09 Kuliah Nyeri Kepala Dr RD-1
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Transcript of 09 Kuliah Nyeri Kepala Dr RD-1
Blok Neurologi:Blok Neurologi:Nyeri KepalaNyeri KepalaRivan Danuaji, dr, M.Kes, Sp.S
OutlineOutline Introduction and approach Pathophysiology Classification:
◦ Primary Headache◦ Secondary Headache
Migraine TTH Cluster Other Headache Conclution
AcuanAcuan
IntroductionIntroduction Headache is the Most Common Symptom that Humans Experience in 99.9% of people with headache there is no sign of tissue damage injuring the brain itself does not cause pain – it causes altered brain function however the membrane and blood vessels of the brain are very pain sensitive
Scale of the problemScale of the problem At least 10% population suffer from headache 1-2% suffer chronic migraine (>15 days/month) 4.4% per year consult GP for headache1
20% of sickness absence from work2
1 Latinovic R et al. JNNP 2006;77:385-387 2 Rasmussen BK. Cephalalgia 2001; 21:774-7
Classification of HeadacheClassification of HeadachePrimary headaches (No underlying cause)
◦Migraine◦Tension-type◦TACs◦Other
Secondary headaches (Underlying cause)◦Medication overuse◦Head/neck injury◦Space-occupying lesion (i.e. brain tumour)◦Vascular cause (i.e. Subarachnoid hemorrhage, intracranial bleed)◦Infectious cause (i.e. meningitis or upper respiratory tract infection)◦+ many others
Headache Classification Committee of the International Headache Society,1988
>65% in patients older than 50
Headache diagnosisHeadache diagnosis Almost entirely on the patients story --> Red Flag Physical Examination always needed Tests, scans etc rarely helpful.
Headache Red Flags - Headache Red Flags - “SNOOP”“SNOOP” Systemic symptoms (fever, weight loss) Secondary risk factors (cancer,
HIV/immunocompromised) Neurologic symptoms or abnormal signs Onset (i.e. new-onset chronic headache) Older patient (i.e. new headaches at age >50 yrs) Previous headache different (i.e. significant
change in headache frequency or clinical features)
Positional component (i.e. increases when upright)
Provocative factors (precipitated by coughing, exercise, sex)
Neurologic Examination of Neurologic Examination of Headache PatientsHeadache Patients Vitals (particularly BP) and Severity of pain (i.e
using VAS) Pupil symmetry, reactivity and fundoscopy Visual fields Eye movements Motor – look for asymmetrical weakness R vs L Reflexes – look for asymmetry (increased
reflexes) R vs L Sensation – extinction to double simultaneous
tactile stimuli Coordination – finger-nose-finger, gain and
tandem gait Examine/touch the head and neck
Olesen J , et al., 2006Pryse –Phyllips WEM, et al., 1997
Adult with Headache
Refer to appropriate on-call hospital team Yes
Headache Management Headache Management PathwayPathwayEmergency
symptoms?
• Thunderclap onset• Accelerated/Malignant hypertension• Acute onset with papilloedema• Acute onset with focal neurological signs• Head trauma with raised ICP headache(see red flags)
• Photophobia + nuchal rigidity + fever +/-rash• Reduced consciousness• Acute red eye: ?acute angle closure glaucoma• New onset headache in:
• 3rd trimester pregnancy/early postpartum• Significant head injury
(esp. elderly/ alcoholics / on anticoagulants)
Adult with Headache
Emergency symptoms? Refer to appropriate on-call hospital team Ye
s
Check ESR, CRP, FBC, LFTPrednisolone 60mg o.d. immediately
Urine and CXR
Consider urgent referral to rheumatology, ophthalmology or
neurology(consideration of temporal artery
biopsy)
Yes
Headache Management PathwayHeadache Management Pathway
Giant cell arteritis?
No
• Symptoms and signs:-• jaw/tongue claudication, amaurosis, scalp
tenderness• temporal artery: prominent, tender, diminished
pulse• other cranial nerve palsies, limb claudication• PMR
• Many headaches respond to high dose steroids, so do not use response as the sole diagnostic factor
• ESR can be normal in 10% (check CRP as well)www.rheumatology.org.uk/includes/documents/cm_docs/2010/m/2_management_of_giant_cell_arteritis.pdf
Adult with Headache
Emergency symptoms? Refer to appropriate on-call hospital team Ye
s
Red flags?
