WHAT TYPES OF SENSORY INFORMATION DO

THE POSTERIOR COLUMN-MEDIAL LEMNISCUS

PATHWAY AND THE ANTEROLATERAL PATHWAY

CONVEY

Posterior column-medial lemniscus pathway (PCML): proprioception, vibration

sense, and fine discriminative touch

Anterolateral pathway: pain, temperature sense, and crude touch

Spinothalamic

Spinoreticular

Spinomesencephalic

WHY IS TOUCH SENSATION NOT ELIMINATED BY

A LESION IN EITHER PATHWAY.

Some aspects of touch sensation are carried by both pathways touch

sensation is not eliminated in isolated lesions to either pathway

DEFINE THE TERM DERMATOME.

Dermatome: a peripheral region innervated by sensory fibers from a single

nerve root; dermatomes form a map over the surface of the body that is useful

for localizing lesions

STATE THE LOCATION OF THE 1° NEURONS IN

THE POSTERIOR COLUMN-MEDIAL LEMNISCUS

PATHWAY AND NAME THE FIBER TRACTS

THROUGH WHICH 1° NEURONS PROJECT

Location of first order neurons in PC-ML pathway: dorsal root ganglion

Fiber tracts through which they project:

Medially: Gracile fasciculus--carries information from the legs and lower

trunk

Laterally: Cuneate Fasciculus--carries information from the upper trunk

above T6, arms, and neck

Note that below T6, the gracile fasciculus ecompasses the entire posterior

column.

STATE THE LOCATION OF THE 2° NEURONS IN

THE PC-ML. NAME THE TRACT FORMED AND

IDENTIFY THE LOCATION OF THE NEURAXIS AT

WHICH THEY DECUSSATE.

The first order neurons synapse onto the second-order neurons in the nucleus

gracilis and nucleus cuneatus, respectively, which are located in the caudal

medulla.

The decussation of the axons of the 2°neurons is termed the internal arcuate

fibers.

These fibers form the medial lemniscus on the other side of the medulla and

ascend.

Ventral SpinocellebellarTract

Dorsal Spinocellebellar

Tract

Spinal TrigeminalNucleus (includes pink)

Spinal Trigeminal Tract

Cuneate Tract

Graciile Tract

Graciile Nucleus

Cuneate Nucleus

Spinal Accessory NucleusAnterolateral System

Rubrospinal Tract

Medulla

STATE THE LOCATION OF THE 3° NEURONS IN

THE PC-ML AND DESCRIBE THE PATH OF THEIR

ASCENT TO THE PRIMARY SOMATOSENSORY

CORTEX.

Third order neurons in the PC-ML pathway are located in the thalamus.

They synapse with the second-order neurons at the ventral posterior lateral

nucleus These axons project through the posterior limb of the internal capsule

in tracts called thalamic somatosensory radiations

They continue to primary somatosensory cortex in the Postcentral gyrus

DESCRIBE THE SOMATOTOPY OF THE MEDIAL

LEMNISCUS IN THE MEDULLA, THE PONS AND

THE MIDBRAIN. The Medial lemniscus forms in the caudal medulla after PC-ML fibers

decussate.

legs= medial

arms= lateral

In the caudal medulla (right after decussation)the medial lemniscus is vertical

legs=ventral

arms=dorsal

In the pons the organization is inclined

leg=lateral

arms=medial

as it moves up to the midbrain it becomes more lateral

PREDICT THE FINDINGS ON NEUROLOGICAL

EXAM OF A LESION IN THE DC-ML

Lesion in the PC-ML: Complete loss of vibration and position sense on both

sides

caused by trauma, compression due to tumor, multiple sclerosis

tingling, numb sensation, a feeling of tight band-like sensation on trunk or

limbs, or a sensation similar to gauze on the fingers when trying to palpate

objects

LESION OF THE MEDIAL LEMNISCUS

Deficit is contralateral to lesion

Lesion would be in the medial medulla or above

Contralateral loss of vibration and joint position sense

Sensory ataxia possible

LESION OF THE THALAMUS

Complete sensory loss on contralateral side

Can be more noticeable in hand, feet, and face than in trunk and proximal

extremities

If the lesion is large enough all sensory modalities can be involved with no

motor deficits

Dejerine-Roussy syndrome: lesion to thalamus that causes severe contralateral

pain

LESION OF THE PRIMARY SOMATOSENSORY

CORTEX

Complete loss on contralateral side

Discriminative touch and joint position sense are often most severely affected

but all modalities can be involved

“cortical sensory loss”= all primary modalities are relatively spared but with

extinction or decrease in stereognosis and graphesthesia

STATE THE LOCATION OF THE 1° NEURONS IN

THE SPINOTHALAMIC TRACT AND WHERE THEY

SYNAPSE ONTO 2°NEURONS.

Small diameter, unmyelinated 1° axons send info of pain and temp

Enter the spinal cord at dorsal root ganglion.

Synapse with 2nd order neurons in the gray matter of spinal cord- mainly dorsal

horn marginal zone (lamina I) and deep in the dorsal horn in lamina V.

Some axon collaterals may ascend or descend a few segments in Lissauer

tract before synapsing with 2nd neurons

NAME THE TRACT FORMED BY 2° NEURONS

AND STATE WHERE THIS TRACT DECUSSATES.

The 2nd order neurons crossover in the spinal cord anterior (ventral)

commissure to ascend in the anterolateral white matter (tracts ascend 2-3

spinal segments before fully crossing, so lateral cord lesions will affect

contralateral pain and temp beginning a few segments below the level of the

lesion)

EXPLAIN WHY LESIONS IN THE SPINOTHALAMIC

TRACT PRODUCE LOSS OF PAIN AND TEMP. A

FEW SEGMENTS BELOW THE LEVEL OF THE

LESION.

It takes 2-3 segments for the spinothalamic tract neurons to reach the opposite

side of the spinal cord in the anterior commissure

Lateral cord lesions will affect contralateral pain and temperature sensation

below level of lesion

NAME THE NUCLEUS IN WHICH 2° NEURONS

SYNAPSE ONTO 3° NEURONS IN THE

SPINOTHALAMIC PATHWAY. NAME THE TRACT

THROUGH WHICH THE 3°NEURONS PROJECT.

The spinothalamic tract neurons synapse with 3rd order neurons mainly in the

Ventral posterolateral nucleus (VPL)

These 3rd order neurons in the VPL project to the somatosensory cortex in the

postcentral gyrus

They ascend through posterior limb of internal capsule in the thalamic

somatosensory radiations to reach the primary somatosensory cortex

DESCRIBE THE SOMATOTOPY OF THE

SPINOTHALAMIC TRACT WITHIN THE SPINAL

CORD.

The somatotopic organization of the spinothalamic tract

Feet are most laterally (and ventrally) represented

Neck is most medially (and dorsally) represented.

DC-ML ANTEROLATERAL

Dorsal root ganglion Dorsal root ganglion

Gracile and cuneate

fasciculus

Lissauer tracts

Gracile/cuneate nuclei in

caudal medulla

Marginal zone of gray

matter

Internal arcuate fibers Anterior commissure

Medial lemniscus Anterolateral white matter

VPL nucleus VPL nucleus

Posterior limb of Internal

capsule

Posterior limb of internal

capsule

Somatosensory cortex Somatosensory cortex

NAME THAT PATHWAY THAT CONVEYS TOUCH

INFORMATION FROM THE FACE TO THE CORTEX,

AND NAME THE THALAMIC NUCLEUS THROUGH

WHICH IT RELAYS.

The Trigeminal lemniscus conveys sensory info from the face via the ventral

posterior medial nucleus of the thalamus (VPM) to the somatosensory cortex

NAME THE PATHWAY THAT CONVEYS PAIN AND

TEMPERATURE INFORMATION FROM THE FACE

TO THE CORTEX, AND NAME THE THALAMIC

NUCLEUS THROUGH WHICH IT RELAYS.

Pain and temperature sensation for the face is carried by the trigeminothalamic

tract to the primary somatosensory cortex. It relays information through the

ventral posterior MEDIAL (VPM) nucleus of the thalamus.

SENSATION TO THE FACE

Discriminatory touch to Face Pain and Temperature to Face

Trigeminal ganglion Trigeminal ganglion

Trigeminal sensory nucleus of

pons

Spinal trigeminal tract

Trigeminal lemniscus Spinal trigeminal nucleus

*Pain/temp circuit descends to

medulla and then ascends

Trigeminothalamic tract

VPM VPM

Somatosensory Cortex Somatosensory Cortex

DESCRIBE THE ROLES OF THE PERIAQUEDUCTAL

GRAY IN MEDIATING PAIN SENSATION.

The spinomesencephalic projects to the midbrain periaqueductal gray matter, which participates in central modulation of pain.

Interacts with local circuits of spinal cord dorsal horn and long-range modulatory inputs via gate-control theory: sensory inputs from large-diameter non-pain A-ß fibers reduce pain transmission through dorsal horn.

The periaqueductal gray receives inputs from the hypothalamus, amygdala, and cortex. It inhibits pain transmission in the dorsal horn via a relay in a region at the

pontomedullary junction called the rostral ventral medulla (RVM). Includes (5-HT) neurons of the raphe nuclei that project to the spinal cord,

modulating pain in the dorsal horn. The RVM also sends inputs mediated by the neuropeptide substance P to

the locus ceruleus which in turn sends (NE) projections to modulate pain in the spinal cord dorsal horn.

DESCRIBE THE SOMATOTOPIC ORGANIZATION

OF THE TONGUE, FACE, HANDS, ARMS, TRUNK,

KNEES AND LEGS AND TOES ALONG THE

SOMATOSENSORY CORTEX.

The primary somatosensory cortex is somatotopically organized with the face

represented most laterally, and the leg represented most medially.

Toes are represented medially within the longitudinal fissure.

The tongue is represented inferiorly to the face, at the superior border of the

sylvian fissure.

Head and neck are NOT located with face, and are represented superiorly

and medially.

LISSAUER’S TRACT

Path of the axons of the first order neurons of the spinothalamic tract that

ascend one or two vertebral levels before synapsing on second order sensory

neurons in the gray matter of the dorsal horn

VPL OF THE THALAMUS

VPL of the thalamus: where the second order neurons of spinothalamic tract

and the posterior column-medial lemniscal tract (PCML) synapse onto third

order neurons, to relay information to the cortex.

MARGINAL ZONE,

The most dorsal part of the gray matter of the spinal cord

LESIONS TO ISOLATED NERVES

Dermatomal distribution of sensory loss or cutaneous domain distribution if

more peripheral

DISTAL SYMMETRICAL POLYNEUROPATHY,

Bilateral hand and stocking distribution

HEMICORD LESIONS (BROWN-SEQUARD

SYNDROME)

Complete lesion of one half of the spinal cord at a specific

level.

Damage to lateral corticospinal tract causes ipsilateral upper

motor neuron-type weakness.

Damage to the posterior columns of the PCML will cause

ipsilateral loss of vibration and joint position sense.

