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FUNCTIONAL LOCALIZATION OF
BRAINSTEM AND CRANIAL NERVES
Presenter: Dr Yilkal Y ( IMR3 )
Moderator: Dr Nebiyu B ( Consultant neurologist )
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OUTLINES
 Neuroanatomy of brainstem
 Midbrain
 Pons
 Medulla oblengata
 Neuroanatomy of cranial nerves
 Functional localization of brainstem and cranial nerves
 References
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Objective
 By the end 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 neuroanatomical area
 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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6
Brainstem Organization
 Composed of three parts:
 Tectum (roof)
 Midbrain
 quadrigeminal plate.
 pons and medulla
 nonfunctional tissue
 Tegmentum (midportion)
 CN motor and sensory nuclei
 Reticular Formation
 long ascending and descending tracts
 Base
 Descending corticospinal and corticobulbar
fibers
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Brainstem Organization…
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10
Brainstem Organization…
11
Brainstem Organization…
12
Midbrain
13
Midbrain…
14
Vascular supply
15
Ventral mid brain syndromes
 WEBER’S SYNDROME
 pyramidal fibers and the
fascicle of cranial nerve III
 Contralateral hemiplegia
 Ipsilateral oculomotor paresis
 Stroke ,MS
16
Ventral mid brain syndromes…
 Claude’s syndrome
 dorsal midbrain tegmental
lesions
 fascicle of cranial nerve III
 Red nucleus
 prominent
 cerebellar signs (e.g., asynergia,
ataxia, dysmetria,
dysdiadochokinesia)
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Ventral mid brain syndromes…
 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 brain syndrome
 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 brain syndrome…
20
Dorsal mid brain syndrome…
 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 1 inch (2.5 cm)
long
 A bridge Connecting the
right and left cerebellar
hemispheres
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Upper pons
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Mid pon
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Lower pon
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Vascular supply of pons
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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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Dorsal pontine syndromes…
32
 PARAMEDIAN PONTINE SYNDROMES
 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
 Most inferior 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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Upper medulla
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Mid medulla
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Lower medulla
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Vascular supply of medulla
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Medullary Syndromes
 Results from 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 to a 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…
 The reticular 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
 Most of 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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Cranial nerves
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Olfactory Nerve
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Localization of Lesions
Affecting the 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
Affecting the 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…
 Foster Kennedy 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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Cranial nerve II
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Cranial nerve II
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Localization of Lesions in 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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Localization of Lesions in the Optic Pathways
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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
 Exits the 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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Oculomotor nucleus
63
Localization of lesions
 Supra nuclear
 Pupillary and accommodation
reflex
 Horizontal gaze palsy
 INO
 Vertical gaze palsy
 Nuclear
 Fascicular
 Peripheral nerves
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Anisocoria
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TROCHLEAR NERVE
 Winding around 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 cranial nerve 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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Localization of trochlear lesions
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Abducent nerve
 Exits from 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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Localization of lesions
73
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Functional classes of eye 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 of eye 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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Horizontal saccade
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Localization of horizontal saccades
 Supra nuclear gaze
palsy
 Saccades away from
the lesion will be
slow/absent
 Intact VOR by
ocuiocephalic
manuever
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Localization of horizontal saccades pathway…
 Interferes with ipsilateral
horizontal saccade
 Pursuit and VOR will be
impaired
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Localization of horizontal saccades pathway…
 Ipsilateral abduction deficient
 No horizontal gaze
deficient ,rather isotropia

