2
OUTLINES
Neuroanatomy ofbrainstem
Midbrain
Pons
Medulla oblengata
Neuroanatomy of cranial nerves
Functional localization of brainstem and cranial nerves
References
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Objective
By theend of this seminar you will be familiar with
Anatomical organization of brainstem
Functional localization of brainstem and cranial nerves
Common brainstem and cranial nerve syndromes
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Introduction
Small neuroanatomicalarea
approximate 8 to 9 cm of length
Act as conduit(for some as relay
station) between cortex,
diencephalon ,cerebellum and spinal
cord.
Contains the reticular formation as its
central core
Ten of the twelve cranial nuclei
Receives blood supply from the
vertebrobasilar system.
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Ventral mid brainsyndromes…
BENEDIKT’S SYNDROME
affect the red nucleus, the brachium
conjunctivum, and the fascicle of
cranial nerve III
More ventral tegmental lesions
Ipsilateral oculomotor paresis,
usually with a dilated pupil
Contralateral involuntary movements,
including intention tremor,
hemichorea, or hemiathetosis, due to
destruction of the red nucleus
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Dorsal mid brainsyndrome
Parinaud’s syndrome
Most often seen with hydrocephalus or
tumors of the pineal region.
Paralysis of conjugate upward gaze
(occasionally down-gaze)
Pupillary abnormalities (pupils are
usually large with light-near
dissociation)
Convergence-retraction nystagmus on
upward gaze (especially elicited by
inducing upward saccades by a down-
moving optokinetic target)
Pathologic lid retraction (Collier’s sign)
Lid lag During horizontal refixations
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Dorsal mid brainsyndrome…
TOP OF THE BASILAR SYNDROME
Occlusive vascular disease of the rostral basilar artery, usually embolic
Infarction of the midbrain, thalamus, and portions of the temporal and
occipital lobes
Disorders of eye movements
Pupillary abnormalities
Behavioral abnormalities
Visual defects
Motor and sensory deficits.
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PONS
About 1inch (2.5 cm)
long
A bridge Connecting the
right and left cerebellar
hemispheres
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Ventral pontine syndromes…
Millard-Gubler Syndrome
A unilateral lesion of the ventrocaudal
pons
Involve the basis pontis and the fascicles
of cranial nerves VI and VII.
Contralateral hemiplegia (sparing the
face) is due to pyramidal tract
involvement.
Ipsilateral lateral rectus paresis (cranial
nerve VI) with diplopia that is
accentuated when the patient “looks
toward” the lesion.
Ipsilateral peripheral facial paresis
(cranial nerve VII).
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Ventral pontine syndromes…
Raymond Syndrome
A unilateral lesion of the ventral
medial pons, which affects the
ipsilateral abducens nerve
fascicles and the corticospinal
tract but spares cranial nerve VII
. Ipsilateral lateral rectus paresis
(cranial nerve VI)
Contralateral hemiplegia, sparing
the face, due to pyramidal tract
involvement
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Ventral pontine syndromes…
Pure Motor Hemiparesis
corticospinal tracts in the basis pontis
may produce a pure motor
hemiplegia with or without facial
involvement
Dysarthria—Clumsy Hand
Syndrome
facial weakness and severe
dysarthria and dysphagia occur
along with clumsiness, impaired finger
dexterity, and paresis of the hand.
Ataxic Hemiparesis
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Ventral pontine syndromes…
Locked-in Syndrome
Bilateral ventral pontine lesions
Quadriplegia due to bilateral
corticospinal tract involvement in
the basis pontis
Aphonia due to involvement of the
corticobulbar fibers innervating
the lower cranial nerve nuclei
Occasional impairment of
horizontal eye movements due to
bilateral involvement of the
fascicles of cranial nerve VI
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Dorsal pontine syndromes…
Foville Syndrome
lesions involving the dorsal pontine
tegmentum in the caudal third of the pons
Contralateral hemiplegia (with facial
sparing) which is due to interruption of the
corticospinal tract.
Ipsilateral peripheral-type facial palsy
which is due to involvement of the nucleus
and fascicle (or both) of cranial nerve VII.
Inability to move the eyes conjugately to
the ipsilateral side (gaze is “away from”
the lesion) due to involvement of the PPRF
or abducens nucleus, or both
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PARAMEDIAN PONTINESYNDROMES
Unilateral mediobasal infarcts. These
patients
present with severe facio-brachio-
crural hemiparesis, dysarthria, and
homolateral or bilateral ataxia.