Damage to anterolateral systems (including spinothalamic

tract) will cause contralateral loss of pain and temperature

sensation

often beginning slightly below the level of the lesion.

POSTERIOR CORD SYNDROME VS. ANTERIOR

CORD SYNDROME

Posterior cord syndrome: loss of vibration and position sense below the level of

the lesion, due to damage to PCML tract.

If lesion is to one side of midline, deficits will be ipsilateral

If lesion involves both sides of the posterior cords, deficits will be bilateral.

Anterior cord syndrome: loss of pain and temperature sensation beginning

slightly below the level of the lesion, due to damage to the anterolateral tracts.

If lesion is to one side of midline, contralateral deficits. Note: there may also

be some ipsilateral deficits, caused by damage to posterior horn cells before

their axons have crossed over the anterior commisure.

If lesion involves both sides, bilateral deficits.

DISTINGUISH THE TYPES OF STIMULI THAT

ACTIVATE MECHANICAL AND POLYMODAL

NOCICEPTORS.

Nociceptors respond to stimuli that can produce tissue damage.

Nociceptors are divided into two major classes: Thermal or mechanical

nociceptors and polymodal nociceptors

Mechanical nociceptors respond to mechanical stimuli (sharp, pricking pain)

myelinated A-delta fibers

Polymodal nociceptors respond to high-intensity mechanical or chemical stimuli

and hot/cold stimuli (extreme temperatures, e.g. above 45 degrees Celsius).

unmyelinated C fibers

Dysesthesia Unpleasant sensation produced in

response to normal stimuli

Sensory level Diminished sensation in all

dermatomes below the level of the

lesion

Suspended sensory loss Central cord syndrome that affects

only the anterolateral system due

to damage to anterior commissure

Radicular pain Pain in a dermatomal distribution

indicating a single nerve root lesion

Allodynia Pain due to a stimulus that does

not normally provoke pain

Hyperalgesia Increased sensitivity to pain

Paresthesia Sensation of tingling, tickling,

prickling of skin

Dissociated sensory loss Pattern of sensory loss in which only 1 of the

2 primary sensory modalities is affected

Large fiber neuropathy Injury to PC-ML pathways in PNS

Small fiber neuropathy Injury to spinothalamic pathways in PNS

Sensory neglect Lack of response to stimuli

Romberg test Test of proprioception and vestibular function.

Patient stands with feet together and balance

is tested with eyes closed.

Segmental sensory loss Sensory loss in dermatomal distribution

Sensory ataxia Loss of coordination due to lack of sensory

input (proprioception), worse with eyes

closed

Sensory drift Movement of arms in space due to loss of

proprioception

Syrinx Pathological cavity in spinal cord

Synesthesia Strange sensory experiences where

stimulation of one modality leads to addition

unrelated perception

DESCRIBE THE NEUROLOGICAL TESTS FOR

PRIMARY SOMATOSENSORY FUNCTION

These tests probe primary somatosensory function:

Test vibration sense by placing a vibrating tuning fork on the ball of the patient's

right or left large toe or fingers and asking him to report when the vibration

stops.

Test joint position sense by moving one of the patient's fingers or toes up and

down and asking the patient to report which way it moves

Two-point discrimination can be tested with a special pair of calipers, or a bent

paper clip, alternating randomly between touching the patient with one or both

points. The minimal separation (in millimeters) at which the patient can

distinguish these stimuli should be recorded in each extremity.

DESCRIBE THE NEUROLOGICAL TESTS FOR

HIGHER ORDER SENSORY FUNCTION

To test graphesthesia, ask the patient to close their eyes and identify letters or

numbers that are being traced onto their palm or the tip of their finger.

To test stereognosis, ask the patient to close their eyes and identify various

objects by touch using one hand at a time.

EXTRAPYRAMIDAL MOTOR TRACTS

DISTINGUISH BETWEEN THE MEDIAL AND

LATERAL BRAINSTEM MOTOR SYSTEMS

Medial: Anterior Corticospinal Tract, Vestibulospinal Tracts, Reticulospinal Tracts, Tectospinal Tract

Portion of the body: Proximal Axial and Girdle Muscles

Function: Postural tone, balance, orienting movements of the head/neck, and automatic gait-related movements.

Activates Extensors. Inhibits Flexors

The vestibulospinal tract facilitates the activity of the extensor (antigravity) muscles and inhibits the activity of the flexor muscles in association with the maintenance of balance.

Lateral: Lateral Corticospinal tract, Rubrospinal tract

Portion of the body: Distal muscles, Extremities

Function: Move the extremities, Flexion. The Lateral tract is “essential for rapid, dexterous movements at individual digits”

DEFINE SPASTICITY. DISTINGUISH BETWEEN

DECORTICATE AND DECEREBRATE POSTURES.

Spasticity: Strong, exaggerated muscle tone. Rigidity due to overactive

muscles. This can interfere with normal motion and activity.

Decerebrate posturing = EXTENSION. Indicates brainstem damage BELOW

the level of the red nucleus, and is believed to be a result of descending input

from brainstem circuits that predominately influences extensor motor neurons.

Decorticate posturing = FLEXION. This posture is believed to be a result of a

lesion rostral to the midbrain which simultaneously disinhibits the red nucleus.

MEDIAL EXTRAPYRAMIDAL MOTOR TRACTS

PROJECT BILATERALLY!!! DECUSSATION

PATTERNS ARE NOT CLINICALLY RELEVANT.

VESTIBULOSPINAL TRACT

The vestibular nuclei are situated in the pons and medulla.

They receive afferent information from the semicircular canals and otolith

organs via cranial nerve (CN) VIII and from the cerebellum.

Fibers from the vestibular nuclei (lateral and medial) descend uncrossed

through the medulla and through the length of the spinal cord in the ventral

(anterior) white column.

The vestibulospinal tract facilitates the activity of the extensor (antigravity)

muscles and inhibits the activity of the flexor muscles in association with the

maintenance of balance.

Medullary Pyramids

Medial Lemniscus

Inferior Olivary Nucleus

Anterolateral System

Ventral SpinocellebellarTract

Medial Vestibular NucleusTectospinal Tract

Spinal VestibularNucleus

Inferior Cerebellar Peduncle

Spinal TrigeminalTract

Rubrospinal Tract

Medulla

RETICULOSPINAL TRACT

Increase and decrease tone.

Cell bodies of upper motor neurons in the reticulospinal tract reside in the pontine

and medullary portions of the reticular formation. The reticular formation is a

collection of diffusely organized nuclei in the brainstem.

Receives input from numerous systems and interconnects heavily with the

cerebellum and the limbic system. The largely uncrossed fibers from the pons

descend through the ventral white column; the crossed and uncrossed fibers from

the medulla descend in the ventrolateral white column. Both sets of fibers enter the

ventral gray horn of the spinal cord and may facilitate or inhibit the activity of the

alpha and gamma motor neurons.

The reticulospinal tract influences voluntary movements and reflex activity in a

manner that stabilizes posture during ongoing movement.

CLINICAL NOTE

The reticular formation normally tends to increase muscle tone, but its activity is

inhibited by higher cerebral centers. Therefore it follows that if the higher

cerebral control is interfered with by trauma or disease, the inhibition is lost and

the muscle tone is exaggerated (spasticity or hypertonia)

TECTOSPINAL TRACT

Cell bodies of brainstem motor neurons in the tectospinal tract are located in

the superior colliculus. Axons of these cells decussate in the midbrain and

descend within the ventral white column.

These fibers project contralaterally to the medial group of interneurons and

motor neurons in the cervical spinal cord that control muscles of the neck.

The tectospinal tract is important for coordinating head and eye movements.

Middle Cerebellar Peduncles

Corticobulbar and Corticospinal Tracts(all of the green fibers)

Pontine Nuclei (all the light pink between green and gray tracts)

Pontocerebellar fibers(all of the gray)

Medial Lemniscus

Trigeminal Nerve

Superior Cerebellar Peduncle

Trigemnial Motor Nucleus

Anterolateral System

Fourth Ventricle Tectospinal Tract

Pons

RUBROSPINAL TRACT

Flexion

The rubrospinal tract originates in the red nucleus, situated in the tegmentum of

the midbrain, at the level of the superior colliculus.

The rubrospinal tract crosses the midline within the midbrain and descends to

cervical levels through the lateral white matter of the spinal cord. Its axons

terminate on ventral horn circuits that control distal limb musculature.

In humans the rubrospinal tract facilitates spinal cord flexor motor neuron

activity.

It receives ipsilateral inhibition from the cortical upper motor neurons.

Middle Cerebellar Peduncles

Corticobulbar and Corticospinal Tracts(all of the green fibers

Medial Lemniscus

Superior Cerebellar Peduncle

Cerebral Aqueduct

Trigeminal Nucleus, mesencephalic (lateral part) Mesencephalic

Trigeminal Tract (medial part)

Anterolateral System Rubrospinal Tract

Pontocerebellar fibers(all of the gray)

Trigeminal Nerve

Tectospinal Tract

Pons

CORTICOSPINAL TRACTS

Fibers of the corticospinal tract arise as axons of pyramidal cells situated in the

fifth layer of the cerebral cortex.

One-third of the fibers of the corticospinal tract arise from the primary motor

cortex (Brodmann’s area 4) Frontal lobe

One-third originate from the secondary motor cortex (premotor cortex) Frontal

lobe

One-third originate from the somatic sensory cortex of the parietal lobe. The

latter are involved in regulating ascending sensory information; these project to

the dorsal horn.

FROM WHAT LAYER OF THE CORTEX TO FIBERS

OF THE CORTICOSPINAL TRACTS ARISE?

Layer V

WHAT ARE THE TWO EXCEPTIONS TO THE

MEDIAL LATERAL ORGANIZATION OF THE

CERVICAL LOWER EXTREMITIES

1. The cuneate and gracile fasciculi and nuclei

2. The motor and somatosensory homunculi in the cortex

All other tracts run with cervical innervation represented more medially and

lower extremity more laterally.

WHICH OF THE VESTIBULOSPINAL,

RETICULOSPINAL, AND TECTOSPINAL TRACTS

DECUSSATE?

Tectospinal decussates in the dorsal tegmentum of the midbrain

PATH OF CORTICOSPINAL TRACT

The descending fibers of the corticospinal tract converge in the corona radiata and then pass through the posterior limb of the internal capsule.

The tract continues through the middle 3/5 of the cerebral peduncle in the midbrain.

On entering the pons the fibers of the corticospinal tract diverge into separate bundles that travel in the base of the pons.

As the fibers descend into the ventral aspect of medulla, they reconverge and form the medullary pyramids; most of the fibers (90%) decussate.

The fibers that decussate form the lateral corticospinal tract, which resides in the lateral column of the spinal cord.

The remaining fibers form the ventral (anterior) corticospinal tract; some fibers in this tract remain ipsilateral, while others cross over in the anterior commissure when they reach their destination.