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INO
 Interferes with ipsilateral
adduction
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Localization of horizontal saccades pathway…
 One and half syndrome
 Horizontal gaze palsy ---one
 INO of CL--half
 Lesion is ipsilateral 6th
nerve
nucleus , PPRF and , MLF.
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Vertical saccades
83
Vertical saccades
Upward gaze Downward gaze
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Localization of vertical gaze
 Vertical supranuclear gaze
palsy
 Impaired upward and downward
saccades with intact VOR.
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Localization of vertical gaze…
 Disrupt upward saccades
 May result downward gaze
deviation---sun set eyes
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Localization of vertical gaze…
 Impair downward saccades
 May cause up gaze deviation
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Pursuit
 Slowly moving targets
(up to 70 degrees/sec)
to maintain the image
stable on the fovea.
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Persuit…
 Lesions present with catch up
saccades
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Vergence
 A means of
maintaining
ocular alignment
on an
approaching or
retreating object
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Lesions
 Exo / Esotropia reviled with
cover testing.
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VOR (horizontal)
92
Lesions
 Compensatory jerk nystagmus
 Acute lesions result in absent
VOR on that side
 Positive head impulse test
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Vertical VOR
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Localization
 Down or up beat nystagmus---
vestibular nucleus
 MLF---Skew deviation
 INC---oscillating type of skew
deviation
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Trigeminal nerve
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Localization of Lesions Affecting 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).
97
lesions Clinical manifestations causes
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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Corneal reflex
99
Cranial nerve VII
SVE
GVE
GSA
SA
100
101
Localization of Lesions Affecting 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
102
PERIPHERAL FACIAL LESSIONS CLINICAL 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….
103
Vestibulocochlear nerve
 Eighth cranial nerve consists of
two separate functional
components:
 the auditory (cochlear) nerve
concerned with hearing
 the vestibular nerve concerned
with equilibrium
104
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
105
Clinical localization
 Sensorineural Deafness
 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
106
Localization of Lesions Causing 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)
107
Vestibular pathways
 Monitors angular and linear
accelerations of the head
 Membranous labyrinth.
 otolith organ (utricle and saccule)
and
 the three semicircular canals
 Vestibular nerve and central
pathways
108
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
109
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)
110
Localization of vertigo
111
Cranial Nerves IX
112
113
Supranuclear Lesions Bilateral corticobulbar lesions
(pseudo-bulbar palsy)
severe dysphagia
other pseudo-bulbar
signs (e.g., pathologic laughter
and crying, spastic tongue, explosive
spastic dysarthria)
Nuclear and Intramedullary Lesions Wallenberg syndrome syringobulbia, demyelinating
disease, vascular disease, motor
neuron disease, and malignancy.
Extramedullary Lesions CEREBELLOPONTINE ANGLE
SYNDROME
JUGULAR FORAMEN SYNDROME
(VERNET’S SYNDROME)
WITHIN THE RETROPHARYNGEAL
AND RETROPAROTID SPACE
Cranial nerve VII,VIII,IX
injure cranial nerves IX, X, and XI
Collet-Sicard syndrome (affecting
cranial nerves IX, X, XI, and XII)
and Villaret’s syndrome (affecting
cranial nerves IX,
X, XI, and XII, the sympathetic chain,
and occasionally cranial nerve VII)
114
Localization of Lesions Affecting the Glossopharyngeal Nerve
115
Cranial Nerves X
116
Supranuclear Lesions supranuclear control 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
117
 Lesions within the Posterior Fossa
118
Cranial Nerve XI
119
Localization of Lesions Affecting Cranial Nerve XI
 muscle on the side of the hemiplegia is paretic.
 the hemiplegia (i.e. ipsilateral to the cerebral lesion).
120
Supranuclear Lesions Contralateral hemiplegia, 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
121
122
Cranial Nerve XII
123
124
Localization of Lesions Affecting Cranial Nerve XII
Supranuclear Lesions
Above the pons
lateral
tongue paralysis
Ipsilateral
ischemia
cortico-lingual pathway dysarthria
Nuclear Lesions and Intramedullary paresis, atrophy, furrowing,
fibrillations, and
Fasciculations
multiple sclerosis, syringobulbia
motor neuron disease
Intramedullary hypoglossal
involvement
Medial medullary syndrome
(Dejerine’s anterior bulbar syndrome
tumor, demyelinating
disease, syringobulbia, and vascular
insult
Peripheral Lesions Deviation to side of the lession
Collet-Sicard syndrome
basilar skull lesion
multiple lower cranial nerve palsy
syndromes
125
126
References
 Localization in Clinical Neurology 2017
 DeJong’s The Neurologic Examination 8th edition
 CRANIAL NERVES Function and Dysfunction 3rd
edition
 Cranial Nerves:Anatomy, Pathology, Imaging 2009
 NETTER’S ATLAS OF NEUROSCIENCE 3rd Edition
 Brainstem Disorders 2011
 NEUROANATOMICAL BASIS of CLINICAL NEUROLOGY 2nd
Edition
 Anatomic Basis of Neurologic Diagnosis 2023
 FUNCTIONAL NEUROANATOMY 2nd
edition
 Bradley neurology 8th
edition
 Google scholar
127
Thank you !!!

