuracy of the neck torsion test is questionable, there was diagnostic concordance of both the history and physical examination findings. A positive right Hallpike-Dix maneuver with up-beating horizontal-rotary nystagmus implicated nonidiopathic right poste-rior canal BPPV, likely due to the head trauma described. With a specificity for the Hallpike-Dix reported as high as 88%,30 the therapist felt confident that this positive test result ruled in the diagnosis of right posterior canal BPPV. The therapist suspected that the muscle relaxant (Skelaxin) contributed to the patient’s complaint of diz-ziness, as the patient experienced an increased sense of lightheadedness 1 hour after taking this medication. In summary, the history and physical examination findings indicated that cervicogenic dizziness and BPPV were concurrently present, complicated by a potential side effect of Skelaxin. Poor ergonomics and body mechan-ics awareness were suspected given the results from the visual posture assessment and reported occupational demands.

The pain and lightheadedness reproduced with active cervical motions and the neck torsion test was likely from abnormal afferent somatosensory input stemming from the upper cervical spine where irritated muscle spindles and joint mechanoreceptors contributed to altered postural control experienced by the patient as a sense of lightheadedness.181 This was evident during the gait assessment when concurrent head rotation caused a decreased cadence and mild deviation from a straight line. The findings on the right Hallpike-Dix maneuver were consistent with canalithiasis, as there was a delayed onset of symptoms lasting less than 60 seconds. Dizziness has been reported as a potential medication-related side

46

effect of Skelaxin. Also, a potential result of overdosage is low blood pressure.191 The normal blood pressure mea-surements noted above led the therapist to suspect not an overdosage but rather a medication-related side effect of dizziness. Head trauma may affect central structures, such as the brainstem, and thereby cause dizziness symptoms. However, the history and physical examination were not consistent with a central cause of dizziness. Poor ergo-nomics and body mechanics awareness at work may have further contributed to the patient’s pain and dizziness, as abnormal stresses are applied on the cervical and thoracic spines with the forward head, rounded shoulder posture.

Guide to Physical Therapist Practice diagnosisThe diagnosis according to the Guide to Physical

Therapist Practice189 is:• Practice pattern 4B: impaired posture• Practice pattern 4E: impaired joint mobility, motor

function, muscle performance, and range of motion associated with localized inflammation

• Practice pattern 5D: impaired motor function and sen-sory integrity associated with nonprogressive disorders of the central nervous system acquired in adolescence or adulthood

Physical therapy management and outcomesPhysical therapy management began following the

examination. The examination findings, diagnosis, prog-nosis, and proposed plan of care were discussed with the patient. A brief telephone conversation was held between the therapist and the referring physician. The therapist reviewed the examination findings with the referring physician with particular focus on the patient’s complaint of dizziness as the complaint of dizziness began after the physician examination. In addition, the therapist inquired about the current dosage (800 milligrams) of Skelaxin, as the use of Skelaxin appeared to increase the patient com-plaints of dizziness. The therapist and physician have a close working relationship and they mutually agreed that right BPPV was likely and the patient would most likely benefit from canalith repositioning maneuvers. The physi-cian also instructed the patient to decrease her dosage of Skelaxin by half to 400 milligrams.

The patient agreed to the proposed plan of care, which started with patient education regarding proper ergo-nomic set-up at her workstation and body mechanics and postural awareness. The intention of this education was to facilitate minimizing external stresses that are applied to the cervical spine and to promote healing of irritated soft tissue structures. A moist heat pack was applied to the cervical spine for 15 minutes followed by soft tissue manipulation to the cervical spine, focusing on the right sternocleidomastoid. Following this cervical intervention intended to increase range of motion and tissue exten-sibility and to decrease pain, a canalith repositioning maneuver (right Epley maneuver) was performed to ad-dress the right BPPV. A home exercise program was then prescribed, including gentle self-stretching of the right

sternocleidomastoid (3 times for 15 seconds), pain-free cervical range-of-motion exercises, and postural correc-tion exercises (axial extension and scapular retraction). The patient was instructed to perform these exercises 3 times per day. At the end of visit 1, retesting with the Hallpike-Dix maneuver was negative for right BPPV.

On the second visit, 1 week later, the patient reported that she had not experienced any vertiginous dizziness since the first visit. She also reported decreased cervi-cal pain (4 out of 10 at worst; 2 out of 10 at best) and decreased lightheadedness. The patient also reported that she no longer experienced increased lightheaded-ness after taking the muscle relaxant. She also reported having made changes to her workstation, which seemed to help decrease her neck pain. Upon reexamination, the Hallpike-Dix maneuver was negative for right BPPV. However, active cervical rotation was still limited with left rotation, left side bending, and flexion producing pain and mild lightheadedness but no vertiginous dizziness. The right sternocleidomastoid remained hypertonic, and palpation of this muscle produced mild lightheadedness. The therapist continued with soft tissue manipulation to the right sternocleidomastoid followed by grade III-IV forward-nodding mobilization to the right Occ-C1 ar-ticulation and a muscle energy technique to improve left rotation at C1-C2. Posterior-anterior grade III-IV mobili-zations were also applied to C7-T3 bilaterally. Contract-relax stretching of the right sternocleidomastoid followed these articular manual therapy techniques. The patient was instructed to continue her home exercise program as prescribed during visit 1 but to increase the duration of her right sternocleidomastoid stretch to 30 seconds.