LATERAL VS VENTRAL CORTICOSPINAL TRACT

Fibers in the lateral corticospinal tract project to and facilitate lateral groups of

interneurons and motor neurons that control distal limb muscles ipsilaterally.

Fibers in the ventral corticospinal tract project to medial groups of interneurons

and motor neurons that control axial muscles bilaterally.

CORTICOBULBAR TRACT

Cortical motor neuron fibers that terminate in the cranial nerve nuclei form the

corticobulbar tract.

These fibers descend with neurons in the corticospinal tract through the

internal capsule, passing through the genu of the internal capsule.

Fibers in the corticobulbar tract descend through the cerebral peduncle in the

midbrain, and then gradually exit the tract at different levels to project to the

cranial nerve motor nuclei.

Most of the fibers in the corticobulbar tract project bilaterally to right and left

cranial nerve nuclei

UPPER MOTOR NEURON SYNDROME

Definition: Interruption of the corticospinal tract somewhere along its course.

Symptoms most apparent in distal limb & cranial musculature.

Initial symptoms = flaccid paralysis with hyporeflexia.

Later symptoms = spastic paralysis with hyperreflexia

No signs of muscle denervation – fasciculation

Hypertonia, clonus, absence of abdominal and cremasteric reflexes

Babinski sing

Classic sign: spastic paralysis

LOWER MOTOR NEURON SYNDROME

Paresis or paralysis

Atrophy of denervation; fasciculations/fibrillations

Atonia or hypotonia

Areflexia or hyporeflexia

Plantar reflex, if present, is normal

Classic Sign = Flaccid paralysis

ALS (LOU GEHRIG’S DISEASE)

ALS is characterized by:

Gradually progressive degeneration of BOTH upper motor neurons and lower motor neurons

Muscle weakness, and eventually, paralysis, respiratory failure and death

Age of onset 50-60s, rarely teens

Initial symptoms include:

Weakness or clumsiness, begins focally and then spreads to adjacent muscle groups

Painful muscle cramping and fasciculations

Sometimes dysarthria and dysphagia or respiratory symptoms

On neurologic exam:

UMN findings (increased tone, brisk reflex), and LMN findings (atrophy and fasciculations)

Head droop

Sometimes uncontrollable bouts of laughter or crying

Normal sensory and mental status

Electromyography shows evidence of muscle denervation and reinnervation

PRIMARY LATERAL SCLEROSIS VS ALS

Primary lateral sclerosis is JUST an upper motor neuron disease

LIST THE EIGHT MOTOR NUCLEI OF THE BRAINSTEM

AND THE CRANIAL NERVES THEY SUPPLY.

Motor Nucleus Anatomical Location Cranial

Nerve

Primary Muscles Innervated

Oculomotor Midbrain at superior colliculus III 4 extrinsic eye muscles, Levator

palpebrae

Trochlear Midbrain at inferior colliculus IV Superior oblique muscle

Trigeminal Motor Middle pons V Muscles of mastication

Abducens Caudal pons near 4th ventricle VI Lateral rectus muscle

Facial Motor Caudal pons VII Muscles of facial expression

Nucleus Ambiguus Medulla IX, X Muscles of palate, pharynx and

larynx

Spinal Accessory Ventral horn of cervical spinal

cord

XI Trapezius and Sternocleidomastoid

Hypoglossal Medulla near 4th ventricle XII Muscles of tongue

STATE THE LATERALITY OF THE

CORTICOBULBAR PROJECTIONS TO EACH OF

THE MOTOR NUCLEI OF THE BRAINSTEM.

These fibers descend with neurons in the corticospinal tract, pass through the genu of the internal capsule, descend through the cerebral peduncle, and then gradually exit to project BILATERALLY to right and left cranial nerve nuclei:

trigeminal (CN V)

facial (CN VII)

ambiguus (CNs IX and X)

accessory (CN XI)

Exceptions: Corticobulbar fibers originating from the cortical motor neurons of the contralateral side

Inferior part of the facial nucleus, innervates muscles of facial expression in the lower face

Hypoglossal nucleus, innervates the muscles of the tongue

STATE THE CLINICAL CONSEQUENCES OF A

LESION TO EACH OF THE MOTOR NUCLEI OF THE

BRAINSTEM

DISTINGUISH BETWEEN THE UPPER AND

LOWER MOTOR LESIONS INVOLVING CN VII

Upper Motor neuron lesion symptoms on lower, contralateral face

Lower Motor neuron lesion symptoms on entire, ipsilateral face

Facial paralysis can result from upper motor damage to the corticobulbar tract,

or lower motor damage to the facial motor nucleus or facial nerve. The upper

half of the facial motor nucleus receives bilateral projections and the lower half

receives contralateral projections. Thus, if the lesion is an upper motor lesion,

only the lower half of one side of the face will be paralyzed. This is because

projections to the upper face are bilateral – the fibers from the intact side are

still stimulating motor neurons in the upper facial nucleus. In contrast, a lower

motor lesion causes complete paralysis of one side of the face.

FACIAL NERVE

The facial nerve exits the brainstem ventrolaterally at the pontomedullary junction, lateral to CN VI in a region called the cerebellopontine angle.

Traverses the subarachnoid space and enters the internal auditory meatus to travel in the auditory canal of the petrous temporal bone together with the vestibulocochlear nerve.

At the genu of the facial nerve, the nerve takes a turn posteriorly and inferiorly in the temporal bone to run in the facial canal, just medial to the middle ear.

The geniculate ganglion lies in the genu and contains primary sensory neurons for taste sensation in the anterior two-thirds of the tongue, and for general somatic sensation in a region near the external auditory meatus.

The main portion of the facial nerve exits the skull at the stylomastoid foramen. It then passes through the parotid gland and divides into five major branchial motor branches to control the muscles of facial expression: the temporal, zygomatic, buccal, mandibular, and cervical branches.

Other smaller branchial motor branches innervate the stapedius), occipitalis, posterior belly of the digastric, and stylohyoid muscles.

STATE THE LEVEL AT WHICH THE

INTERMEDIOLATERAL CELL COLUMN IS

LOCATED AND ITS FUNCTIONAL SIGNIFICANCE.

Interomediolateral cell column aka the lateral cell horn is located from spinal

levels T1-L2/L3.

Within Lamina VII (Laminae break the gray matter within the spinal cord into 10

different categories based on cellular structure).

It is the location of preganglionic sympathetic nuclei

STATE THE LEVELS OF THE SPINAL CORD AT

WHICH PELVIC PARASYMPATHETICS ARISE.

S2-S4

These nerves control bladder functioning, bowel movements, and sexual

arousal.

Urinary-Activation allows detrusor muscle contraction and the initiation of flow.

Bowel-Anal sphincter closure is maintained by contraction of internal anal

sphincter

Enables gastric motility beyond the splenic flexure

Sexual-Secretion of mucus by Bartholin’s glands, initiating and maintaining

erection

(Parasympathetics Point, Sympathetics Shoot)

STATE THE LEVELS OF THE SPINAL CORD AT

WHICH THE SYMPATHETICS FOR BOWEL,

BLADDER AND SEXUAL FUNCTION ARISE.

Bladder Function-Voluntary relaxation of the external urethral sphincter triggers

inhibition of sympathetics to the bladder neck, causing it to relax. Sympathetic

innervation goes to bladder neck, urethra, and bladder dome.

Sexual Function-Increased vaginal blood flow and secretions (female),

contributes to erection, initiates the smooth muscle contractions which lead to

ejaculation

Parasympathetics point, sympathetics shoot

DESCRIBE THE ACUTE PHENOMENON OF

SPINAL AND THE LONGER-TERM SIGNS OF

HYPERREFLEXIA AND SPASTICITY. The most common causes of spinal cord dysfunction are compression due to

trauma, and metastatic cancer.

In acute, severe lesions such as trauma, there is often an initial phase of spinal shock: loss of all neurological activity below the level of injury.

Spinal shock is characterized by: flaccid paralysis below the lesion loss of tendon reflexes decreased sympathetic outflow to vascular smooth muscle causing moderately

decreased blood pressure absent sphincteric reflexes and tone

Over the course of weeks to months, spasticity and upper motor neuron signs usually develop. Some sphincteric and erectile reflexes may return, although often without voluntary control.

Phas

e

Time Physical Finding Underlying Event

1 0-1d Areflexia/Hyporeflexia Loss of descending facilitation

2 1-3d Initial Reflex Return Denervation supersensitivity

3 1-4w Hyperreflexia (onset) Axon supported synapse growth

4 1-12m Hyperreflexia, Spasticity Soma supported synapse growth

DESCRIBE THE PHYSIOLOGICAL ROLE OF THE

DORSAL AND VENTRAL SPINOCEREBELLAR

TRACTS OF THE SPINAL CORD.

Dorsal

Spinocerebellar

Tract

Ventral

Spinocerebellar

Tract

Afferent

information about

limb movements

for lower

extremity

Activity of spinal

cord interneurons

(reflects activity in

descending

pathways)

1°: Dorsal root

ganglion

2°: Nucleus

dorsalis of Clark

(C8-L2/L3)

1°: Spinal

Interneurons

2°: Spinal border

cells

No Cross -

Ipsilateral

Double Cross –

Ipsilateral

DEFINE ATAXIA. GIVEN A PATIENT WITH ATAXIA

AND A CEREBELLAR LESION, LATERALIZE THE

LESION IN THE CEREBELLUM.

Ataxia - Uncoordinated movement in the setting of otherwise normal strength.

Lateralization of the lesion - Ataxia would be ipsilateral to the cerebellar lesion.

Dysrhythmia

Dysmetria

DISTINGUISH BETWEEN THE MIDLINE LESIONS

AND LATERAL LESIONS OF THE CEREBELLUM IN

TERMS OF THE SIGNS AND SYMPTOMS IN THE

PATIENT.

Midline lesions of the cerebellar vermis or flocculonodular lobes cause

unsteady gait (truncal ataxia)”Drunk gait” and eye movement abnormalities.

An anterior cerebellar lesion would affect the legs and cause ataxic gait and

poor heel-to-shin.

Posterior midline lesion would cause impaired vestibular input, leading to

unsteady gait and dysequilibration.

Lesions lateral to the vermis cause ataxia of the limbs (appendicular ataxia)

ATAXIA-HEMIPARESIS

Often caused by lacunar infarcts

Both contralateral*

HOW TO DISTINGUISH BETWEEN CEREBELLAR

AND SENSORY ATAXIA

1. With sensory ataxia impaired joint sensation

2. With sensory ataxia improved with visual feedback, worse in darkness

IDENTIFY : VERMIS, CEREBELLAR HEMISPHERES,

FOLIA, MIDDLE, INFERIOR AND SUPERIOR

CEREBELLAR PEDUNCLES, FLOCCULONODULAR

LOBE, CEREBELLAR TONSILS.

NAME THE THREE MAJOR FIBER TRACTS THAT

CONNECT THE CEREBELLUM TO THE BRAINSTEM.

