Posterior Fossa Level (Cerebellar, Auditory and Vestibular System)

Lecturer MED-2023 | Date June 11, 2021

Trans by: Cabalza, R. Dela Cruz, K. Palattao

OUTLINE • Lesion: unsteady, staggering gait (gait ataxia).

Posterior lobe
I. Anatomy of the VI. Neurologic Examination of
• Largest portion
Cerebellum the Posterior Fossa
A. Cerebellum Level • Responsible for coordinated movements of the extremities.
B. Cerebellar Peduncle A. The Ocular Motor • Lesion: loss of motor coordination, dysmetria, if the dentate
C. Cerebellar Cortex System and Cranial nucleus is involved, intention tremor (limb ataxia).
II. Ocular System Nerves III, IV, and
A. Neural mechanisms VI
used for eye B. Cranial Nerve VII
movements C. The Auditory and
III. The Auditory System Vestibular Systems
A. Anatomy of the and Cranial Nerve
Auditory System VII
B. Physiology D. Cranial Nerves IX
C. Pathophysiology And X
IV. The Vestibular System E. Cranial Nerve XI
V. Clinical Correlations F. Cranial Nerve XII
A. Ischemic Lesions of G. Speech
the Brainstem VII. References
B. Vascular Lesions of VIII. Appendix
the Brainstem
Figure 2. Lobes of the cerebellum
C. Vascular Lesions of
the Pons Vermal Zone/ midline cerebellar zone
D. Vascular Lesions of
the Midbrain • Vermis of the anterior and posterior lobes
E. Neoplasm of the • Receives the spinocerebellar afferents and is concerned
Posterior Fossa mainly with the muscle synergies involved in walking.
• Paleocerebellum – phylogenetic origin
I. ANATOMY OF THE CEREBELLUM • Spinocerebellum
A. CEREBELLUM
Lateral zone
• Largest structure in the posterior fossa
• Major part of the posterior lobe
• A derivative of the metencephalon
• Receives the corticopontocerebellar afferents.
• Dorsal to the pons and medulla and consists of a midline vermis
• Involved in the coordination of ipsilateral limb movement.
and two lateral hemispheres.
• Neocerebellum
• Forms the roof of the fourth ventricle.
• Corticocerebellum
• Divided functionally and anatomically into three lobes.
Paravermal/ intermediate zone
B. CEREBELLAR PEDUNCLE
• Cerebellum is connected to the brainstem by three pairs of
peduncles that contain cerebellar afferents and efferents.

Figure 1. Picture shows the different parts of the cerebellum.

Flocculonodular lobe
• Caudal lobule of the vermis, nodulus and flocculus.
• Archicerebellum or vestibulocerebellum because it receives
input from the vestibular system.
• Responsible for equilibrium and balance
• Lesion: inability to sit or stand without swaying or falling (truncal
ataxia).
Anterior lobe
• Consists of the vermis and cerebellar hemispheres anterior
Figure 3. Afferent and efferent fibers in the cerebellar peduncles
to the primary fissure.
• Responsible for coordination of gait and posture