No
Giant cell arteritis?
No
Yes Refer
Headache Management Headache Management PathwayPathway
Check ESR, CRP, FBC, LFTPrednisolone 60mg o.d. immediately
Urine and CXR
Consider urgent referral to rheumatology, ophthalmology or
neurology(consideration of temporal artery
biopsy)
Yes
•Raised intracranial pressure:-•Wakes from sleep (but not migraine or cluster)•Precipitated by Valsalva manoeuvres (cough, straining at stool)•Papilloedema•Other symptoms of raised ICP headache include:-
oPresent upon waking and easing once up (MOH can cause this phenomenon)
oWhooshing pulse-synchronous tinnitusoEpisodes of transient visual loss when changing posture (e.g. upon
standing)oVomiting (in context as migraine causes this!)
•New onset seizures•Persistent new or progressive neurological deficit•Increasing in severity and frequency despite appropriate treatment
•Undifferentiated headache of recent origin and present for >8 weeks
•Triggered by exertion•New onset headache (< 6 months) in:-
>50 years old (consider giant cell arteritis); interrogate patient about previous ‘normal headaches’ as it might not be ‘new’Immunosuppressed / HIV / relevant history of cancer
Adult with Headache
Emergency symptoms? Refer to appropriate on-call hospital team Ye
s
Migraineor
tension headache?
No
Red flags?
No
Giant cell arteritis?
No
Yes Refer
Headache Management Headache Management PathwayPathway
Check ESR, CRP, FBC, LFTPrednisolone 60mg o.d. immediately
Urine and CXR
Consider urgent referral to rheumatology, ophthalmology or
neurology(consideration of temporal artery
biopsy)
Yes
Primary or Secondary?
Headache: historyHeadache: history How old were you when the headaches started? How often do they come? Do they come in relationship to anything else? At what time do they come on? How do they start? Where is the pain? How long does it last? How bad is it? Are there other symptoms? Does anything bring it on? What helps? How long does it last?
Overall Approach to Overall Approach to HeadacheHeadache
Wolff HG, et al., 2001
Any secondary Headache disorder can mimic a primary headache disorder
Adult with Headache
•If relevant, stop combined oral contraceptive•Ensure not overusing analgesics or triptans•Modify lifestyle (adequate sleep, hydration, reduce caffeine intake, trigger avoidance)•If prophylaxis necessary, try the following for 3 months at the target dose before judging efficacy:-Migraine prophylaxisa)Propranolol SR 80mg o.d. increase gradually to 240mg o.d. or maximum tolerated below that• If ineffective or contraind: Amitriptyline 10mg o.n. increasing by 10mg/week to ≤75mg• Don’t bother with pizotifen (weight gain, sedation, little benefit)• If above ineffective/not tolerated, try Topiramate 25mg o.d. increasing by 25mg every 2-weeks aiming for a target of 50mg b.d. NOTE: teratogenic and potential interaction with combined oral contraceptive
Tension Type Headache prophylaxisAmitriptyline 10mg o.n. increasing by 10mg a week up to 75mg or maximum tolerated below that
Emergency symptoms? Refer to appropriate on-call hospital team Ye
s
Cluster headache
?
No
Continue treatment
for 9-12 months;then consider
stopping
Still troublesome
?
No
Still troublesome
?
No
Nofurther
treatment
Migraineor
tension headache?
No
Red flags?
No
Giant cell arteritis?
No
No
Stop offending medication
(for 2 months if MOH)
Yes
Yes
Yes Refer
Try acute treatments
Yes
Can you diagnose migraine or
tension headache?
Yes
No
Refer
Yes
Prescribe acute treatment (< 10 times/month)
Yes
Secondary causes?
e.g. sinusitis, TMJ pain
Hb, Ca2+, TFT,ESR, CRP
R/V lifestyle & medication
Treat as necessary
No
Suspect:-•Medication overuse headache (MOH)?•Drug induced?
Yes
Still troublesome
?