Superior cerebellar peduncle - efferent from the dentate nucleus (one of deep

cerebellar nuclei) to the contralateral red nucleus (in midbrain) & thalamus

Middle cerebellar peduncle - afferent from contralateral pons. This carries

impulses from motor & sensory cortex to pons. These motor & sensory

neurons synapse in pontine nuclei. Then, pontine axons cross the midline and

enter the contralateral cerebellum via the middle cerebellar peduncle.

Inferior cerebellar peduncle - afferent from below: from principle olivary nuclei,

dorsal spinocerebellar tract, and vestibular system.

THE DEEP CEREBELLAR NUCLEI FROM LATERAL

TO MEDIAL

Dentate emboliform globose fastigial

Don’t eat greasy foods

NAME THE FOUR DEEP NUCLEI OF THE CEREBELLUM.

Dentate nucleus Largest of the deep cerebellar nuclei.

Receives projections from the lateral

cerebellar hemispheres, efferent fibers

through superior cerebellar peduncle

to red nucleus and VL of thalamus.

Emboliform nucleus,

Globose nucleus

Together called the “interposed nuclei”

Receive projections from the

intermediate part of the cerebellar

hemispheres, project to red nucleus of

midbrain.

Fastigial nucleus Receive input from the medial zone:

vermis and a small input from the

flocculonodular lobe, efferent fibers

through inferior cerebellar peduncle to

corticospinal, vestibulospinal,

reticulospinal tracts.

Vestibular Nuclei (in medulla) Receive input from flocculonodular

lobes projects to PPRF and spinal cord

STATE THE ROLE OF THE PURKINJE CELLS OF

THE CEREBELLUM IN INFLUENCING THE

EXCITABILITY OF THE DEEP CEREBELLAR

NUCLEI.

All output from the cerebellar cortex is carried by Purkinje cell axons into

cerebellar white matter.

Purkinje cells form inhibitory synapses onto deep cerebellar nuclei and

vestibular nuclei, which then convey outputs from the cerebellum to other

regions through excitatory synapses.

GRANULE CELLS

Granule cells are very small, densely packed neurons that account for the huge

majority of neurons in the cerebellum. Found in the granular layer.

These cells receive input from mossy fibers and project to the molecular layer

to form parallel fibers that run parallel to the folia and perpendicular to the

Purkinje cells. Parallel fibers form excitatory synapses with numerous Purkinje

cells.

MOSSY FIBERS

Originate in the pontine nuclei, the spinal cord, the brainstem reticular

formation, and the vestibular nuclei

Form excitatory synapses onto dendrites of granule cells and cerebellar nuclei.

Granule cells send axons into the molecular layer, then bifurcate, forming

parallel fibers that run parallel to the folia.

Parallel fibers run perpendicular to Purkinje cell dendritic trees.

Each parallel fiber forms excitatory synaptic contacts with numerous Purkinje

cells.

CLIMBING FIBERS

Originate exclusively in the inferior olive

They wrap around the cell body and dendritic tree of Purkinje cells, forming

powerful excitatory synapses.

1 climbing fiber will branch to ~10 Purkinje cells; however, each Purkinje cell

is excited by just 1 climbing fiber.

Strong modulatory effect on the response of Purkinje cells, causing a

sustained decrease in their response to synaptic inputs from parallel fibers.

EXPLAIN WHY DEFICITS IN COORDINATION DUE

TO CEREBELLAR LESIONS OCCUR IPSILATERAL

TO THE LESION. EXPLAIN WHY LESIONS TO THE

VERMIS DO NOT TYPICALLY CAUSE UNILATERAL

DEFICITS

Cerebellar lesions The lateral motor system of

the cerebellum is either

ipsilateral or crosses twice

and affects distal limb

coordination.

1. (superior cerebellar

peduncle)

2. (pyramidal decussation)

Ataxia in ipsilateral

extremities

Vermis lesions The medial motor system of

the cerebellum causes

truncal ataxia bilaterally.

DENTATE NUCLEUS

Largest of the deep cerebellar nuclei

Active just before voluntary movement: involved in motor planning

Input: Lateral cerebellar hemisphere

Output: Dentate nucleus projects via the superior cerebellar peduncle

(efferent), which decussates in the midbrain to reach the contralateral ventral

lateral nucleus (VL) of the thalamus.

VL projects to the motor cortex, premotor cortex, SMA, and parietal lobe to

influence motor planning in the corticospinal systems

Ipsilateral control

INTERPOSED NUCLEI

Receive input from intermediate hemisphere

Project via superior cerebellar peduncle to contralateral VL of thalamus

motor, supplementary motor and premotor cortex to influence the lateral

corticospinal tract

Also project to red nucleus to influece rubrospinal systems

FASTIGIAL NUCLEUS

Receives input from the vermis

Projects via the superior cerebella peduncle to the VL

Influences the anterior corticospinal tract

Also projects via uncinate fasciculus and juxtarestiform body to the vestibular

nuclei

Influences reticulospinal and vestibulospinal tracts

NAME THE TWO MOST COMMON CAUSES OF

ACUTE ATAXIA IN ADULTS. NAME THE THREE

MOST COMMON CAUSES OF ACUTE ATAXIA IN

CHILDREN:

Cause of acute ataxia in adults:

Toxin ingestion (alcohol, didn’t need Blumenfeld to tell me that one)

Ischemic or hemorrhagic stroke

Cause of acute ataxia in children:

Toxin ingestion

Varicella-associated cerebellitis

Brainstem encephalitis

Migraine

DESCRIBE WHICH SIDE OF THE CEREBELLUM

MAKES SYNAPTIC CONNECTIONS WITH WHICH

SIDE OF THE CORTEX:

Cortex contralateral innervation to cerebellum

Cerebullum ipsilateral body innervation

NAME THREE MOTOR PATHWAYS THAT ARE

INFLUENCED BY THE OUTPUT OF THE FASTIGIAL

NUCLEI.

Anterior corticospinal tract

Reticulospinal tract

Vestibulospinal tract

NAME THE TARGET(S) OF

VESTIBULOCEREBELLUM OUTPUT:

Vestibulocerebellum = flocculonodular lobe + inferior vermis

vestibular nuclei

fastigial nuclei (a little)

DESCRIBE THE FUNCTION OF THE

SPINOCEREBELLAR PATHWAY

Function of the spinocerebellar pathway:

Input to cerebellum of limb movements (lower--dorsal spinocerebellar, upper--

cuneocerebellar) and info about the activity of spinal cord interneurons (lower--

ventral spinocerebellar, upper-rostral spinocerebellar)

Spinocerebellar pathways provide feedback information of two kinds to the

cerebellum:

afferent info about limb movements is conveyed to the cerebellum by the

dorsal spinocerebellar and cuneocerbellar tracts.

information about the activity of spinal cord interneurons, which is thought to

reflect the amount of activity in descending pathways, is carried by the

ventral and rostral spinocerebellar tracts.

DEFINE THE FOLLOWING CLINICAL TERMS:

OVERSHOOT, POSTURAL TREMOR,

ACTION/INTENTION TREMOR

Overshoot: An example of Dysmetria where a body part in movement goes past a target. This is the converse of undershoot where the body part does not get to the target

Postural tremor: Tremor (rhythmic, oscillatory movement that is typically involuntary) that is present when a body part, typically limb, is held against gravity (such as placing hands outstretched). This can be immediately seen upon holding of a posture or can be delayed after prolonged posture holding (or re-emergent)

Action tremor: literally any tremor present with volitional movement. Intention tremor: A subset of Action tremor that emerges or worsens at a target. Also

termed terminal tremor. A classic example is cerebellar tremor where tremor may be mild or absent on finger to nose until the patient reaches to finger or nose itself and tremor becomes more prominent.

DEFINE THE FOLLOWING CLINICAL TERMS:

NYSTAGMUS, DYSMETRIA, DYSRHYTHMIA.

Nystagmus: Rhythmic eye movements typically with a slow and fast component

(e.g. slow movement in one direction and a corrective fast movement in the

opposite direction). Can be seen in vestibular processes where the nystagmus

typically has slow face towards the side of lesion (i.e. vestibulopathy) and fast

face away.

Dysmetria: Abnormally measured, or metered, movement. This can be

undershoot or overshoot and can apply to finger to nose testing, ocular

movements or other body parts.

Dysrhythmia: Abnormal rhythm of movements.

THE GENICULOSTRIATE PATHWAY AND THE

EXTRA-GENICULOSTRIATE PATHWAY.

Geniculostriate pathway is specialized for form or pattern vision

It allows us to identify objects in the environment.

Extra-geniculostriate pathways:

Pretectum participates in pupillary responses to visual stimuli.

Tectum (superior colliculus) is specialized for visually guided behaviors

Suprachiasmatic nucleus is involved in visual control of circadian rhythms

Pregeniculate nucleus is thought to play a role in eye-head coordination, via

connections with the vestibular system.

DISTINGUISH BETWEEN THE DIRECT AND THE

CONSENSUAL PUPILLARY RESPONSES

1. Afferent pathway CN II extra-geniculostriate pathway coursing via the

optic nerve to the optic chiasm, bilaterally to both optic tracts, and to the

midbrain (pretectal nucleus)

2. Interneuron synapses to the edinger westphal nuclei bilaterally

3. Efferent pathway CN III to ciliary ganglion which produces pupil

contraction

The direct response is the constrictor response observed in the illuminated

eye

The consensual response is the constrictor response observed in the

contralateral eye

DEFINE ANISOCORIA

Pupillary inequality

NAME THE ROLE OF THE SUPERCHIASMATIC

NUCLEI IN VISION

A small number of retinal axons terminate in the suprachiasmatic nucleus of the

hypothalamus. This nucleus is critical for circadian behaviors (those with a 24-

hour cycle).

NAME THE KEY ORGANIZING PRINCIPLES FOR

THE RETINOGENICULOSTRIATE PATHWAY

4 organization principles for understanding retinotopy

1. Topography

Mapping of visual field on retina

2. Parallel Projections

Specialized ganglion cells form the origin of parallel pathways

3. Homonomy

Information about a portion of the visual field derived from two eyes

converges

4. Hierarchical Systems

DEFINE WHERE THE VISUAL FIELDS ARE MAPPED

Temporal visual fields cross

at optic chiasm bilateral

temporal hemianopia with

lesion of optic chiasm

DISTINGUISH THE SAME RELATIONSHIPS FOR

THE SUPERIOR/ INFERIOR VISUAL FIELDS AND

THE SUPERIOR/INFERIOR PARTS OF THE

RETINA.

DISTINGUISH BETWEEN THE UPPER AND

LOWER (MYERS LOOP) PORTIONS OF THE

GENICULOCALCARINE TRACT IN TERMS OF THE

VISUAL FIELD INFORMATION THEY CARRY.

• Light from the upper temporal (left) visual

field hits the lower nasal retina of the left

eye. Signals travel down optic nerve and

cross at the optic chiasm and synapses

at the (dLGN).