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 Inferior cerebellar peduncle / restiform body
• receives information from the spinal cord and medulla.
• Connects it to the midbrain.
Middle cerebellar peduncle / brachium pontis
• Contains only afferent fibers which originate in the
contralateral pontine nuclei.
• Connects it to the pons.
Superior cerebellar peduncle /brachium conjunctivum
• Main outflow pathway from the cerebellum.
• Connects it to the medulla.
C. CEREBELLAR CORTEX
• Is a highly convoluted structure- folia.
• deep to it is a white matter that consists of the fiber tracts
entering and leaving the cortex.
• relay stations for efferent fibers from the cerebellar cortex:
o Dentate
o Emboliform
o Globose
o Fastigial nuclei
Figure 4. Afferent and efferent fibers in the cerebellar peduncles
• Histologically, the cerebellar cortex consists of three layers:
the molecular layer, Purkinje cell layer, and granule cell
layer.
• Afferent fibers entering the cerebellar cortex terminate as
either mossy fibers or climbing fibers.
• Activation of a single incoming mossy fiber can produce
excitation of a small, rectangular array of Purkinje cells,
because the mossy fiber contacts multiple granule cells
whose parallel fibers contact multiple Purkinje cells.
Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System)
Figure 5. Cell layers and connections of the cerebellar cortex
Molecular layer
• Consists mainly of axons and dendrites
• Basket cells
• Stellate cells
Purkinje cell layer
• Consists of a single layer of large goblet-shaped purkinje cells.
Granule cell layer
• Granule cells - densely packed small neurons
• Golgi cells- scattered larger neurons.
Mossy fibers
• Represent the cerebellar afferent fibers from all except the
inferior olivary nucleus.
• Mossy fiber synapses and parallel fiber synapses are
excitatory.
• All the other neurons activated by parallel fibers (Golgi, basket,
and stellate cells) are inhibitory to purkinje cells.
• The mossy fiber system constantly modulates cerebellar
activity during voluntary movement.
Climbing fibers
• axons of the olivocerebellar pathway
• synapse directly on Purkinje cells with excitatory input
• Signals errors in motor performance important in motor
learning.
Purkinje cells
• Mediates all output from the cerebellar cortex which project to
the deep cerebellar nuclei and form inhibitory synapses.
II. OCULAR SYSTEM
• Eye movement is accomplished through the action of the
extraocular muscles, which are activated by cranial nerves III,
IV, and VI.
• Paramedian reticular formation
o most of the input to the nuclei CN
o determines the activity of lower motor neurons for
both reflex and voluntary eye movements.
• Reflex movements are mediated by input from the vestibular
nuclei in the medulla to the abducens nucleus (cranial nerve
VI) and then through the medial longitudinal fasciculus to the
trochlear (cranial nerve IV) and oculomotor (cranial nerve III)
nuclei.
• Input from the retina travels to the superior colliculus and the
pretectal region and then to the brainstem reticular formation.
• Voluntary and pursuit movements come by way of descending
supranuclear pathways from the frontal eye fields and parieto-
occipital visual cortex.
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 A. NEURAL MECHANISMS USED FOR EYE
MOVEMENTS
Saccadic eye movements
• rapid reflex movements that bring a visual image to the fovea.
• voluntary saccades depend on the frontal eye fields.
• reflex saccades involve the superior colliculus.
• The frontal eye fields and superior colliculus project to the
brainstem.
• Pause cell, burst and tonic cells act to hold the eye at the new
desired position.
• Saccade, the pause cells are inhibited. Burst cells then fire
briefly, driving the eyes to their new position. Tonic cells also
begin to fire, and their discharge frequency is just enough to
hold the eye at the new desired position.
Burst neurons
• Pontine paramedian reticular formation- for horizontal
saccades
• Lesion: interrupt horizontal conjugate eye movements toward
the side of the lesion
• Rostral interstitial nucleus of the medial longitudinal
fasciculus- vertical -eye movements
• Lesion: affect both upward and downward vertical gaze.
Superior colliculus and the pretectal region
• Receive input from relay station in the auditory pathway.
• mediate eye movements in response to targets picked up in the
peripheral vision and in response to sound.
Smooth pursuit movements
• keep the fovea focused on a moving target.
• visual input from the retina is integrated, through the thalamus,
in both the primary visual cortex and parieto-occipital cortex.
• The parieto-occipital eye field- responsible for involuntary
smooth pursuit movements in which the eyes are fixated on an
object and maintain visual fixation as the object moves.
• Optokinetic nystagmus- eyes then make a quick movement
in the opposite direction to fixate on a new target when the
visual field reached its limit. Example: When watching a
passing train.
Vergence movements
• Maintain the visual image on the fovea when objects move
toward the eyes (convergence) or away from them
(divergence).
• Accommodation and miosis – reflexes mediated by the
edinger-westphal nucleus, the origin of the parasympathetic
fibers of the oculomotor nerve.
Vestibulo-ocular reflexes
• Hold images steady on the retina during brief head rotations.
• Involves conjugate movement of the eyes in the direction
opposite to that of head movement.
o Example: rotation of the head to the right- reflex involves
vestibular input from the right ear (semicircular canals are
stimulated) that relays in the ipsilateral
• Vestibular nucleus and crossed excitatory connections of the
vestibular nucleus with the contralateral abducens nucleus.
• Each of these eye movements is mediated by the nuclei of
cranial nerves III, IV, and VI and coordinated through neurons
in the brainstem paramedian reticular Formation.
Optokinetic movements
• Hold stable images on the retina as long as possible when
object filled space is moving past the eyes and then quickly
refixates on the next available target.
Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System)
Hering’s law
• Principle of equal innervation of yoked pairs of extraocular
muscles
• The muscles that turn the two eyeballs are yoked in pairs so
that the eyes move conjugately in the same direction with the
same velocity and force. Example: right lateral gaze- left
medial rectus and right lateral rectus
• Upward gaze depends on activation of the superior rectus and
inferior oblique muscles.
• Downward gaze depends on activation of the inferior rectus
and superior oblique muscles.
Table 1. The superior and inferior recti muscles move the eye up and down when
it is turned outward, and the inferior and superior oblique muscles move the eye
up and down when it is turned inward
Brainstem paramedian reticular formation
• Receives input from all prenuclear areas concerned with eye
movements.
• pause cells, burst cells, and tonic cells- different firing patterns
with different types of eyes movement
Conjugate horizontal eye movements
• integrated primarily at the level of the pons where the
abducens nucleus innervate the ipsilateral lateral rectus
muscle and the commissural neurons cross the midline
ascend in the contralateral medial longitudinal fasciculus to
innervate the motor neurons in the midbrain oculomotor
nucleus that innervate the medial rectus muscle.
Vertical eye movements
• control at the level of the midbrain
• Maintenance of the eyes in a particular position in the orbit
depends on tonic input from neurons in the neuronal
integrator.
o neurons in the vestibulocerebellum and medial
vestibular nucleus,
o nucleus prepositus hypoglossi in rostral
medulla – horizontal eye movements
o interstitial nucleus of Cajal in the midbrain -
vertical eye movements
Diplopia, or double vision
• occurs when an image no longer falls on exactly
corresponding areas of the two retinas.
• occurs from a lesion that affects one or more of the ocular
nerves or extraocular muscles, posterior fossa level or the
peripheral level.
Internuclear ophthalmoplegia
• Clinical syndrome when the lesion in the medial longitudinal
fasciculus prevents adduction of the eye on the side of the
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 lesion when the patient attempts to gaze toward the opposite lateral lemniscus. Fibers thus ascend bilaterally to the inferior colliculus, medial
side. genticulate body, and auditory cortex.