Headache Management PathwayHeadache Management Pathway
Check ESR, CRP, FBC, LFTPrednisolone 60mg o.d. immediately
Urine and CXR
Consider urgent referral to rheumatology, ophthalmology or
neurology(consideration of temporal artery
biopsy)
Yes
PATOPHYSIOLOGYPATOPHYSIOLOGY
Basic Pathophysiology of Pain ProcessesBasic Pathophysiology of Pain Processes
Devor, 1996
Stimulus Perception
PNSSpinal cord
Brainstem
BRAIN
Gate-control inhibitionInjury triggered
“central sensitization”
Brainstem collaterals
Peripheral(receptor)
sensitization
NervePathophysiology(ectopic)
Sympathetic-sensory
Coupling,neurogenic
Inflammation?
Descending inhibition
PERCEPTION
MODULATION
CONDUCTION
TRANSDUCTION
PAIN – SERIES OF EVENTSPAIN – SERIES OF EVENTS
PAIN
TRANSMISSION
Pathophysiology Primary Pathophysiology Primary HeadacheHeadache AuraAura
◦Spreading cortical depression, not Spreading cortical depression, not ischemiaischemia
BrainstemBrainstem
◦Migraine “generator” in dorsal raphe, locus Migraine “generator” in dorsal raphe, locus ceruleus and periaqueductal gray matterceruleus and periaqueductal gray matter
◦PET scans show increased blood flowPET scans show increased blood flow
PathophysiologyPathophysiology Threshold surpassed:Threshold surpassed:
◦Brainstem “generator” Brainstem “generator” liberates CGRP (Calcitonin liberates CGRP (Calcitonin Gane-Related Peptide)Gane-Related Peptide)
◦Activation of Activation of trigeminovascular systemtrigeminovascular system
CGRP also elevated with pulsating chronic tension-CGRP also elevated with pulsating chronic tension-type headachestype headaches
PathophysiologyPathophysiology Nitric oxideNitric oxide
◦VasodilatorVasodilator◦Promotes central Promotes central
sensitization of trigeminal sensitization of trigeminal nociceptorsnociceptors
◦Sumatriptan decreases Sumatriptan decreases NO release in addition to NO release in addition to inhibiting CGRP releaseinhibiting CGRP release
PathophysiologyPathophysiology Trigeminal StimulationTrigeminal Stimulation
◦Ca channel activation: substance P Ca channel activation: substance P releaserelease
◦Feedback to DRG: NMDA (Feedback to DRG: NMDA (N-Methyl-D-aspartate) & AMPA ( & AMPA ((α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) release, leading to wind uprelease, leading to wind up
◦Release of prostaglandins, kinins that Release of prostaglandins, kinins that induce perivascular inflammationinduce perivascular inflammation
◦NO and CGRP further capillary leakageNO and CGRP further capillary leakage
PathophysiologyPathophysiology Potentials for future abortive treatment:Potentials for future abortive treatment:
◦Antagonists of: CGRP, NO, GlutamateAntagonists of: CGRP, NO, Glutamate◦Agonists of adenosine A1 receptorsAgonists of adenosine A1 receptors
CLASIFICATIONCLASIFICATION
©International Headache Society 2003/5
INTERNATIONAL CLASSIFICATIONINTERNATIONAL CLASSIFICATIONofofHEADACHE DISORDERSHEADACHE DISORDERS
2nd edition (12nd edition (1stst revision) revision)
(ICHD-IIR1)
©International Headache Society 2003/5
ClassificationClassificationPart 1:Primary headache disorders:
no other causative disorderPart 2: Secondary headache disorders
(ie, caused by another disorder):new headache occurring in close
temporal relation to another disorder that is a known cause of headache
coded as attributed to that disorder(in place of previously used term associated
with)
Part 3: Cranial neuralgias, central and primary facial pain and other headaches
©International Headache Society 2003/5
ClassificationClassificationPart 1: The primary headaches
1. Migraine2. Tension-type headache3. Cluster headache
and other trigeminal autonomic cephalalgias4. Other primary headaches
©International Headache Society 2003/5
Part 2: The secondary Part 2: The secondary headachesheadaches
5. Headache attributed to head and/or neck trauma
6. Headache attributed to cranial or cervical vascular disorder
7. Headache attributed to non-vascular intracranial disorder
8.Headache attributed to a substance or its withdrawal
9. Headache attributed to infection.10. Headache attributed to disorder of homoeostasis 11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures12. Headache attributed to psychiatric disorder