Brainstem and CN localization Yilkal.pptx

  • 1.
    1 FUNCTIONAL LOCALIZATION OF BRAINSTEMAND CRANIAL NERVES Presenter: Dr Yilkal Y ( IMR3 ) Moderator: Dr Nebiyu B ( Consultant neurologist )
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    2 OUTLINES  Neuroanatomy ofbrainstem  Midbrain  Pons  Medulla oblengata  Neuroanatomy of cranial nerves  Functional localization of brainstem and cranial nerves  References
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    3 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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    4 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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    6 Brainstem Organization  Composedof three parts:  Tectum (roof)  Midbrain  quadrigeminal plate.  pons and medulla  nonfunctional tissue  Tegmentum (midportion)  CN motor and sensory nuclei  Reticular Formation  long ascending and descending tracts  Base  Descending corticospinal and corticobulbar fibers
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    15 Ventral mid brainsyndromes  WEBER’S SYNDROME  pyramidal fibers and the fascicle of cranial nerve III  Contralateral hemiplegia  Ipsilateral oculomotor paresis  Stroke ,MS
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    16 Ventral mid brainsyndromes…  Claude’s syndrome  dorsal midbrain tegmental lesions  fascicle of cranial nerve III  Red nucleus  prominent  cerebellar signs (e.g., asynergia, ataxia, dysmetria, dysdiadochokinesia)
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    17 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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    18 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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    20 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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    21 PONS  About 1inch (2.5 cm) long  A bridge Connecting the right and left cerebellar hemispheres
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    26 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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    27 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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    28 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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    29 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
  • 30.
    30 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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    32  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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    33 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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    34 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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    39 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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    40  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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    41 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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    42 Reticular formation  Functions Sleep and consciousness  Pain modulation  Cardiovascular control  Respiratory control  Somatic motor control
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    43 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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    44 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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    45 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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    46 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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    51 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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    52 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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    53 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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    56 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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    57 Localization of Lesionsin the Optic Pathways
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    59 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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    61 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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    63 Localization of lesions Supra nuclear  Pupillary and accommodation reflex  Horizontal gaze palsy  INO  Vertical gaze palsy  Nuclear  Fascicular  Peripheral nerves
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    67 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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    68  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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    71 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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    74 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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    75 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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    77 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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    78 Localization of horizontalsaccades pathway…  Interferes with ipsilateral horizontal saccade  Pursuit and VOR will be impaired
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    79 Localization of horizontalsaccades pathway…  Ipsilateral abduction deficient  No horizontal gaze deficient ,rather isotropia 
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    80 INO  Interferes withipsilateral adduction
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    81 Localization of horizontalsaccades pathway…  One and half syndrome  Horizontal gaze palsy ---one  INO of CL--half  Lesion is ipsilateral 6th nerve nucleus , PPRF and , MLF.
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    84 Localization of verticalgaze  Vertical supranuclear gaze palsy  Impaired upward and downward saccades with intact VOR.
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    85 Localization of verticalgaze…  Disrupt upward saccades  May result downward gaze deviation---sun set eyes
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    86 Localization of verticalgaze…  Impair downward saccades  May cause up gaze deviation
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    87 Pursuit  Slowly movingtargets (up to 70 degrees/sec) to maintain the image stable on the fovea.
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    88 Persuit…  Lesions presentwith catch up saccades
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    89 Vergence  A meansof maintaining ocular alignment on an approaching or retreating object
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    90 Lesions  Exo /Esotropia reviled with cover testing.
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    92 Lesions  Compensatory jerknystagmus  Acute lesions result in absent VOR on that side  Positive head impulse test
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    94 Localization  Down orup beat nystagmus--- vestibular nucleus  MLF---Skew deviation  INC---oscillating type of skew deviation
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    96 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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    97 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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    101 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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    102 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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    103 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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    104 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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    105 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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    106 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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    107 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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    108 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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    109 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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    113 Supranuclear Lesions Bilateralcorticobulbar lesions (pseudo-bulbar palsy) severe dysphagia other pseudo-bulbar signs (e.g., pathologic laughter and crying, spastic tongue, explosive spastic dysarthria) Nuclear and Intramedullary Lesions Wallenberg syndrome syringobulbia, demyelinating disease, vascular disease, motor neuron disease, and malignancy. Extramedullary Lesions CEREBELLOPONTINE ANGLE SYNDROME JUGULAR FORAMEN SYNDROME (VERNET’S SYNDROME) WITHIN THE RETROPHARYNGEAL AND RETROPAROTID SPACE Cranial nerve VII,VIII,IX injure cranial nerves IX, X, and XI Collet-Sicard syndrome (affecting cranial nerves IX, X, XI, and XII) and Villaret’s syndrome (affecting cranial nerves IX, X, XI, and XII, the sympathetic chain, and occasionally cranial nerve VII)
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    114 Localization of LesionsAffecting the Glossopharyngeal Nerve
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    116 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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    117  Lesions withinthe Posterior Fossa
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    119 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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    120 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
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    124 Localization of LesionsAffecting Cranial Nerve XII Supranuclear Lesions Above the pons lateral tongue paralysis Ipsilateral ischemia cortico-lingual pathway dysarthria Nuclear Lesions and Intramedullary paresis, atrophy, furrowing, fibrillations, and Fasciculations multiple sclerosis, syringobulbia motor neuron disease Intramedullary hypoglossal involvement Medial medullary syndrome (Dejerine’s anterior bulbar syndrome tumor, demyelinating disease, syringobulbia, and vascular insult Peripheral Lesions Deviation to side of the lession Collet-Sicard syndrome basilar skull lesion multiple lower cranial nerve palsy syndromes
  • 125.
  • 126.
    126 References  Localization inClinical Neurology 2017  DeJong’s The Neurologic Examination 8th edition  CRANIAL NERVES Function and Dysfunction 3rd edition  Cranial Nerves:Anatomy, Pathology, Imaging 2009  NETTER’S ATLAS OF NEUROSCIENCE 3rd Edition  Brainstem Disorders 2011  NEUROANATOMICAL BASIS of CLINICAL NEUROLOGY 2nd Edition  Anatomic Basis of Neurologic Diagnosis 2023  FUNCTIONAL NEUROANATOMY 2nd edition  Bradley neurology 8th edition  Google scholar
  • 127.

Editor's Notes

  • #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