Ipsilateral conjugate gaze palsy

• Lesion in the abducens nucleus itself paralysis of the ipsilateral
Major regions of the Ear
lateral rectus muscle is disproportionately severe.
Nystagmus
• Combination of slow eye movements in one direction followed
by quick saccades in the opposite direction.
• Interactions between the vestibular and ocular motor systems
• Can also be a sign of disease in the vestibular end organ or in
the vestibulocerebellar pathways in the brainstem.
• See appendix types of nystagmus.
A. ANATOMY OF AUDITORY SYSTEM
• External ear consists of the pinna, which collects and directs
sounds through the external auditory canal.
• middle ear, or tympanic cavity, contains the tympanic
membrane (eardrum) and auditory ossicles which convert
soundwaves into waves in a fluid-filled chamber.
• inner ear or labyrinth which is a series of fluid filled
membranous channels in the petrous portion of the temporal
bone.

Frontal eye field

• Tonic influence on the contralateral pontine paramedian
reticular formation causing the eyes to tend to deviate toward
the opposite side is the most important clinical feature of
cortical ocular motor control.

Supratentorial lesions
• Involving the frontal eye fields produce loss of voluntary
conjugate gaze to the opposite side.

III. THE AUDITORY SYSTEM

• Represented at the posterior fossa and supratentorial levels.
• Cell bodies of these first-order neurons for hearing are in the
spiral ganglion in the axis of the helix.
• Afferent impulses pass centrally in the acoustic division of
cranial nerve viii and, synapse in the cochlear nuclei, ascend
bilaterally through a multisynaptic brainstem pathway to
primary auditory cortex in the anterior transverse gyrus of
heschl in the temporal lobe. Figure 7. Anatomy of the auditory system.
• Relay nuclei in the brainstem include the superior olivary nuclei,
Membranous labyrinth
nucleus of the lateral lemniscus, inferior colliculus, and medial
• divided into 2 channels/ membranes.
geniculate body.
• further divided:
• Lesions central to the cochlear nuclei result in some alteration
o Cochlea - contains the receptors for sound
of auditory function.
o Vestibule- contains the receptors of the vestibular
• Unilateral loss of hearing occurs only with lesions of cranial apparatus.
nerve VIII or the peripheral receptors. o Utricle
o Saccule
o Three semicircular canals