©International Headache Society 2003/5
ClassificationClassificationPart 3: Cranial neuralgias, central and primary facial pain and other headaches
13. Cranial neuralgias and central causes of facial pain14. Other headache, cranial neuralgia, central or primary facial pain
MIGRAINEMIGRAINE
MigraineMigraine• Unilateral onset• Throbbing• 4 – 72 hours• Sensory Sensitivity
–Light–Sound–Smells–Movement
migraine behaviour
Common misdiagnosis of Common misdiagnosis of migrainemigraine
Cervicogenic Headache (30% migraine→neck pain)
Chronic Tension Type Headache Eye Strain Dental TMJ dysfunction Sinus headache Hypertensive Headaches
Migraine CriteriaMigraine CriteriaAt least 5 attacks fulfilling the followingHeadache attacks lasting 5 to 72 hours with at least 2 of the following characteristics
◦Unilateral location◦Pulsating quality◦Moderate or severe intensity◦Aggravation by walking stairs or similar
routine physical activity
Migraine Criteria Migraine Criteria (cont.)(cont.) During headache at least 1 of the following
◦Nausea and/or vomiting◦Photophobia and phonophobia
No evidence of organic disorder causing chronic headaches
IHS Migraine Condensed: IHS Migraine Condensed: One Simple QuestionOne Simple Question Have you experienced 5 or more attacks of unprovoked head pain that lasted 4
to 72 hours, were severe enough to inhibit or even prohibit routine activity, and were accompanied by light/sound sensitivity, nausea, or both?
IHC II auraIHC II aura
• focal neurological symptoms• develop over 5-20 minutes• last for < 60 minutes
AurAuraa
• Fortification spectra = teichopsia
• Photopsia• Scotoma• Shimmering• Paraesthesia• HemiparesisVauban 17th
century
Migrainous AuraMigrainous Aura
Migrainous AuraMigrainous Aura
Migrainous AuraMigrainous Aura
What happens during a migraine?What happens during a migraine?
Migraine causeMigraine cause cause unknown but strongly inherited a lower threshold to spontaneously
produce symptoms as if the head and brain had been injured
many effective treatments
TriggersTriggers foods : spices, wine , chocolate, citrus food additives : monosodium
glutamate sleep : both too much and too little stress : mainly offset female hormones : fluctuating or falling
oestrogen
Migraine Treatment: Migraine Treatment: acuteacute
• Aspirin 900mg + metoclopramide (and/or paracetamol)
• NSAID• Triptans: 5-HT 1b/d agonists
– Almotriptan– Eletriptan– Frovatriptan– Naratriptan– Rizatriptan– Sumatriptan
• Antipsychotics: chlorpramazine etc• Steroids?
Generic and fastest acting
Migraine Treatment: Migraine Treatment: ProphylaxisProphylaxis• Propranolol• Amitriptyline• (pizotifen….no evidence…..gain weight and
sleepy)• Topiramate
–Wt loss, paraesthesia common–Memory problems, 1% renal calculi
• Gabapentin
• unusual stuff: Botox, methysergide, lisinopril...• Alternative stuff:
–Feverfew+riboflavin, butterburr, Mg, acupuncture
BMJ 2011;342:d583Pharmacological Prevention of Migraine
TENTION TYPE TENTION TYPE HEADACHEHEADACHE
Tension-Type HeadacheTension-Type Headache Most common headache
syndrome Episodic < 15 days per month Chronic > 15 days per month
TTH - CharacteristicsTTH - Characteristics 30 minutes to 7 days Pressing or tightening Mild to moderate pain Variable location, often bilateral Nausea and vomiting rare
Typical patient : any
Episodic Tension Type Episodic Tension Type HeadacheHeadache..IHS Criteria Tension type headaches < 15 per month. Lasts 30 mins to 7 days No nausea or vomiting No photophobia and phonophobia (1 ok) Headache has at least 2 of the following
criteria:a. pressing/tighteningb. Bilateral Mild-moderate Not aggravated by physical activity.
Chronic Daily HeadacheChronic Daily Headache Affects 4-5% of the population. Definiton: head pain for at least 4
hours for more than 15 days/month. Often develops from an episodic
headache disorder either migraine or episodic tension type headache
Includes chronic tension type headache(CTTH) and chronic daily migraine
Chronic Tension Type Chronic Tension Type Headache.Headache. Develops from episodic tension
type headaches The most common form of CDH. Familial tendency. Medication rebound headache
may be a factor in the transformation of episodic headache to CDH.