Unilateral mediolateral basal infarcts.
Most patients show slight hemiparesis
with ataxia and dysarthria, ataxic
hemiparesis, or dysarthria—clumsy
hand syndrome.
Unilateral mediocentral or
mediotegmental infarcts.
Presentations include dysarthria—
clumsy hand syndrome, ataxic
hemiparesis with prominent sensory or
eye movement disorders, and
hemiparesis with contralateral facial or
abducens palsy.
Bilateral centrobasal infarcts. These
patients have pseudobulbar palsy and
bilateral sensorimotor disturbances.
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Lateral pontine syndrome…
Marie-Foix Syndrome
lateral pontine lesions, especially
those affecting the brachium pontis
Ipsilateral cerebellar ataxia due to
involvement of cerebellar connections
Contralateral hemiparesis due to
involvement of the corticospinal tract
Variable contralateral
hemihypesthesia for pain and
temperature due to involvement of
the spinothalamic tract
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MEDULLA OBLONGATA
Mostinferior region of the brain stem
Becomes the spinal cord at the level
of the foramen magnum
Medulla is broad above, joins with
pons and narrow below, continuous
with spinal cord
Length is about 3cm, width is about
2cm at its upper end
Anteriorly covered by blood vessels
Posteriorly partly by 4th ventricle
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Medullary Syndromes
Resultsfrom atherosclerotic occlusion of the
vertebral artery, anterior spinal artery, or the
lower segment of the basilar artery.
Ipsilateral paresis, atrophy, and fibrillation of the
tongue (due to cranial nerve XII affection). The
protruded tongue deviates toward the lesion (away
from the hemiplegia).
Contralateral hemiplegia (due to involvement of the
pyramid) with sparing of the face
Contralateral loss of position and vibratory
sensation (due to involvement of the medial
lemniscus)
Occasionally, upbeat nystagmus may occur because
of dorsal extension of the infarct toward the medial
longitudinal fasciculus
MEDIAL MEDULLARY SYNDROME (DEJERINE’S ANTERIOR BULBAR SYNDROME)
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damage toa wedge-shaped
area of the lateral medulla
and inferior cerebellum
secondary to intracranial
vertebral artery or posterior
inferior cerebellar artery
occlusion
LATERAL MEDULLARY (WALLENBERG) SYNDROME
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Lateral medullary syndrome…
Ipsilateral facial hypalgesia and
thermoanesthesia (due to trigeminal spinal
nucleus and tract involvement). Ipsilateral facial
pain is common.
Contralateral trunk and extremity hypalgesia
and thermoanesthesia (due to damage to the
spinothalamic tract)
Ipsilateral palatal, pharyngeal, and vocal cord
paralysis with dysphagia and dysarthria (due to
involvement of the nucleus ambiguus).
Ipsilateral Horner syndrome (due to affection of
the descending sympathetic fibers).
Vertigo, nausea, and vomiting (due
to involvement of the vestibular
nuclei).
Ipsilateral cerebellar signs and
symptoms (due to involvement of the
inferior cerebellar peduncle and
cerebellum).
Occasionally, hiccups (singultus)
attributed to lesions of the
dorsolateral region of the middle
medulla and diplopia (perhaps
secondary to involvement of the
lower pons)
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Reticular formation
Functions
Sleep and consciousness
Pain modulation
Cardiovascular control
Respiratory control
Somatic motor control
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Reticular formation…
Thereticular formation nuclei lie in the
brainstem and arranged into three longitudinal
columns
Median column
lies in the midline and consists
intermediate size neuron
The nuclei of this column are termed raphe nuclei
Medial column
made up of large size neurons
also called magnocellular column
Long ascending and descending projections
Lateral column
Made up of small neurons
also termed parvocellular nucleus
Cranial nerve reflexes and visceral functions
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Median RF (Raphe)
The midbrain raphe
Gives rise to ascending serotonergic
projections to higher levels of the CNS
(slepping cycle )
The pontine raphe
projects to the cerebellum.
The medullary raphe:
Gives rise to descending serotonergic
projections to the spinal cord.