• Upper geniculocalcarine tract, carrying

lower visual field passes through the

parietal lobe and terminates in

cuneate/calcarine fissure

• Meyer’s Loop carrying upper visual field

info, travels through the temporal lobe

and terminates in lingual gyrus/calcarine

fissure.

• Damage to the temporal lobe can

therefore affect contralateral upper field

vision for both eyes.

EXPLAIN WHY THE VISUAL FIELD MAP OF THE

FOVEA OCCUPIES A RELATIVELY LARGE REGION

OF THE PRIMARY VISUAL CORTEX.

In the visual cortex and the dorsal lateral geniculate nucleus (dLGN),

retinotopical organization is proportional to the density of receptors, not

physical dimensions.

Put another way, the fovea has the "highest visual acuity" and therefore takes

up a lot of the visual cortex

About half of the visual cortex mass is devoted to the fovea

OCULAR DOMINANCE COLUMNS

Ocular Dominance Columns - In the primary visual cortex, there are ~1 mm

columns or stripes of cells that are primarily activated by one eye. These

columns alternate between left and right eyes, with the areas in between

actively activated by both. These columns are thought to be important in

stereovision.

Monocular deprivation during the critical period causes terminal arbors of axons

from the deprived eye pathway to shrink due to a loss of territory, while the

terminal arbors from the undeprived eye expand.

Cortical blindness - amblyopia

Critical period: 6mo-2yrs

IMPORTANT DEFINITIONS OF VISION

Strabismus: lazy eye, or eyes not aligned with one another. Affects binocular vision & depth

perception.

Cortical blindness: a form of blindness that occurs despite intact function in the retinal & thalamic

cells responsible for visual processing. Due to damage to the brain’s occipital cortex.

Orientation column: vertical columns of simple and complex cells with similar orientations within each

ocular dominance column. The orientation preference shifts in a slight but ordered fashion as you

move between columns (about 10 degrees every 30-100 micrometers)

Achromatopsia: absence of color recognition. Can occur with damage to the transition zone between

the occipital and temporal lobes (the pathway of higher order processing of information from P cells)

Prosopagnosia: inability to recognize faces. Can occur with damage to the inferotemporal cortex

(also a location of higher order processing of information from P cells)

Anopsia: a visual field deficit

Homonymy: Anatomical co-localization of the neural representation of the same region of the visual

field

DISTINGUISH BETWEEN MYOPIA AND

HYPEROPIA IN TERMS OF THE TYPE OF

CORRECTIVE LENS REQUIRED TO CORRECT

REFRACTION. DEFINE ASTIGMATISM

Myopia (near-sighted) results if the shape of

the eye places the retina at a greater

distance.

It is corrected by using concave lenses.

Hyperopia (far-sighted) results if the shape of

the eye places the retina at a smaller

distance.

It is corrected using convex lenses.

Astigmatism: when the amount of refraction

is not the same across the spherical surface

of the cornea

DESCRIBE THE ANATOMICAL BASIS FOR

RETINAL DETACHMENT. DESCRIBE THE

CLINICAL CONSEQUENCES OF RETINAL

DETACHMENT.

Retinal detachment: the separation between the neural retina and the retinal

pigment epithelium.

Consequences of detachment:

- separation of the neural retina from the choroidal vasculature

- dilution of subretinal proteins

- eventual degeneration of the photoreceptors (over the course of months)

DISTINGUISH BETWEEN RODS AND CONES IN

THE RETINA

NAME EACH THE THREE LAYERS OF THE RETINA

THAT CONTAIN CELL BODIES, PROCEEDING

FROM THE OUTSIDE OF THE EYE TO THE CENTER

OF THE EYE.

The layers are (from the vitreous humor to the pigment epithelium)

Ganglion cell layer: contains the ganglion cell bodies

Bipolar cell layer: contains the bipolar cell bodies (also amacrine & horizontal cells)

Outer nuclear layer: contains the photoreceptors (rods and cones)

All of these layers come before the pigment epithelium when entering from the vitreous humor

PHYSIOLOGICAL ROLE OF THE CELL LAYERS OF

THE RETINA. PATH OF LIGHT FROM THE LENS

TO THE PHOTORECEPTOR CELL LAYER.

Photoreceptor layer: capture the light and translate it into signal for CNS processing. They absorb photons and that causes a change in the membrane potential.

Bipolar cell layer: found in between the photoreceptor layer and the ganglion layer. Their function is to transmit information (directly or indirectly) from the photoreceptor layer to the ganglion cell layer

Ganglion cell layer: receives visual information from photoreceptors via bipolar cells, modulated by horizontal cells and amacrine cells. They transmit this information to several regions of the thalamus, hypothalamus, and midbrain.

Path of light:

cornea → pupil→ lens→ vitreous humor→ retina (photon passes through the ganglion and bipolar layers until finally reaching photoreceptors, except at the fovea, where there is only the photoreceptor layer so that light can reach cones without distortion.

Once the photon stimulates the photoreceptors, signals travel back “outward” from photoreceptors → bipolar cells → ganglion cells (whose axons form optic nerve).

MACULAR SPARING

Partial lesions of the visual pathways occasionally result in a phenomenon

called macular sparing.

This occurs because the fovea has a relatively large representation for its size,

beginning in the optic nerve and continuing to the primary visual cortex.

Macular sparing can also occur in visual cortex because either the MCA or the

PCA may provide collateral flow to the representation of the macula in the

occipital pole

Although the term “macular sparing” is usually used in the context of cortical

lesions, other lesions may cause a relative sparing of central vision as well.

CORNEAL LAYERS

Epithelium – richly innervated by opthalmic n. of CN V

Bowman membrane

Stroma

Descemet’s membrane

Endothelium

PUPILLARY DEFECTS

DIPLOPIA

Diplopia: double vision

Binocular diplopia: double vision that resolves with closing either eye, most

often due to eye misalignment

Monocular diplopia: double vision that persists with other eye closed, can be

unilateral or bilateral, usually caused by corneal defect or uncorrected

refraction; not caused by eye misalignment

MADDOX ROD TEST

MADDOX ROD:

WHY DOES THE IMAGE SEEN BY THE WEAK EYE

APPEAR LATERAL TO THE IMAGE SEEN BY THE

NORMAL EYE?

Image should fall fovea in

each eye if gaze is conjugate.

In the weak right eye the image

falls on nasal retina. The brain

interprets images seen by nasal

retina of the right eye as being in

the lateral portion of the visual field.

EXTRAOCULAR MUSCLES

Muscle Innervation Action

Levator palpebrae superioris

CN III Elevates eyelid

Superior Oblique CN IV Depression, abduction,

intortion

Inferior Oblique CN III Elevation, abduction, extortion

Superior Rectus CN III Elevation, adduction, intortion

Inferior Rectus CN III

Depression, adduction,

extortion

Medial Rectus CN III Adduction

Lateral Rectus CN VI Abduction

1. MUSCLES ARE ELASTIC FORWARD GAZE

2. UPON STIMULATION, ANTAGONIST IS INHIBITED

OCULOMOTOR NERVE

OCULOMOTOR PALSY – “DOWN AND OUT”

Complete disruption of oculomotor nerve function causes paralysis of all

extraocular muscles except for the lateral rectus and superior oblique.

Because of decreased tone in all muscles except the lateral rectus and superior

oblique, the eye may come to lie in a “down and out” position at rest.

In addition, paralysis of the levator palpebrae superior causes the eye to be

closed (complete ptosis) unless the upper lid is raised with a finger.

The pupil is dilated and unresponsive to light because of involvement of the

parasympathetic fibers that run with the oculomotor nerve.

TROCHLEAR NERVE

WHAT IS THE MOST COMMON CAUSE OF

TROCHLEAR NERVE PALSY

Diabetes

Also sensitive to raised intracranial pressure

ABDUCENS NERVE

ABDUCENS NERVE PALSY

PUPILLARY REFLEXES

CAVERNOUS SINUS

AMBLYOPIA

If vision in one or both eyes is impaired early in life due to cataracts, severe

focus or accommodation problems, or if eyes are misaligned, normal cortical

development of the visual system is impaired. This can lead to permanent

visual impairment up to total blindness, with no detectable neurological lesion.

STRABISMUS

Conjugate gaze and binocular vision develop throughout early childhood.

Normally, input from both eyes is perceived and the eyes are held in alignment,

or fusion, referring to fusion of the foveal visual fields, which is required for

binocular vision. If fusion is broken, the brain will favor input from one eye,

ignoring the input from the other eye. Strabismus, misalignment of the eyes,

can develop in the absence of any discernable motor lesion. In strabismus, one

eye is fixated on a visual target while the other eye is deviated.

Esotropia is medial deviation of the non-fixated eye

Exotropia is lateral deviation

Hypertropia is upward deviation

PHORIA

Mild latent weakness present only when eye is covered

In phorias, fusion is normally maintained, but if fusion is broken (by covering

one eye, or under conditions of fatigue or inattention), deviation of one eye

occurs (esophoria, exophoria, etc.). In the cover-uncover test, both eyes are

aligned when uncovered. The covered eye deviates, then realigns when

uncovered.

SACCADES

Rapid eye movements that function to bring targets of interest into the field of

view

Vision is transiently suppressed during saccades

Can be performed voluntarily or reflexively

Test saccades by having the patient shift gaze to different locations, on both

horizontal and vertical axes.

Normal saccades are conjugate.

same time

same speed

same target

Lesions may result in movements that are slow, disconjugate or absent,

sometimes only to specific areas of the visual field.

CENTRAL CONTROL OF SACCADES

Horizontal = paramedian pontine reticular formation (PPRF)

Vertical = rostral interstitial nucleus of the MLF (riMLF)

in the midbrain reticular formation

Oblique movements require contributions from both centers

Frontal eye fields generate saccades in the contralateral direction

Superior colliculus generates fast reflexive “express” saccades through

contralateral gaze centers

HORIZONTAL GAZE PATHWAY

VERGENCE

Adjusts eye positions to view objects at different distances.

Convergence = both eyes adduct via medial recuts

Divergence = both eyes abduct via lateral recus

Vergence movements are disconjugate

Activation of parasympathetics as well to improve close focus

Test vergence by providing a slowly approaching visual target. Lesions may be

unilateral, resulting in slow or absent adduction only on the side of the lesion.

Vergence is the most sensitive of the eye movements to fatigue or drugs,

something to keep in mind when a patient exhibits a deficit.

CENTRAL CONTROL OF VERGENCE

Skip gaze centers and MLF because movement is disconjugate

Pathway from occipital cortex to pretectal nuclei

Parasympathetic responses through Edinger-Westphal nucleus

Potential to drive abduction without going through gaze centers

SMOOTH PURSUIT

Smooth pursuit movements use visual feedback to follow a moving object of

interest against a non-moving background.

Smooth pursuit movements cannot be made voluntarily; there must be a

moving stimulus to follow.

Long latency, to calculate the target position and speed. Top speed is ~100o/s,

much slower than saccades.