Chronic Tension Type Chronic Tension Type HeadacheHeadache Affect women more than men Most common in middle age Stress is often a trigger Average duration is 4-13 hours.
Treatment of CTTH.Treatment of CTTH. Treating each headache increases
the frequency and severity of the headaches.
Reserve medications for worse than usual headache.
Expert opinion: treat 2 headaches a week.
Treatment of TTHTreatment of TTH Simple analgesia:ibuprofen is
more effective than acetaminophen.
Combine analgesics with a sedating anit-histamine eg diphenhydramine.
Limit treatment to 2 days a week to prevent rebound headaches.
TTH - TreatmentTTH - Treatment Stress
management◦ Biofeedback◦ Stress reduction◦ Posture correction
Medication rarely needed in ETTH◦ Benzodiazepines◦ amitriptyline
CTTH◦ Abortive
NSAIDs ASA-caffeine-
butalbital Phenacetin
◦ Preventative Antidepressants Muscle relaxants NSAIDs
Prevention of CTTHPrevention of CTTH Tricyclic antidepressants. Stress management Tizanidine SSRIs:prozac Anticonvulsants:gabapentin and
topiramate. Acupuncture
CLUSTER HEADACHECLUSTER HEADACHE
©International Headache Society 2003/5
3.1 Cluster headache (IHS)3.1 Cluster headache (IHS)A. At least 5 attacks fulfilling criteria B-DB. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 min if untreatedC. Headache is accompanied by ≥1 of the following:
1. ipsilateral conjunctival injection and/or lacrimation2. ipsilateral nasal congestion and/or rhinorrhoea3. ipsilateral eyelid oedema4. ipsilateral forehead and facial sweating5. ipsilateral miosis and/or ptosis6. a sense of restlessness or agitation
D. Attacks have a frequency from 1/2 d to 8/dE. Not attributed to another disorder
Cluster HeadacheCluster Headache Frequency clusters – every time each year or season,
then free
Pain excruciating penetrating, boring continuous, non-
throbbing
Duration 15mins-3 hrs; same clock time each day (2am);
several episodes / day
Location ALWAYS the same side
Symptoms watering eyes nasal stuffiness, runny nosered eye, swollen eyelids osweating
Typical patient : middle aged male smoker
Cluster HeadacheCluster Headache
ClusterCluster Intensely severe
pain Unilateral Periorbital 15 to 180 minutes Nausea and
vomiting uncommon
No aura
Alcohol intolerance
Male predominance
Autonomic hyperactivity◦ Conjunctival
injection◦ Lacrimation◦ Nasal congestion◦ Ptosis
ClusterCluster Episodic
◦ Two episodes per year to one every two or more years 7 days to a year
Chronic◦ Remission phases
less than 14 days◦ Prolonged
remission absent for > one year
Cluster - TreatmentCluster - Treatment Preventative
◦ Calcium channel blockers
◦ Bellergal◦ Lithium◦ Methysergide◦ Steroids◦ Valproate◦ Antihistamines
Abortive◦ Oxygen◦ 5-HT receptor
agonists◦ Intranasal
lidocaine
OTHER HEADACHEOTHER HEADACHE
Secondary headache after injury Should begin within 7 days of head injury
(to meet IHS criteria) Consider diagnosis: subdural, CSF leak,
dissection Headaches may resemble primary
headache disorders (i.e. migraine, tension)
Often assoc with other “post-concussive” symptoms: vertigo, tinnitus, cognitive changes, sleep problems, depression, medication overuse
There is no evidence-based approach and no guidelines
Post-Traumatic HeadachePost-Traumatic Headache
-anterior communicating artery (30-35%),-the bifurcation of the internal carotid and posterior communicating artery (30-35%) --the bifurcation of the middle cerebral artery (20%) -bifurcation of the basilar artery, and the remaining posterior circulation arteries (5%)
SymptomsSymptoms Headache 85-95% Neck stiffness 74-84% n/v , photophobia 48% Mental status 43%
Less common:◦ Focal deficit, seizures, coma, CN palsy, papilledema, ocular
hemorrhage
*sentinel bleed
First primary sexual or exertional First primary sexual or exertional headacheheadache
SAH has to be excluded as 1/3 of SAHs occur during activities such as bending, lifting, defecation or sexual intercourse.
Copyright restrictions may apply.