The patient returned 3 days later and reported no vertiginous dizziness and only mild lightheadedness: 0 at its best and 1 to 2 at its worst on a 0 to 10 numeric rating scale used to measure intensity of dizziness com-plaints. Similarly, she rated her neck pain as 0 at its best and 1 to 2 on a 0 to 10 numeric pain rating scale; these higher pain ratings were still experienced at the end of the day. She reported that she was taking the Skelaxin only as needed as compared to previously 3 times per day. Active cervical range-of-motion tests revealed full motion with a gentle stretching pain at end-range left side bending. The AROM tests reproduced no lightheaded-ness. Passive segmental mobility testing revealed normal forward nodding at the right Occ-C1 joint and normal left rotation at C1-C2. Mild restrictions were still noted with bilateral rotation at the C7-T3 levels. Upper thoracic traction thrust manipulation was applied to address these remaining C7-T3 restrictions. Palpation still revealed mild hypertonicity of the right sternocleidomastoid, but this palpation no longer resulted in reproduction of lightheadedness. Cervical deep flexor exercises using a blood pressure cuff to provide feedback to the patient with regard to effort were initiated to improve endurance and followed the protocol as outlined by Jull et al.36,38 The patient’s home program was progressed to include resistance bands for strengthening scapular retraction.

47

The patient was instructed to perform craniocervical flex-ion exercises in supine 3 times per day for 10 repetitions with a 10-second hold.

The patient returned 1 week later for visit 4. She re-ported no complaints of dizziness and very minimal neck pain (1 out of 10 at worst). Active cervical range of mo-tion was full and pain-free. Passive segmental mobility of the cervical and upper thoracic spine was unrestricted. The right sternocleidomastoid demonstrated normal tone. Improvement was observed in cervical deep flexor endurance. The patient’s home exercise program was reviewed for comprehension and proper performance. As the patient had met all previously agreed upon long-term goals, she agreed to discharge from physical therapy intervention. A 1-month follow-up via a telephone call

found that the patient was doing well with no symptoms of dizziness or neck pain.

ACKNOWLEDGEMENTSThe authors would like to thank Maureen McKenna,

PT, MS, OCS, for her willingness to serve as a model, as well as Paul Mensack, PTA, for their assistance with the pictures included in this monograph. The material in this monograph was based to a large extent on the articles “Dizziness in Orthopaedic Physical Therapy Practice: Classification and Pathophysiology” and “Dizziness in Orthopaedic Physical Therapy Practice: History and Physical Examination,” both previously published in the Journal of Manual and Manipulative Therapy and used here with permission.

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NOTES

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NOTES

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1. The most common peripheral vestibular disorder is: a. acoustic neuroma. b. benign paroxysmal positional vertigo. c. Ménière disease. d. perilymphatic fistula.

2. Benign paroxysmal positional vertigo of the left pos-terior canal due to adherent otoconia on the cupula is characterized by:

a. down-beating torsional nystagmus lasting less than 60 seconds.

b. down-beating torsional nystagmus lasting more than 60 seconds.

c. up-beating torsional nystagmus lasting less than 60 seconds.

d. up-beating torsional nystagmus lasting more than 60 seconds.

3. What finding indicates a positive Weber test for unilateral sensorineural hearing loss?

a. air conduction is louder than bone conduction. b. bone conduction is louder than air conduction. c. patient perceives sound coming from normal

ear. d. patient perceives sound coming from abnormal

ear.

4. To differentiate dizziness originating from the pe-ripheral vestibular system versus the upper cervical spine, the therapist would compare active cervical rotation with the:

a. Hallpike-Dix maneuver. b. Fukuda step test. c. head-thrust test. d. neck torsion test. 5. The diagnosis of cervicogenic dizziness is compli-

cated by the fact that neck movements can affect the:

a. cardiovascular system. b. cervical musculoskeletal system. c. vestibular and visual systems. d. all of the above.

Orthopaedic Section Independent Study Course 17.3.3

Cervicogenic Dizziness and Differential Diagnosis of Dizziness in the Orthopaedic Physical Therapy Setting

REVIEW QUESTIONS

6. Which symptoms best describe an acute episode of Ménière disease?

a. constant, severe vertigo with aural fullness and severe tinnitus.

b. constant, severe vertigo without tinnitus but with nausea and vomiting.

c. position-dependent, severe vertigo with tinnitus and nausea.

d. position-dependent vertigo with mild tinnitus and spontaneous nystagmus.

7. Disproportionate weakness in the sternocleido-mastoid and trapezius muscles has been associated with:

a. Arnold-Chiari malformation. b. cervicogenic dizziness. c. toxic vestibulopathy. d. vertebrobasilar ischemia.

8. Which symptoms best describe basilar-type mi-graine?

a. dysarthria, vertigo, ataxia, and bilateral paresthe-sia.

b. hyperacusis, vertigo, unilateral visual symptoms, and quadrilateral paresis.

c. vertigo, bilateral diplopia, ataxia, and ipsilateral arm and leg paresis.

d. vertigo, stupor, tinnitus, and ipsilateral arm and leg paresthesia.

9. Which diagnosis is associated with vertigo brought on with arm exertion but not neck movements?

a. multiple sclerosis. b. subclavian steal syndrome. c. vertebrobasilar ischemia. d. Wernicke encephalopathy.

10. A patient may report a sensation of tilting of the environment as a the result of:

a. mal de debarquement syndrome. b. unilateral otolith dysfunction. c. vertebrobasilar infarction. d. all of the above.

ANSWERS

1.b2.d3.c4.d5.d6.a7.a8.a9.b10.d