Figure 6. Auditory pathways. Auditory impulses can ascend directly in the Figure 8. Anatomy of membranous labyrynth.
ipsilateral lateral lemniscus or synapse in the trapezoid body or superior olivary
nucleus. They also may cross to the opposite side and ascend in the contralateral

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 Cochlea
• contains contains three parallel chambers and is shaped like a
snail.

Scala vestibuli and scala tympani

• Outer chambers contain perilymph – ionic composition similar
to cerebrospinal fluid

Scala media/ cochlear duct

• Middle chamber contains endolymph - high potassium and low
sodium content

Vestibular (Reissner) membrane

• Separates the scala vestibuli and scala media.

Basilar membrane.
• Separates the the scala tympani and scala media.

Scala vestibuli
• Ends at the oval window.

Scala tympani
• Ends at the round window.

Organ of Corti Figure 9. Conversion of sound waves in the external environment into action
potentials in the auditory nerves.
• Lies on the surface of the basilar membrane and contains
mechanically sensitive hair cells, the auditory receptors.

Stereocilia
• processes of the hair cells that generate electrotonic
potentials in response to movement of the basilar membrane
produced by sound waves.
• These electrotonic potentials will be converted into action
potentials in the auditory nerve fibers.

B. PHYSIOLOGY
• The ear converts sound waves in the external environment into
action potentials in the auditory nerves.
• Sound waves entering the external auditory canal move the
tympanic membrane. This movement is transmitted to the Figure 9 and 10. Conversion of sound waves in the external environment into
ossicles (malleus, incus, and stapes) of the middle ear, which action potentials in the auditory nerves.
amplify and transform the movements of the eardrum into smaller
and more forceful movements of the footplate of the stapes, C. PATHOPHYSIOLOGY
which rests against the oval window of the inner ear.
• As the sound waves enter the perilymph of the scala vestibuli, • Tinnitus or unilateral loss of hearing
they are transmitted through the vestibular membrane to the → Present in patients with disease of the auditory division of
endolymph of the scala media. cranial nerve VIII or its receptors or disease in the ipsilateral
• This causes displacement of the basilar membrane, which in turn ear.
stimulates the hair cells in the organ of Corti • Conduction deafness
→ Disease of the external or middle ear that prevents sound
waves from being transmitted to the cochlea.
→ Middle ear disease is associated with low-frequency loss
• Sensorineural deafness
→ Disease of the cochlea or the auditory nerve or its nuclei.
→ Nerve damage is associated with high-frequency loss.
• Audiometric testing
→ Identifies the frequencies most impaired
• Lesions central to the cochlear nuclei
→ Do not complain of hearing loss.
• Unilateral lesions in auditory receptive areas
→ Do not cause hearing loss, but they produce a deficit in sound
localization or discrimination.
• Focal seizures
→ Involving the cortical auditory receptive area in the temporal
lobe produce hallucinations of sound
• Brainstem auditory evoked potentials
→ Electrical potentials evoked by click stimulation