Wityk, R. J. JAMA 2001;285:2757-2762.
Imaging of Stroke
Copyright restrictions may apply.
Wityk, R. J. JAMA 2001;285:2757-2762.
Anatomy of Carotid Artery Dissection
2cm distal to carotid origin-ends at skull base
Subintimal dissection -stenosis
Mickey mouse ears: expansion by hyperintense hematoma of the outer lumen of the artery
Carotid DissectionCarotid Dissection Fronto-orbital headache before ischemia: 55-100%
Painful Horner’s, Painful tinnitus Carotid bruit, dysguesia, ipsilateral neck pain,
cerebral or retinal ischemia
Triggers: cough, sneeze, trauma Risks: syphilis, Marfans, Ehlers-Danlos, FMD Prognosis: good (60% resolve spont.;85% do well)
37 year old after a motorcycle accident Sara Mazzucco, MD; and Nicolo` Rizzuto, MD
Neurology 2006
cavernomacavernoma
MRI demonstrating a left-sided cavernoma (a and b) with an associated developmental venous anomaly (c) in the dorsal midbrain region adjacent to the periaqueductal grey matter. Cephalalgia, Vol. 22, No. 2, 107-111 (2002)
MSMS
MS patients with a plaque located within the midbrain, in proximity to the PAG, showed a four-fold increase in migraine-like headaches (odds ratio 3.91, 95% confidence interval 2.01 to 7.32; P < .0001) when compared to MS patients without a plaque in this location
Headache 2005 Jun;45(6):670-7
occipital arteriovenous malformationoccipital arteriovenous malformation
Kurita, H. et al. Arch Neurol 2000;57:1219
34-year-old man started to experience monthly headaches: visual prodrome consisting of scintillating bright lights in the left visual field that slowly expanded over several minutes. Shortly after the visual symptom subsided, right-sided throbbing headaches developed along with nausea and vomiting, which usually lasted 2 to 4 hours. Normal neuro exam. He was treated by radiosurgery with obliteration of the AVM and resolution of the headaches
Erle C.H. Lim, Raymond C.S. Seet: Sudden-Onset Headache And Seizures In A Young Man. The Internet Journal of Neurology. 2005. Volume 4 Number 2
Trigeminal NeuralgiaTrigeminal Neuralgia
VERY short (<1 sec) severe pain
Knife-like Local triggering : eating
etc
Typical patient : middle aged / elderly woman
Sinus InnervationSinus Innervation Ophthalmic and maxillary
branches of 5th cranial nerve Greater superficial petrosal
branch of 7th cranial nerve Ostiomeatal complex > turbinates
> septum > sinus mucosa
Frontal SinusFrontal Sinus Ophthalmic
branch of 5th cranial nerve
Pain referred to forehead and anterior cranial fossa
Anterior EthmoidAnterior Ethmoid Ophthalmic
division Anterior ethmoid
nerve off nasociliary
Anterior septum, turbinates, ostiomeatal complex
Posterior Ethmoid and Posterior Ethmoid and SphenoidSphenoid Maxillary division
◦ Posterior ethmoid nerve
◦ Posterior septum, parts of superior and middle turbinates
Ophthalmic division
Greater superficial petrosal nerve
Maxillary SinusMaxillary Sinus Maxillary
division of 5th cranial nerve◦Posterior
superior alveolar◦Infraorbital◦Anterior superior
alveolar
Referred OtalgiaReferred Otalgia Oral cavity
◦Mandibular division of 5th cranial nerve
◦Auriculotemporal nerve Pharynx
◦Jacobson’s branch of 9th cranial nerve Hypopharynx and supraglottic
larynx◦Arnold’s branch of 10th cranial nerve
HistoryHistory First occurrence Timing Quality Treatments Associated symptoms Precipitating factors
Past Medical HistoryPast Medical History Head injuries, infections,
surgeries Psychiatric diagnoses Medications
◦OTC analgesics ◦OCP ◦Herbal medications◦Antihypertensives & vasodilators
Alcohol, tobacco, drugs
Physical ExaminationPhysical Examination Complete head & neck exam
◦Cranial nerves◦TMJ & muscles of mastication◦Scalp vessels◦Trigger points
Neurological exam
Diagnostic TestsDiagnostic Tests EEG CT and/or MRI EMG TMJ radiography Cervical spine films Labs Psychometric testing
Conclusion of Secondary causesConclusion of Secondary causesDisruption of outflow-venous thrombosis, dural fistula-radical neck dissection-right heart failure-COPD-(obesity)
Hormonal-hypoparathyroidism-hyper/hypothyroidism-Cushing's ?Addison's-PCO
Toxins/meds-vitamin A-Nalidixic acid,tetracycline,nitrofurantoin,indocid,steroids/withdrawal,others
Medical conditionsCRF, SLE, Anemia/polycythemia
Infectious-meningitis,encephalitis,Lyme,HIV
Trauma
MANAGEMENTMANAGEMENT
TreatmentTreatmentExplanation, set realistic objectives
Lifestyle change
Treatment of the attack
Treatment to reduce attack frequency
Treatment of the attackTreatment of the attack1. General pain relievers2. Migraine-specific treatments
- triptans and ergots
3. Cluster specific treatment- oxygen- triptans
General pain relievers : General pain relievers : migraine, tensionmigraine, tension
aspirin
paracetamol
ibuprofen
codeine
tramadol
Fast? ✔✔ ✔ ✔Safe? ✔✔OK
for long term?
