MBB Localizing Lesions

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.

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.

Dorsal
Spinocellebellar
Tract
Ventral Spinocellebellar
Tract
Spinal Trigeminal Tract
Spinal Trigeminal
Nucleus (includes pink)
Cuneate Tract
Graciile Nucleus
Graciile Tract
Cuneate Nucleus
Spinal Accessory Nucleus
Rubrospinal Tract
Anterolateral System
Medulla

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

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
Lissauer tracts
fasciculus
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
Posterior limb of internal
capsule
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
Spinal trigeminal tract
pons
Trigeminal lemniscus Spinal trigeminal nucleus
*Pain/temp circuit descends to
Trigeminothalamic tract
medulla and then ascends
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.

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
Ventral Spinocellebellar
Tract
Tectospinal Tract Medial Vestibular Nucleus
Spinal Vestibular
Nucleus
Inferior Cerebellar Peduncle
Spinal Trigeminal
Tract
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)
Pons
Pontine Nuclei (all the
light pink between
green and gray tracts)
Pontocerebellar fibers
(all of the gray)
Medial Lemniscus
Trigeminal Nerve
Superior Cerebellar Peduncle
TrigemnialMotor
Nucleus
Fourth Ventricle Tectospinal Tract

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

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:
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 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.

WHAT IS THE MOST COMMON CAUSE OF
TROCHLEAR NERVE PALSY
 Diabetes
 Also sensitive to raised intracranial pressure

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

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 ipsilateral
ear.
 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:
 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

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
 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
 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

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
Tectospinal Superior colliculus
Dorsal tegmental decussation in
midbrain
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.

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 Spinocerebellar
pathways
 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 pterygopalatine
and 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 otic
ganglion. 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 supranuclear
ocular 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
 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 thalamocapsular
lesions, 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
 Contralateral Weakness – upper and lower extremity - Corticospinal tract
 Ipsilateral Lateral gaze weakness - CN 3

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