Receive primary nociceptive (pain)
Nuclei are serotonergic
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Medial RF
Mostof the largest neurons are found in
the pons and medulla
Have long ascending and descending
collaterals
Ascending branches: Reticulo thalamics
Primarily in the intralaminar nuclei of
thalamus
Activated the cortical EEG (waking state)
Descending branches: Reticulo spinals
To affect muscle tone on spinal motoneurons
Pontine reticulospinals are excitatory
Medullary reticulospinals are inhibitory
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Lateral RF
1.Dorsolateral Pons
Locus Ceruleus (NE): projects throughout
CNS
Its connections facilitate broad CNS
activation during “fight or flight
Pedunculopontine Nucleus (ACh):
Gives rise to cholinergic trigger for the onset
of REM sleep
2. Caudal Pons- Pressor Area (NE)
Ascending branches to the hypothalamus
To control of autonomic activities
Descending projections
Concerned with the control of blood pressure
3. Medulla
Dorsal Respiratory Area
Chemical aspects of respiration
(pCO2)
Ventral Respiratory Area
Mechanical aspects of
respiration (inspiration,
expiration)
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Localization of Lesions
Affectingthe Olfactory Nerve
Lesions Causing Anosmia/hyposmia
Age
younger than 65 years 2% of the population
65-80 ---50%
older than 80--- 75%
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Localization of Lesions
Affectingthe Olfactory Nerve
Neuronal olfactory disorders
lesions that affect the olfactory
nerve, bulb, tract or the olfactory
cortex
Conductive olfactory disorders
conditions that affect the bony
and soft tissue structures in the
nasal cavity, nasopharynx, and
paranasal air sinuses
Bilateral anosmia
Local nasal disease
most common cause of transient
and bilateral anosmia is the
common cold
several airborne toxins
Unilateral anosmia
Lesion affecting the olfactory nerve
filaments, bulb, tract, or stria.
Head injury
A unilateral lesion distal to the decussation of the olfactory fibers causes no olfactory impairment.
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CN I…
FosterKennedy Syndrome
olfactory groove or sphenoid
ridge masses (especially
meningiomas) or space-
occupying lesions of the frontal
lobe
Ipsilateral anosmia
Ipsilateral optic atrophy
Contralateral papilledema due
to raised intracranial pressure
secondary to the mass lesion.
Pseudo–Foster Kennedy
syndrome
noted when increased intracranial
pressure of any cause occurs in a
patient who has previous
unilateral optic atrophy.
most often due to sequential
anterior ischemic optic
neuropathy (arteritic or
nonarteritic) or optic neuritis
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Localization of Lesionsin the Optic Pathways
Impaired visual perception
poor discrimination of fine details
of high contrast (visual acuity),
which results in difficulty with tasks
such as reading a printed page
Impaired color recognition
impaired discrimination of objects
that have little contrast with the
background (contrast
discrimination)
visual field defects
Objective deficits
Along the visual pathway
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Ocular motor system
Includes
The cranial nerve III
(oculomotor) nucleus in
the midbrain
The cranial nerve IV
(trochlear) nucleus at
the level of the
midbrain-pontine
junction
The cranial nerve VI
(abducens) nucleus in
the lower pons.
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Oculomotor Nerve
Exitsthe ventral midbrain in
the interpeduncular fossa
Pierces the dura mater pass
below PCA and above SCA
Lateral wall of the
cavernous sinus
Inters orbit through superior
orbital fissure
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TROCHLEAR NERVE
Windingaround the
periaqueductal grey matter
and comes out posteriorly
through the opposite side.
Crosses the tentorium->enters
middle cranial fossa->lateral
wall of cavernous sinus
Enters Superior orbital fissure-
>supplies Sup. Oblique
muscle.
Down and out movement of
eyeball
Reading muscle
Intorsion – axis of vision is
kept parallel
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Fourth cranialnerve palsies may
cause
Incomitant hypertropia
hypertropia increases on head tilt
toward the paralyzed side (positive
Bielschowsky’s test).
Excyclotropia
torsion of one eye (or both) about the
eye's visual axis
Head tilt
eliminate the hypertropia and rarely
the cyclotropia
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Abducent nerve
Exitsfrom pontomedullary junction
At petrous temporal bone it makes a sharp
turn forward to enter the cavernous sinus.
In the cavernous sinus it runs alongside the
ICA. (internal carotid artery)
It then enters the orbit through the SOF and
innervates the lateral rectus.
The abducens nucleus is located in the pons
PPRF connections-lateral conjugate gaze
center.