✖ ✔✔ ✖ ✖✖✖
Not suitable : dextropropoxyphene “Doloxene; Di-Gesic” morphine, pethidine
Additives : metoclopramide (nausea) caffeine
Effective Abortive AgentsEffective Abortive Agents TriptansTriptans DihydroergotamineDihydroergotamine NSAIDsNSAIDs Anti-emeticsAnti-emetics Lidocaine?Lidocaine? Opioids?Opioids?
TriptansTriptans 5-HT5-HT1B 1B action: vasoconstriction by action: vasoconstriction by
acting against NOacting against NO 5-HT5-HT1D1D action: inhibit CGRP release action: inhibit CGRP release
Should be very effective, yet only Should be very effective, yet only 70-80% effective, with 50% 70-80% effective, with 50% headache recurrence.headache recurrence.◦Cardiac risk, side effects further limit Cardiac risk, side effects further limit
useuse
TriptansTriptans PO versions require 60-90 PO versions require 60-90
minutes to effectminutes to effect 50% success rate PO vs. 75-80% 50% success rate PO vs. 75-80%
s/cs/c Newer triptans offer no real Newer triptans offer no real
advantage over originaladvantage over original Subset of patients do respond Subset of patients do respond
well to this abortive agent in well to this abortive agent in home settinghome setting
DihydroergotamineDihydroergotamine Same 5-HT action, but slower bindingSame 5-HT action, but slower binding
◦Impact of IM may require 2 hoursImpact of IM may require 2 hours◦Nasal version requires up to 4 hoursNasal version requires up to 4 hours
If given IV may initially increase CGRP If given IV may initially increase CGRP release, producing dramatic headache release, producing dramatic headache increaseincrease
Does not increase N&VDoes not increase N&V Most initial research success probably Most initial research success probably
due to adjunctive anti-emeticsdue to adjunctive anti-emetics
NSAIDsNSAIDs Excellent for mild to moderate Excellent for mild to moderate
migrainesmigraines No effect on neurotransmittersNo effect on neurotransmitters Direct inhibition of most Direct inhibition of most
perivascular inflammationperivascular inflammation Ketorolac at best 50-60% success Ketorolac at best 50-60% success
as abortive for severe migrainesas abortive for severe migraines
Dopamine AntagonistsDopamine Antagonists PhenothiazinesPhenothiazines ButyrophenonesButyrophenones MetoclopramideMetoclopramide
Dopamine AntagonistsDopamine Antagonists High adverse event rateHigh adverse event rate
◦Need to treat prophylactically: Need to treat prophylactically: benztropine, lorazepam, benztropine, lorazepam, diphenhydraminediphenhydramine
Low headache recurrence rateLow headache recurrence rate Only droperidol as effective IM as Only droperidol as effective IM as
IVIV Dysphoria cannot be treated, found Dysphoria cannot be treated, found
to be horrible by some patientsto be horrible by some patients
LidocaineLidocaine Intranasal lidocaine found Intranasal lidocaine found
effective in two studies, but of effective in two studies, but of very short duration, 70% very short duration, 70% headache recurrenceheadache recurrence
Mechanism of action uncertain as Mechanism of action uncertain as blocks Na+ channels not Ca++ blocks Na+ channels not Ca++ onesones
OpioidsOpioids At best 50% effective, high At best 50% effective, high
recurrence raterecurrence rate Often required in combination for Often required in combination for
complex casescomplex cases Biggest effect: allows patient to Biggest effect: allows patient to