CENTRAL CONTROL OF SMOOTH PURSUIT

Controlled by extrastriate occupital cortex via cerebellum and IPSILATERAL

gaze center

Lesion in smooth pursuit saccadic pursuit in direction of lesion

LESIONS AFFECTING HORIZONTAL GAZE

Right abducens nerve – CN VI palsy

Right abducens nucleus – right lateral gaze palsy

Ask if eyes can converge to test if muscles and LMN are functional

Right PPRF – right lateral gaze palsy

Left MLF – left INO

ipsilateral eye cannot adduct, nystagmus on contralateral eye

Also test vergence

Left MLF and left abducens nucleus – 1 and ½ syndrome

OTHER LESIONS

Gaze centers:

PPRF - disrupts gaze toward lesion (ipsilateral to LMN)

riMLF - disrupts vertical gaze, sometimes just in one direction

Cortex:

Frontal eye fields - disrupts gaze away from lesion (contralateral to LMN), eyes

deviate toward lesion (no inhibitory circuit)

Occipital cortex - disrupts smooth pursuit toward lesion (ipsilateral)

VESTIBULO-OCULAR REFLEX

Rapid, no visual input, decays quickly

Pairs of muscles that receive input from semicircular canal yoke muscles

Gaze center not involved

TEST THE VOR REFLEX

Oculocephalic test (doll’s eye maneuver)

Can be performed on unconscious patient

Prop eyes open and rock head eyes should remain fixed

Caloric test:

Cool water – nystagmus in opposite direction

Warm water – nystagmus in same direction

Use ice water in potentially brain dead patient

CALORIC TEST

Ice cold or warm water or air is irrigated into the external auditory canal. The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal. Hot and cold water produce currents in opposite directions and therefore a horizontal nystagmus in opposite directions.

In patients with an intact brainstem:

If the water is warm (44°C or above) endolymph in the ipsilateral horizontal canal rises, causing an increased rate of firing in the vestibular afferent nerve. This situation mimics a head turn to the ipsilateral side. Both eyes will turn toward the contralateral ear, with horizontal nystagmus to the ipsilateralear.

If the water is cold, relative to body temperature (30°C or below), the endolymph falls within the semicircular canal, decreasing the rate of vestibular afferent firing. The eyes then turn toward the ipsilateral ear, with horizontal nystagmus (quick horizontal eye movements) to the contralateral ear.

OPTOKINETIC NYSTAGMUS

Slower, takes over as VOR decays, uses visual input

Eyes track in smooth pursuit and then saccade in opposite direction

nystagmus

ROLE OF CEREBELLUM

Adaptation: quality control

Compensation for lesions

ROLE OF BASAL GANGLIA

Gating

IMPORTANT POINTS TO REMEMBER

Vergence - no MLF or gaze centers

VOR tests brainstem from vestibular nucleus

to oculomotor nucleus (medulla to midbrain)

-bypasses gaze centers, but does use MLF

Sympathetics supply dilator of pupil and superior

tarsal muscle

Visual defects are not motor defects

LEFT HEMIPARESIS, LEFT BABINKSKI, VISUAL

AND TACTILE EXTINCTION ON LEFT, RIGHT

SIDED HEADACHES, FATIGUE

Right hemisphere cortical or subcortical lesion affecting corticospinal and

attentional pathways

LESION CONTALATERAL TO WEAKNESS

Elderly patient with headaches following MVA subdural hematoma

COMA, BLOWN PUPIL AND HEMIPLEGIA

Uncal herniation

WITH FACIAL WEAKNESS, LESIONS MUST BE

ABOVE WHAT POINT?

At or above the pons

The facial nerve nucleus is in the pons and exits at the pontomedullary junction

UPPER MOTOR NEURON LESION CONTRALATERAL TO WEAKNESS

LOWER HALF OF FACE

LOWER MOTOR NEURON LESION ISPILATERAL WEAKNESS OF ENTIRE

FACE

HEADACHE, NAUSEA, PAPILLEDEMA, DIPLOPIA,

INCOMPLETE ABDUCTION OF LEFT EYE

Increased intracranial pressure aducens palsy

This can begin unilateral and progress to bilateral

SHUFFLING “MAGENTIC GAIT”, INCONTINENCE,

MENTAL DECLINE + ENLARGED VENTRICLES

Normal pressure hydrocephalus

UNILATERAL FACE, ARM AND LEG WEAKNESS

WITH NO SENSORY DEFICITS

Corticospinal and corticobulbar tracts below cortex and above pons

Corona radiata

Posterior limb of internal capsule

Basis pontis

Middle third of cerebral peduncle

Lacunar infarct of internal capsule

Lenticulostriate or anterior choroidal

LESION CONTRALATERAL TO WEAKNESS

HEMIPARESIS WITH SOMATOSENSORY,

OCULOMOTOR, VISUAL OR HIGHER CORTICAL

DEFICITS

Entire primary motor cortex

LESION IS CONTRALATERAL TO WEAKNESS

HEMIPLEGIA SPARING THE FACE

Not likely to be corticospinal tract between cortex and medulla because

corticobulbar tract runs so closely

Arm and leg area of motor cortex:

LESION CONTRALATERAL TO WEAKNESS

OR

Corticospinal tract from lower medulla to C5:

LESION IPSILATERAL TO WEAKNESS if below pyramidal decussation

LESION CONTRALATERAL TO WEAKNESS if above pyramidal decussation

UNILATERAL FACE WEAKNESS

Bells palsy

Peripheral facial nerve or nucleus

Forehead and obicularis oculi are not spared

LESION IPSILATERAL TO WEAKNESS

Lower half of face

Motor cortex or capsular genu lesions

Forehead is spared

LESION CONTRALATERAL TO WEAKNESS

WEAKNESS OF ALL RIGHT FINGER, HAND AND

WRIST MUSCLES WITH NO SENSORY LOSS AND

NO PROXIMAL WEAKNESS

NOT A PERIPHERAL LESION

Most likely: left precentral gyrus, primary motor cortex hand area

LESION CONTRALATERAL TO WEAKNESS

With prior cardiac arrest

Embolic infarct occlusion of small cortical branch of MCA

RIGHT EYEBROWS DEPRESSED, RIGHT LOWER

FACE DELAY OF MOVEMENT, SPEECH SLURRED,

TRACE CURLING OF FINGERTIPS

Unilateral facial weakness without other deficits is most commonly caused by

peripheral lesions of facial nerve BUT mild dysarthria and finger curling suggest

minor involvement of corticobulbar and corticospinal tracts

Thus MOST LIKELY left motor cortex face area

LESION CONTRALATERAL TO WEAKNESS

Eyebrow is not usually depressed in UMN lesion of facial nerve

PROGRESSIVE WEAKNESS, MUSCLE

TWITCHING, AND CRAMPS, UMN AND LMN

SIGNS AND NO SENSORY DEFICITS

Amyotrophic lateral sclerosis

LOSS OF SENSATION TO UNILATERAL LOWER

FACE AND BODY

Primary somatosensory or thalamic lesion

LESION CONTRALATERAL TO WEAKNESS

LOSS OF PAIN AND TEMPERATURE ON RIGHT

FACE AND LEFT BODY

Right Lateral pontine or medullary lesion

Anterolateral pathway crosses below, so CONTRALATERAL

Spinal trigeminal nucleus is on IPSILATERAL side

LEFT SIDED LOSS OF VIBRATION AND JOINT

POSITION SENSE BELOW FACE

Right medial lemniscus lesion in medial medulla

RIGHT SIDE LOSS OF VIBRATION AND JOINT

SENSE AND MOTOR NEURON WEAKNESS, LEFT

SIDE LOSS OF PAIN AND TEMP.

Brown Séquard – hemicord lesion

RIGHT ARM NUMBNESS, AGRAPHESTHESIA,

ASTEREOGNOSIS WITH PRESERVED PRIMARY

SENSORY MODALITIES, MILD FLUENT APHASIA,

DIFFICULTY SEEING FINGERS ON RIGHT SIDE,

RIGHT PRONATOR DRIFT

Left postcentral gyrus, primary somatosensory cortex in arm area and some

adjacent left parietal cortex.

WEAKNESS OF LEFT LEG AND MILD WEAKNESS

OF LEFT ARM AND FACE, MILD DYSARTHRIA*,

LEFT LEG HYPERREFLEXIA, BABINKSI, LEFT

GRASP REFLEX **, LEFT ARM “OUT OF

CONTROL”, UNAWARE OF WEAKNESS,

DECREASED RESPONSE TO L PINPRICK, L.

TACTILE EXTINCTION

*Rules out spinal cord lesion

** Suggests frontal lobe lesion

Primary motor cortex, supplementary motor area, adjacent frontal and parietal

lobe lesion

Right ACA infarct

RIGHT HOMONYMOUS HEMIANOPIA

Lesion in left hemisphere visual pathways from left optic tract to left primary

visual cortex

Most common cause is infarction of primary visual cortex caused by PCA

occlusion.

RIGHT HAND WEAKNESS AND SPEECH

DIFFICULTY, DIM BLURRY VISION, HIGH

PITCHED BRUIT OVER CAROTID ARTERY

Carotid stenosis TIAS

Right hand weakness and speech

Left MCA superior division

Decreased left vision

Left opthalmic artery

DECREASED MOVEMENTS OF RIGHT FACE

(SPARING FOREHEAD), PROFOUND RIGHT ARM

WEAKNESS, MILD RIGHT LEG WEAKNESS,

BROCA’S APHASIA

Left primary motor cortex, face and arm areas, Broca’s area, adjacent left

frontal cortex

Left MCA

HEMIBALLISMUS

Lesion of contralateral subthalamic nucleus

FLUENT APHASIA, GREATER GRIMACE TO

PINPRICK ON LEFT, INCREASED TONE ON RIGHT

WITH RIGHT BABINSKI, RIGHT VISUAL FIELD

DEFICIT

Left temporal and parietal lobes including Wernicke’s area, optic radiations and

somatosensory cortex

SCOTOMA IN UPPER NASAL QUADRANT OF

RIGHT EYE AND RIGHT CAROTID BRUIT

Lesion of lower temporal retina of right eye arising from carotid embolus

MONOCULAR VISUAL LOSS IN LEFT EYE

IMPROVING TO CENTRAL SCOTOMA, LEFT

AFFERENT PUPILLARY DEFECT, LEFT OPTIC

DISC PALLOR

Left optic nerve lesion

Most likely due to optic neuritis in young patients

MENSTRUAL IRREGULARITY AND BITEMPORAL

HEMIANOPIA

Lesion in optic chiasm due to pituitary adenoma

DO LESIONS OF TRIGEMINAL NUCLEI IN

BRAINSTEM CAUSE IPSILATERAL OR

CONTRALATERAL LOSS OF PAIN AND TEMP?

IPSILATERAL loss of facial senation to pain and temp because they do not

cross before entering the nucleus

Often involve spinothalamic tract

ipsilateral loss of pain and temp in face and contralateral loss of pain and

temp in body

DECREASED CORNEAL REFLEX CAN BE CAUSED

BY LESIONS IN WHAT AREAS?