Send their axons across the midline to the
opposite MLF and then third nerve nucleus.
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Functional classes ofeye movements
Place and maintain an object of visual interest on each fovea
To allow visualization of a single, stable object.
Accomplish it by
Saccades
Pursuit
Vergence
Oculocephalic reflex
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Functional classes ofeye movements
Saccades
Moves the eyes rapidly (up to 800 degrees/sec) and conjugately to fixate new
targets
Voluntarily
in response to verbal commands in the absence of a visible target
generated in the contralateral frontal cortex
Reflexive saccades
occur in response to peripheral retinal stimuli such as visual threat or to sounds.
in the contralateral parietal cortex
Horizontal vs Vertical
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Localization of horizontalsaccades
Supra nuclear gaze
palsy
Saccades away from
the lesion will be
slow/absent
Intact VOR by
ocuiocephalic
manuever
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Localization of horizontalsaccades pathway…
Interferes with ipsilateral
horizontal saccade
Pursuit and VOR will be
impaired
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Localization of horizontalsaccades pathway…
Ipsilateral abduction deficient
No horizontal gaze
deficient ,rather isotropia
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Localization of LesionsAffecting Cranial Nerve V
Supranuclear
Lesions
Contralateral trigeminal motor paresis ( for masseter predominant CL )
Bilateral upper motor neuron lesions (pseudobulbar palsy)
anesthesia of the contralateral face.
Ischemia
Nuclear Lesions
Motor Ipsilateral paresis, atrophy, and fasciculations of the muscles of mastication Mid pontine
lesions
Sensory Ipsilateral hemianesthesia of the face (due to affection of the main sensory
nucleus of the trigeminal nerve), contralateral hemisensory loss of the limbs
and trunk (due to spinothalamic tract affection), and ipsilateral tremor (due to
affection of the brachium conjunctivum).
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lesions Clinical manifestationscauses
Preganglionic
Trigeminal Nerve Roots
ipsilateral facial pain, paresthesias,
numbness, and sensory loss
involvement of the neighboring
cranial nerves (especially cranial
nerves VI, VII, and VIII).
corneal reflex is depressed and a
trigeminal motor paresis may occur
tumors
Gasserian Ganglion Facial numbness with or without
paresthesias, often associated with
facial pain
hemifacial or involve only select
divisions of the trigeminal nerve
tumors
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Localization of LesionsAffecting Cranial Nerve VII
FACIAL NERVE LESSIOS CLINICAL MANIFESTATIONS CAUSES
Supranuclear Lesions (Central Facial
Palsy)
contralateral paresis of the lower
portion of the face with relative
sparing of upper facial function
Ischemia
Nuclear and Fascicular Lesions
(Pontine Lesions)
a peripheral type of facial nerve
palsy.
unilateral paralysis of all mimetic
facial muscles, with loss of frontal
wrinkling and facial asymmetry
MILLARD-GUBLER SYNDROME
FOVILLE SYNDROME
EIGHT-AND-A-HALF SYNDROME
PERIPHERAL FACIAL flaccid weakness of all the muscles of
facial expression on the
involved side, both upper and lower
face
Cerebellopontine Angle Lesions
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PERIPHERAL FACIAL LESSIONSCLINICAL MANIFESTATIONS CAUSES
Meatal
(Canal) Segment of the Facial
Nerve in the Temporal Bone
unilateral facial motor paralysis,
impairment of taste over the
ipsilateral anterior two-thirds of the
tongue, impaired lacrimation, and
deafness (rather than hyperacusis).
temporal bone fracture and
primary or secondary
tumors.
Facial Canal Distal to
the Meatal Segment but Proximal
to the Departure of the Nerve to the
Stapedius Muscle
Facial Canal Distal to
the Meatal Segment but Proximal
to the Departure of the Nerve to the
Stapedius Muscle
Ramsay Hunt syndrome
Within the Facial Canal Between the
Departure of the Nerve to the
Stapedius and the Departure of the
Chorda tympani
facial motor paralysis with loss of
taste on the anterior two-thirds of the
tongue
hearing is spared
Metabolic, infectious, neoplastic…
in the facial Canal Distal to the
Departure of the Chorda Tympani
facial motor paralysis without
associated hyperacusis or loss of
taste.
Metabolic, infectious, neoplastic…
Distal to the
Stylomastoid Foramen
isolated facial motor paralysis
paralysis of individual facial muscles.