enter REM sleep, which shuts enter REM sleep, which shuts down dorsal raphe activitydown dorsal raphe activity
Analgesia-induced rebound Analgesia-induced rebound headachesheadaches Obtain good headache medication Obtain good headache medication
historyhistory May occur with simple analgesics or May occur with simple analgesics or
with opioidswith opioids If cessation of medication may take 3 If cessation of medication may take 3
months to return to baseline headache months to return to baseline headache frequencyfrequency
DHE IV q8h x 2-3 days resolves DHE IV q8h x 2-3 days resolves problemproblem
Preventing Future Preventing Future HeadachesHeadaches Headache diary: identifying Headache diary: identifying
triggerstriggers ProphylaxisProphylaxis
◦DietDiet◦ExerciseExercise◦SleepSleep◦Stress modificationStress modification
Preventing Future Preventing Future HeadachesHeadaches Medications:Medications:
◦Valproate: 45% patients more than Valproate: 45% patients more than placebo with 50% decrease in placebo with 50% decrease in headache rateheadache rate
◦Beta Blockers: 40%Beta Blockers: 40%◦Flunarazine: 42%Flunarazine: 42%◦Pizotifen: 20%Pizotifen: 20%◦Riboflavin: 37%Riboflavin: 37%
Preventative drugsPreventative drugs “mixed bag” of drugs used for other conditions
found to be effective in headache usually by chance usually for high blood pressure, depression,
epilepsy all work in somebody ; none works in everybody generally reduce frequency but do not change
attacks key to success : trial and error : persist need to start at low dose and increase until effective
or not tolerated about 50 % of patients will get 50% or more
reduction in attacks
Main migraine preventersMain migraine preventersEffectiveness
Tolerability / safety
Good Fair Poor
Good propranolol verapamilBotox
Fair amitriptylinetopiramatevalproate
pizotifenibuprofen
Poor methysergide
Tension preventersTension preventersEffectiveness
Tolerability / safety
Good Fair Poor
Good
Fair amitriptyline ibuprofen
Poor
Cluster preventers - balance of Cluster preventers - balance of effectiveness and safety / tolerabilityeffectiveness and safety / tolerability
Effectiveness
Tolerability / safety
Good Fair Poor
Good verapamil
Fair topiramate
Poor methysergidesteroids
lithium
Non drugNon drugHerbalManual therapies
◦physiotherapy – caution◦acupuncture – probable
Electrical occipital nerve stimulation : possiblyClosure of hole in heart - no
Anger
Fear
Anxiety
Depression
PERCEPTION OF PAIN
Noxious Stimuli
PS Y
CH
OL O
GI C
AL
NOCICEPTIVE
A
B
MELIALA 2004
PERILAKU NYERI(PAIN BEHAVIOUR)
PENDERITAAN(SUFFERING)
NYERI(PAIN)
BIOPSIKOSOSIAL(BIOPSYCHOSOCIAL)
NOSISEPSI(NOCICEPTION)
PENGERTIAN MODEL NYERI
BYERS AND BONICA, 2001MODIFIKASI PENULIS
•Terapi kognitif•Restorasi fungsional
•Opioid•Tramadol
•Oxcarbazepine•Gabapentin
•Eperisone HCL•Paracetamol
•OAINS
•Antidepresan•Psikotropika•Relaksasi•Spiritual
•Diklofenak•Etodolac•Dexketoprofen•Celecoxib•Modalitas fisik
ConclusionConclusion Headache & facial pain are
common complaints History most important in making
accurate diagnosis Recognize psychological aspects
of pain Recognize “Red Flag” Do a proper management based
on pathophysiology
The task of a doctor:The task of a doctor:
TO CURE IS SOMETIMES TO TREAT IS OFTEN TO COMFORT IS ALWAYS
A. Pare (1598)
AKU TELAH MEMBERIKAN OBAT YANG AKU KENAL TERHADAP PENYAKIT
YANG AKU PAHAMI KEPADA PASIEN YANG
SEBAGIAN BESAR TIDAK TAHU APA-APA
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