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 → Abnormalities in these potentials can identify and localize Important components
lesions in the auditory system. • Receptors
→ Hair cells that respond to mechanical movement and initiate
impulses that are transmitted in the vestibular division of CN
VIII to the vestibular nuclei in the medulla and pons.
→ Hair cells within the semicircular canals (angular acceleration)
and otoliths (linear acceleration)
→ These receptors are enclosed in the vestibular portion of
labyrinth in the urticle, the saccule, and semicicular canals.
Receptors that detect gravitational pull, rotational
→ Movements, and acceleration and these are located in the
utricle, saccule, and semicircular canals of the inner ear. They
transmit information to the central nervous system through the
vestibular division of cranial nerve VIII
→ Movement of the hair cell stereocilia (one direction) – it
produce local potentials that increase action potentials in the
nerve, (opposite direction) which inhibit nerve discharge
→ Angular acceleration – shake or nod of head, changes in head
rotation
→ Linear acceleration – elevator drops, lean to one side
→ Macula – present in the urticle and sacculae,
→ When the head is tilted from the vertical position, gravitational
pull on the otoliths distorts the hair cells and initiates an action
potential in the vestibular nerve.The
three semicircular canals monitor acceleration in any plane.
→ Each macula tuft of ciliated columnar epithelial cells
embedded in a gelatinous matrix that contains small calcified
particles (otoliths).
Figure 10. Rinne Test and Weber Test
• Cranial nerve
→ vestibular division of cranial nerve VIII
• Central nuclei
→ superior, medial, lateral, and inferior vestibular nuclei
• Vestibulo-ocular connections
→ the vestibulocerebellum (flocculonodular lobe) and vestibular
input to nuclei of cranial nerves III, IV, and VI.
• Vestibulospinal connections
→ lateral and medial vestibulospinal tracts
• Vestibulo-cortical connections
→ cerebral cortex(temporal lobes)
• Fibers of the vestibular division of cranial nerve VIII synapse in
the superior, medial, lateral, and inferior vestibular nuclei located
in the floor of the fourth ventricle.

Table 2. Difference of Weber and Rinne Test in terms of Method, Normal

Response, Conduction Deafness and Sensorineural deafness.

IV. THE VESTIBULAR SYSTEM

• Provide the nervous system with information about gravity,
rotation, and acceleration necessary for maintenance of balance
and equilibrium
• Located primarily in the posterior fossa
• Vestibular nuclei connected to cerebellum, spinal cord, reticular
formation (internal regulation and consciousness systems),
medial longitudinal fasciculus (for coordination of head and eye
movements), and cerebral cortex to allow integration of vestibular
impulses with other sensory information for normal balance and
equilibrium
• It is also for maintaining posture and for maintaining steady vision
Table 3. Comparison of Function and Connections of Vestibular Organs
with change in position.
• vestibular function is represented in the temporal lobes
• The oculocephalic (doll’s eye) reflex involves rapidly turning the
• Lesions - dysequilibrium (sense of imbalance)
head from side to side or up and down. This movement
→ Vertigo - symptom of vestibular system dysfunction. stimulates the semicircular canals and causes the eyes to move
→ Nystagmus - occurs with lesions of the vestibular system. conjugately in the opposite direction.
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• Vertigo may result from dysfunction of the vestibular system.
• Hyperkinetic dysarthria
→ occurs in dystonias and choreas in which there are
uncontrolled and unpredictable movements of the laryngeal,
pharyngeal, lingual, and facial muscles that interrupt and
distort phonation, resonation, and articulation.

Figure 11. Oculocephalic (Dell’s Eyes)

V. CLINICAL CORRELATIONS
Dysarthria
• motor speech impairment, must be distinguished clearly from
aphasia, a disorder of symbolic language function
• clear speech involves closely coordinated and modulated activity
of muscles supplied by cranial nerves V, VII, IX, X, and XII as
well as the respiratory muscles, especially the diaphragm,
innervated by the phrenic nerve (spinal level C4)
Table 4. Types pf Dysarthrias