Bell’s palsy….
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Vestibulocochlear nerve
Eighthcranial nerve consists of
two separate functional
components:
the auditory (cochlear) nerve
concerned with hearing
the vestibular nerve concerned
with equilibrium
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The Auditory Pathways
Four-tiered neuronal network
Auditory (cochlear) nerve extending
from the organ of Corti to the cochlear
nucleus
Fibers from the cochlear nucleus crossing
to the contralateral inferior colliculus
Fibers from the inferior colliculus
extending to the medial geniculate body
Fibers from the medial geniculate body
projecting to the auditory cortex in the
superior temporal gyrus
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Clinical localization
SensorineuralDeafness
deficit in perceiving either tones
or speech, which is due to a
lesion central to the oval window
involve the cochlea (sensory),
the cochlear nerve and nuclei
(neural), or the central auditory
pathways
Conductive
lesion located between the
environment and the organ of
Corti
Mixed
By Weber, rinne, audiogram
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Localization of LesionsCausing Sensorineural Deafness
LESSIONS CLINICAL MANIFESTATIONS CAUSES
CEREBRAL LESIONS auditory cortex do not cause complete
deafness
Unilateral dominant posterior
temporal lesions
Difficulties in localizing sounds.
auditory verbal agnosia, in bilateral
Ischemia
BRAINSTEM LESIONS ascending auditory tracts above the
level of the cochlear nuclei
do not cause hearing impairment.
sudden and complete bilateral deafness
(central stem deafness of Brunner)
Pineal and midbrain tumors
PERIPHERAL NERVE LESIONS AND
THE CEREBELLOPONTINE ANGLE
SYNDROME
Partial or complete deafness
ipsilateral tinnitus.
vestibular schwannoma (acoustic
neuroma)
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Vestibular pathways
Monitorsangular and linear
accelerations of the head
Membranous labyrinth.
otolith organ (utricle and saccule)
and
the three semicircular canals
Vestibular nerve and central
pathways
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Vertigo
ETIOLOGIC SEARCH
1.Blood pressure evaluation in
both arms
2. A detailed cranial nerve
examination
3. Cerebellar testing
4. Evaluation of vestibular control
of balance and movement
Romberg test
5. Provocative tests
head-thrust test
Dix-Hallpike test
caloric testing
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Etiologies of vertigo
Three general categories:
Peripheral causes (vestibular
labyrinthine disease)
Central causes (dysfunction of
the vestibular connections)
Systemic causes (e.g., endocrine,
hemopoietic, metabolic diseases)
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Supranuclear Lesions supranuclearcontrol is bilateral.
Bilateral upper motor neuron lesions
result in pseudo-bulbar palsy
Ischemia…
Nuclear Lesions and Lesions
Within the Brainstem
Wallenberg syndrome
ipsilateral palatal, pharyngeal, and
laryngeal paralysis
Wallenberg syndrome), tumors,
syringobulbia, motor neuron disease,
and inflammatory disease.
Lesions Affecting the
Vagus Nerve Proper
complete ipsilateral
vocal cord paralysis associated with
unilateral laryngeal anesthesia.
Neoplasm
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Localization of LesionsAffecting Cranial Nerve XI
muscle on the side of the hemiplegia is paretic.
the hemiplegia (i.e. ipsilateral to the cerebral lesion).
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Supranuclear Lesions Contralateralhemiplegia, the
trapezius
head is turned away from the
hemiplegic side indicating paresis of
the sternocleidomastoid muscle on the
side opposite
Head turning
Stroke
Mass
Nuclear Lesions paresis with
prominent atrophy and fasciculations
cord-low medulla
Lesions
motor neuron disease
Infranuclear Lesions paresis with
prominent atrophy and fasciculations
LESIONS WITHIN THE SKULL AND
FORAMEN MAGNUM
JUGULAR FORAMEN SYNDROME
(VERNET’S SYNDROME)
Collet-Sicard syndrome
#4 Extends from the pyramidal decussation to the posterior commissure.
#51 The basis for age-related changes in smell function is multiple and includes ossification and closure of the foramina of the cribriform plate, development of early neurodegenerative disease pathology, and cumulative damage to the olfactory receptors from repeated viral and other insults throughout life
#60 Oculomotor system is to stabilize images of the visual world on the retina