Trigeminal sensory pathways

Facial nerve

Sensorimotor cortex contralateral to decreased reflex

DOUBLE VISION AND UNILATERAL EYE PAIN,

HEADACHES, LEFT EYE DRIFTS TO LEFT, LEFT

EYE LIMITED UPGAZE, DOWNGAZE, ADDUCTION,

LEFT PTOSIS AND FIXED DILATED PUPIL

Oculomotor palsy

ON RIGHT GAZE: L. EYE PAIN, LIMITED

ADDUCTION, HORIZONTAL DIPLOPIA

ON LEFT GAZE: MILD HORIZONTAL DIPLOPIA

PAIN AND ERYTHEMA OF LEFT CONJUNCTIVA

Lesion restricting movement of left lateral rectus muscle

Limited ability to stretch and contract

UNILATERAL HEADACHE, OPTHALMOPLEGIA,

AND FOREHEAD NUMBNESS

Cavernous sinus syndrome

PSTOSIS, MIOSIS AND ANHIDROSIS

Horner’s syndrome

Left sympathetic chain in lower neck, lung apex or carotid plexus

LEFT HORIZONTAL GAZE PALSY AND RIGHT

HEMIPARESIS

Wrong way eyes

Infarct of left pons involving corticospinal and corticobulbar tracts as well as left

abducens nucleus or PPRF

LEFT EYE DOES NO ADDUCT PAST MIDLINE,

RIGHT EYE HAD SUSTAINED NYSTAGMUS ON

ABDUCTION

INO to left MLF

FACE AND CONTRALATERAL BODY NUMBNESS,

HOARSENESS, HORNER’S SYNDROME AND

ATAXIA

Wallenberg’s syndrome

Lateral medullary syndrome (thrombosis of vertebral artery)

HEMIPARESIS OF RIGHT ARM AND LEG, RIGHT

BABINSKI, RIGHT PARESTHESIAS, DECREASED

VIBRATION AND JOINT POSITION SENSE, FACE

SPARING

Medial medulla involving pyramid and medial lemniscus

UNILATERAL FACE NUMBNESS, HEARING LOSS

AND ATAXIA

Most likely brainstem dysfunction localized to pons

DIPLOPIA AND UNILATERAL ATAXIA

Oculomotor fascicles in midbrain with involvement of superior cerebellar

peduncle (ataxia) in left midbrain

Left midbrain tegmentum

riMLF can cause difficulty in vertical eye movements

Reticular formation can cause somnolence and delirium

SUDDEN ONSET LEFT ARM AND LEG ATAXIA,

UNSTEADINESS, SLURRED SPEECH, NAUSEA

AND VOMITING

Most likely left cerebellar hemisphere extending to vermis or one of the

cerebellar peduncles.

HEADACHE AND UNSTEADY, WIDE-BASED GAIT

WITH FALLING TO LEFT SIDE

Cerebellar vermis

HEADACHES, NAUSEA, SLURRED SPEECH, ARM

AND LEG ATAXIA GREATER ON LEFT,

HORIZONTAL AND VERTICAL NYSTAGMUS,

STAGGERING GAIT, PAPILLEDEMA

Left cerebellar lesion causing compression of fourth ventricle leading to

increased intracranial pressure.

NAUSEA, PROGRESSIVE UNILATERAL ATAXIA

AND RIGHT FACE NUMBNESS

Right middle or inferior cerebellar peduncle along with right spinal trigeminal

nucleus

SENSORY TRACTS

Tract Decussation Laterality

DC-ML Internal arcuate fibers in

caudal medulla

Contralateral loss of

sensation above medulla,

Ipsilateral below

Anterolateral Anterior commissure Contralateral loss of

sensation

Trigeminothalamic Spinal trigeminal nucleus

from medulla to upper

cervical spine

Lesions of trigeminal nuclei

cause ipsilateral loss of

pain/temp sensation often

involve spinothalamic tract to

affect contralateral body.

Trigeminal lemniscus Chief trigeminal nucleus to

trigeminal lemnsicus in pons

Above pons contralateral

face affected.

Below pons ispilateral face

MOTOR TRACTS

Tract Origin and Decussation Laterality

Anterior corticospinal No decussation Bilateral no obvious deficits

Reticulospinal Pontine and medullary reticular

formation

No decussation

Bilateral no obvious deficits

Vestibulospinal Medial and lateral nuclei

No decussation

Bilateral no obvious deficits

Tectospinal Superior colliculus

Dorsal tegmental decussation in

midbrain

Bilateral no obvious deficits

Corticobulbar No decussation except facial and

hypoglossal

Bilateral

Facial Decussate at pons to reach the

facial nucleus in caudal pons.

Facial nucleus recieves bilateral

projection for the upper face and

contralateral for the lower face.

The facial nerve leaves the

brainstem at the pontomedullary

junction

Above the pons – contralateral

lower facial weakness

Below the facial nucleus –

ipsilateral full facial weakness

Hypoglossal Hypoglossal nerve decussates in

the medulla and exits ventral

medulla between pyramid and

inferior olivary nucleus

Lesions above medulla will cause

contralateral tongue weakness,

while lesions of nucleus, exiting

fascicles or nerve cause ipsilateral

weakness. Tongue deviates

towards weak side.

VISUAL TRACTS

Tract Pathway Laterality

Pupillary Optic nerve pretectal nuclei

(temporal retina to ipsilateral,

nasal retina to contralateral).

Bilateral projections to Edinger

Westphal nucleus and to ciliary

ganglion.

Bilateral lesion leads to loss of

reflex

Horizontal saccades PPRF Abducens nucleus

ipsilateral projection to lateral

rectus and contralateral projection

via MLF to oculomotor nucleus to

medial rectus.

Lesion of PPRF or abducens

ipsilateral lateral gaze palsy

Lesion of MLF ipsilateral INO –

ipsilateral adduction impairment +

contralateral nystagmus + normal

convergence

Vertical saccades Gaze center – rostral midbrain

reticular formation and pretectal

areas.

Ventral riMLF downgaze

Dorsal upgaze

Frontal eye fields Frontal lobe PPRF Contralateral saccades

Lesions of cerebral hemispheres

disrupts contralateral

saccades fixed gaze to side of

lesion

Smooth pursuit Controlled by extrastriate occipital

cortex via cerebellum and

ipsilateral gaze centers.

Ipsilateral smooth pursuit

Occipital cortex disrupts smooth

pursuit towards lesions

Vergence Pathway from occipital cortex to

pretectal nuclei- bypasses gaze

centers and MLF

Sensitive to fatigue and drugs.

CEREBELLAR OUTPUT PATHWAYS

Area Pathway Laterality

Lateral hemispheres

Motor planning

Projects to dentate nucleus and to superior

cerebellar peduncle which decussates in

midbrain to reach VL of thalamaus and

project to motor and premotor cortex

Hemispheric or

peduncle lesions

Ipsilateral

ataxia

Intermediate hemispheres

Control of distal

extremities

Projects to emboliform and globose nuclei

and to superior cerebellar peduncle

(ventral tegmental decussation) to reach

VL in thalamus and project to motor and

premotor cortex

Hemispheric or

peduncle lesions

Ipsilateral ataxia

Cerebellar vermis and

folcculonodular lobes

Proximal trunk movements

and VOR control

Projects to fastigial nuclei and to superior

cerebellar peduncle (decussation) to reach

VL in thalamus and influence the anterior

corticospinal tract and tectal area,

reticulospinal tracts and vestibulospinal

tracts.

Lesions to medial

system cause

bilateral truncal

ataxia, but

patients may fall

towards side of

lesion

CEREBELLAR INPUT PATHWAYS

Input pathway Origin, nuclei,

peduncle

Laterality

Pontocerebellar Cortex, pontine

nuclei, middle

cerebellar

peduncle

Ipsilateral

Dorsal

spinocerebellar

Leg

proprioceptors,

nucleus dorsalis

of clark (C8-L2),

inferior cerebellar

peduncle

Ipsilateral

Ventral

spinocerebellar

Leg interneurons,

spinal cord

neurons, superior

cerebellar

peduncle

Ipsilateral

INTERNAL CAPSULE STROKE

The presence of these cortical signs may exclude an internal capsule stroke:

gaze preference or gaze deviation

expressive or receptive aphasia

visual field deficits

visual or spatial neglect

If any of these signs are present, the patient may have a cortical stroke, not

an internal capsule stroke.

IMPORTANT STRUCTURES

ACUTE STROKE: CT SHOWS ACUTE BLEEDS (NOT

ISCHEMIA) VERY EARLY, FAST, NON CONTRAST.

ON A BRAIN IMAGE, YOU CAN DISTINGUISH

BETWEEN ISCHEMIC AND HEMORRHAGIC BY

FINDING IF THE LESION FOLLOWS A VASCULAR

REGION OR NOT.

RELATIVE AFFERENT PUPILLARY DEFECT

(RAPD, MARCUS GUNN PUPIL)

An RAPD is a defect in the direct response. It is due to damage in optic nerve

or severe retinal disease.

It is important to be able to differentiate whether a patient is complaining of

decreased vision from an ocular problem such as cataract or from a defect of

the optic nerve.

If an optic nerve lesion is present the affected pupil will not constrict to light

when light is shone in the that pupil during the swinging flashlight test.

However, it will constrict if light is shone in the other eye (consensual

response). The swinging flashlight test is helpful in separating these two

etiologies as only patients with optic nerve damage will have a positive RAPD.

ARGYLL ROBERTSON PUPIL

This lesion is a hallmark of tertiary neurosyphillis

Pupils will NOT constrict to light but they WILL constrict with accommodation

Pupils are small at baseline and usually both involved (although degree may be

asymmetrical)

BRAINSTEM LESIONS ARE VERY UNLIKELY TO

CAUSE UNILATERAL HEARING LOSS.

CEREBELLAR OR VESTIBULAR LESIONS WILL

CAUSE OPEN EYE INSTABILITY, SO ROMBERG IS

TECHNICALLY A BETTER TEST FOR SENSORY

PROPRIOCEPTIVE LOSS

RULE OF FOUR

4 Medial Structures: Motor Nuclei: Oculomotor, Trochlear, Abducens, Hypoglossal Motor Pathway Medial Lemniscus MLF

4 Lateral Structures Spinothalamic Pathway Sensory trigeminal nucleus Spinocerebellar Sympathetic

Cranial Nerves Medulla: Glossopharyngeal, Vagus, SA, Hypoglossal Pons: Trigeminal, Abducens, Facial, Auditory Midbrain: Olfactory, Optic (not in midbrain) Trochlear, Oculomotor

MEDIAL BRAINSTEM LESIONS

If you find upper motor neuron signs in the arm and the leg on one side then you know the patient has a medial brainstem syndrome because the motor pathway is paramedian and crosses at the level of the foramen magnum (decussation of the pyramids). If the face is affected it must be above the level of the midpons.

The motor cranial nerve ‘the parallels of latitude’ indicates whether the lesion is in the medulla (12th), pons (6th) or midbrain (3rd). Remember the cranial nerve palsy will be ipsilateral to the side of the lesion and the hemiparesis will be contralateral.

If the medial lemniscus is also affected then you will find a contralateral loss of vibration and proprioception in the arm and leg (the same side affected by the hemiparesis) as the posterior columns also cross at or just above the level of the foramen magnum.

The median longitudinal fasciculus (MLF) is usually not affected when there is a hemiparesis as the MLF is further back in the brainstem.

LATERAL BRAINSTEM LESION

Ipsilateral ataxia of the arm and leg as a result of involvement of the Spinocerebellarpathways

Contralateral alteration of pain and temperature sensation as a result of involvement of the Spinothalamic pathway

Ipsilateral loss of pain and temperature sensation affecting the face within the distribution of the Sensory nucleus of the trigeminal nerve (light touch may also be affected with involvement of the spinothalamic pathway and/or sensory nucleus of the trigeminal nerve).

Ipsilateral Horner’s syndrome with partial ptosis and a small pupil (miosis) is because of involvement of the Sympathetic pathway.

The power tone and the reflexes should all be normal.

LATERAL MEDULLARY SYNDROME

(WALLENBERG) VASCULAR

Vertebral artery: Distal branches

Vertebral artery: Superior lateral medullary artery

Posterior inferior cerebellar artery: Less common than vertebral

SYMPTOMS

CN V nuclei: sensory loss, facial pain

Restiform body, inferior cerebellar peduncle: limb and gait ataxia

Vestibular nuclei: nystagmus, nausea/vomiting, vertigo

Nucleus ambiguus: hoarseness, dysphagia

Sympathetics: Horner syndrome

Spinothalamic tract: Hemisensory loss of pain and temp

LATERAL PONS

General symptoms plus:

Ipsilateral facial weakness

Weakness of the ipsilateral masseter and pterygoid muscles

Occasionally ipsilateral deafness.

GENERAL SOMATIC EFFERENT – EXTRAOCULAR,

STRIATE, TONGUE

1. Oculomotor nucleus (CN III): midbrain. Sends fibers to oculomotor nerve,

innervating the levator palpebrae superioris (the muscle that lifts the eyelid) and 4 of

the extraocularmuscles (superior and inferior recti, medial rectus, and inferior

oblique).

2. Trochlear nucleus (CN IV): caudal midbrain. Efferent fibers cross the midline

before exiting the brainstem as the trochlear nerve (exits from superior aspect just

behind the inferior colliculus), which innervates the superior oblique muscle. Other

neurons project through the MLF to coodinate conjugate eye movements.

3. Abducens nucleus (CN VI): caudal pons. The abducens motoneurons send their

axons into the abducens nerve, innervating the lateral rectus muscle.

4. Hypoglossal nucleus (CN XII): rostral medulla. Fibers enter the hypoglossal nerve

and innervate the musculature of the tongue. Lesion: tongue deviates toward lesion.

GENERAL SOMATIC AFFERENT

1. Principal (chief or main) sensory nucleus of the trigeminal (CN V): mid-pons (at the level of the trigeminal nerve). Receives mainly large diameter primary afferents and mediates discriminative touch; it gives rise to trigemino-thalamic axons which joins the medial lemniscus.

2. Spinal nucleus of the trigeminal (CN V): from mid-pons to upper cervical cord. Receives mainly small diameter afferents that mediate pain and temperature. Gives rise to trigemino-thalamic fibers that join the anterolateral system. Primary fibers descending to the spinal trigeminal nucleus form the spinal trigeminal tract.

3. Mesencephalic nucleus of the trigeminal (CN V): extending rostrally from mid-pons into the midbrain. Although it lies within the CNS, it contains the cell bodies of primary afferents, just like those found in the trigeminal ganglion. Somata in the mesencephalic nucleus send one branch of their axon to innervate muscle spindles in the jaw musculature, the other terminates in the brainstem. Some of these terminate on motoneurons in the trigeminal motor nucleus, mediating the jaw jerk reflex

GENERAL VISCERAL EFFERENT - BRANCHIAL

1. Edinger-Westphal nucleus (CN III): midbrain (near the oculomotor nucleus). Sends preganglionic parasympathetic fibers to the oculomotor nerve. They synapse in the ciliary ganglion and innervate the constrictor of the iris and ciliary body, mediating pupillary constriction and accomodation.

2. Superior salivatory nucleus (CN VII): pons. Preganglionic parasympathetic neurons travel with branches of the facial nerve and synapse in the pterygopalatineand submandibular ganglia, After a ganglionic synapse, innervates the lacrimal, nasopalatine, and salivary glands (except the parotid).

3. Inferior salivatory nucleus (CN IX): medulla (at the level of the glossopharyngeal nerve). Preganglionic parasynpathetic fibers travel in CN IX and synapse in the oticganglion. Innervates the parotid gland.

4. Dorsal motor nucleus of the vagus (CN X): medulla. Provides the preganglionic parasympathetic innervation to organs in the thorax and abdomen (excluding the bladder and descending colon).

SPECIAL VISCERAL EFFERENT

1. Motor nucleus of the trigeminal (CN V): mid-pons. Innervates the muscles of

mastication as well as the tensor tympani.

2. Facial nucleus (CN VII): caudal pons. Its axons travel dorso-medially, around the

abducens nucleus, forming the facial colliculus. Its axons then enter the facial nerve

and innervate the muscles of facial expression, as well as the stapedius muscle.

3. Nucleus ambiguous (CN IX and X): rostral medulla. It sends axons to the

glossopharyngeal and vagus nerves to innervate the muscles of the pharynx and

larynx.

4. Spinal accessory nucleus (CN XI): upper cervical cord. Its axons travel rostrally

through the foramen magnum, then exit the skull as the spinal accessory nerve; it

innervates the sternocleidomastoid and trapezius muscles.

GENERAL/SPECIAL VISCERAL AFFERENT

1. Solitary nucleus: medulla. TASTE AND SENSATION

Rostral half of the nucleus receives taste fibers (SVA) via inputs from CN VII

(from the anterior 2/3s of the tongue), CN IX (caudal 1/3 of the tongue), and

CN X (epiglottis).

Caudal half of the nucleus receives general visceral afferents (GVA)

mediating sensations from the soft palate CN VII, pharynx and carotid body,

carotid sinus and middle ear CN IX, and the larynx and viscera CN X. The

primary visceral afferents, as they travel caudally, form a prominent tract, the

solitary tract, located in the medulla.

SPECIAL SENSORY AFFERENT

Vestibular nucleus

Cochlear nucleus

LOCKED IN SYNDROME

ANATOMY Bilateral ventral pons

VASCULAR Basilar artery

Signs & Symptoms Bilateral Cortical Spinal tracts Quadriplegia Bilateral corticobulbar tracts Facial weakness

Bilateral ventral pons lesions (iscemic or hemorrhagic) may result in this deefferented state, with preserved consciousness and sensation, but paralysis of all movements except vertical gaze and eyelid opening.

Reticular formation is spared, so the patient is typically fully awake. The supranuclearocular motor pathways lie dorsally, so that vertical eye movements and blinking are intact.

EDINGER WESTPHALL NUCLEUS IS ON

PERIPHERY AND CAN PRESENT PRIOR TO

EXTRAOCULAR PROBLEMS

INTERNAL CAPSULE STROKE

The internal capsule is one of the subcortical structures of the brain. Anterior limb: Frontopontine fibers (frontal cortex to pons), Thalamocortical fibers

(thalamus to frontal lobe) Genu (angle): Corticobulbar fibers (cortex to brainstem) Posterior limb: Corticospinal fibers (cortex to spine), Sensory fibers

Blood Supply: Lenticulostriate branches of MCA & anterior choroidal artery (AChA) of internal carotid artery

Symptoms and Signs: 1. Weakness of the face, arm, and/or leg (pure motor stroke). Pure motor stroke caused

by an infarct in the internal capsule is the most common lacunar syndrome.

2. Upper motor neuron signs hyperreflexia, Babinski sign, Hoffman present, clonus, spasticity

3. Mixed sensorimotor stroke can lead to contralateral weakness and contralateral sensory loss

HOW TO DISTINGUISH CORTICAL FROM

SUBCORTICAL LESIONS

The presence of these cortical signs may exclude an internal capsule stroke:

Gaze preference or gaze deviation

Expressive or receptive aphasia

Visual field deficits

Visual or spatial neglect

If any of these signs are present, the patient may have a cortical stroke, not

an internal capsule stroke.

STROKE PATIENTS OFTEN PRESENT WITH

FLEXED ARM, EXTENDED LEG, SWINGING GAIT.

HORNERS SYNDROME CAN RESULT FROM A

LESION IN ANY LATERAL REGION OF THE

BRAINSTEM

GAG REFLEX INNERVATION

The afferent limb of the reflex is supplied by the glossopharyngeal nerve

(cranial nerve IX), which inputs to the nucleus solitarius and the spinal

trigeminal nucleus. The efferent limb is supplied by the vagus nerve (cranial

nerve X) from the nucleus ambiguus. All of these are located in the medulla.

IN NORMAL OCULOCEPHALIC MANEUVER OF AWAKE

PERSON, EYES DO NOT MOVE RELATIVE TO HEAD

IN COMATOSE PATIENTS, THE EYES DO MOVE

CONJUGATE RELATIVE TO THE HEAD IN OPPOSITE

DIRECTION OF MOVEMENT TO REMAIN FIXED.

IN BRAIN DEAD PATIENT, THE EYES DO NOT MOVE

RELATIVE TO THE HEAD.

ATAXIC HEMIPARESIS

ANATOMY

Cerebral hemisphere: Posterior limb of external capsule, Pons: Basis pontis

VASCULAR

Middle cerebral artery: Small penetrating arteries

Basilar artery: Small penetrating arteries

Signs & Symptoms

Contralateral Weakness – upper and lower extremity

Contralateral Ataxia – arm and leg

Weakness usually more prominent in leg than arm; extensor plantar response; no facial involvement or dysarthria. Other locations include thalamocapsularlesions, red nucleus, anterior cerebral artery distribution. Also called “homolateral ataxia and crural paresis.”

LATERAL PONTINE LESION

VASCULAR

AICA

BASILAR

Lesion in the lateral pons, including the middle cerebellar peduncle.

Ipsilateral cerebellar ataxia due to involvement of cerebellar tracts

Contralateral hemiparesis due to corticospinal tract involvement

Variable contralateral hemihypesthesia for pain and temperature due to

spinothalamic tract involvement

WEBER SYNDROME

ANATOMY

Midbrain: Base

VASCULAR

Posterior cerebral artery: Penetrating branches to midbrain

Signs & Symptoms

Contralateral Weakness – upper and lower extremity - Corticospinal tract

Ipsilateral Lateral gaze weakness - CN 3