Table 5. Differences Between Bulbar and Pseudobulbar Palsies

Coma
• Common result of lesions in the posterior fossa
• Coma due to lesions of the brainstem can be identified and
localized by the presence of associated disturbances in
brainstem function outside the consciousness system such as:
Table 4. Components of Speech Production 1. Dysfunction of the descending motor pathways resulting in
disturbances in posture and tone
• Flaccid dysarthria
2. Dysfunction of the ocular motor system
→ result of lesions of the final common pathways of cranial
3. Disturbances in control of respiratory and cardiovascular
nerves V, VII, IX, X, or XII characterized by breathy voice,
functions
hypernasality, and articulatory imprecision.
• Decorticate posturing
• Spastic dysarthria
→ due to damage of the rostral brainstem(rostral to the red
→ result of bilateral corticobulbar tract lesions and is
nucleus). Flexor tone is increased more than extensor tone in
characterized by a strained hoarseness, hypernasality, and a
the upper extremities, resulting in flexion of the arms.
slow articulatory rate.
• Decerebrate posturing
• Ataxic dysarthria
→ lesions at or caudal to the red nucleus but rostral to the
→ result of lesions in Cerebellum. It causes irregular articulatory
vestibular nuclei. Extensor tone is increased in all four limbs
breakdowns and, less frequently, voice tremor and loss of
causing uninhibited influence of vestibulospinal pathway.
loudness of the voice.
• Oculovestibular reflex
• Hypokinetic and hyperkinetic dysarthrias
→ effects on eye movements by caloric stimulation of the
→ due to Lesions of the basal ganglia circuits.
labyrinth.
• Hypokinetic dysarthria
→ normal = caloric stimulation produces nystagmus.
→ characteristic of Parkinson disease and related syndromes
• Cheyne-Stokes respiration
and features low-volume, monotonous, rapid speech with
→ happens due to loss of cerebral influence because of lesions
indistinct articulation.
rostral to the red nucleus. There is periodic breathing pattern
characterized by waxing-and-waning hyperpnea alternating
with short periods of apnea
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• Central neurogenic hyperventilation C. VASCULAR LESIONS OF THE PONS
→ midbrain and rostral pontine lesions are suggested by
sustained hyperpnea.
• Lesions in the lower brainstem
→ causes slow, arrhythmic, or periodic breathing patterns,
apneustic breathing (long inspiratory pauses), respiration
alternans, and ataxic(Biot)breathing
*see appendix - levels of brainstem involvement

A. ISCHEMIC LESIONS OF THE BRAINSTEM

• The blood supply of the brainstem is derived from the
vertebrobasilar arterial system.
→ Midline region
▪ supplied by small penetrating paramedian branches of the
vertebral and basilar arteries
→ Point lateral area
Figure 13. Paramedian infarct of pons (red area) with involvement of cranial
▪ by larger circumferential branches
nerves VI (abducens nerve) and VII (facial nerve), medial lemniscus, and
→ At the level of the medulla corticospinal tract.
▪ posterior inferior cerebellar artery See Appendix. Table 10.
→ At the level of the pons
▪ anterior inferior cerebellar artery D. VASCULAR LESIONS OF THE MIDBRAIN
→ Superior cerebellar artery • Infarction of the lateral midbrain is uncommon
▪ at the level of the midbrain • Paramedian region – ischemic lesions are seen occasionally
• Ischemic lesions involving the brainstem usually occur either in → produce diplopia, ptosis, and mydriasis due to involvement of
the paramedian region or in the lateral region. cranial nerve III
→ Paramedian Region → contralateral hemiparesis due to involvement of the cerebral
▪ involves the descending motor pathways, medial peduncle
lemniscus, and the nuclei of cranial nerves III,IV,VI, or XII. • This constellation of symptoms is called Weber syndrome.
→ Lateral Region
▪ involves the cerebellum, cerebellar pathways, descending
sympathetic pathways, the lateral spinothalamic tract, and
the nuclei of cranial nerves V, VII,VIII, IX, or X.

B. VASCULAR LESIONS OF THE BRAINSTEM

• Paramedian region
→ supplied by vessels from the anterior spinal and vertebral
arteries
• Infarction in paramedian medulla involves the: medullary
pyramids, medial lemniscus, and cranial nerve XII
→ results in contralateral hemiparesis, impaired conscious
proprioceptive sensation, and ipsilateral tongue weakness

Figure 14. Paramedian infarct (red area) of midbrain (Weber syndrome), with
involvement of cranial nerve III (oculomotor nerve) and cerebral peduncle.

• Certain tumors of the posterior fossa are encountered more

commonly in children and adolescents than in older adults.

Ependymomas and medulloblastomas

• frequently arise in the region of the fourth ventricle
• associated with ataxia, nausea, and vomiting
• As lesions increase in size, they obstruct the outflow of
cerebrospinal fluid from the ventricular system and cause non-
communicating hydrocephalus and signs of increased
intracranial pressure.
Figure 12. Paramedian infarct of medulla (green area) Astrocytomas of the cerebellum
• Common in childhood.
• Arise in the cerebellar hemisphere (resulting in ipsilateral limb
ataxia).
• Display a unique biologic behavior.
• The early diagnosis and surgical removal of cerebellar
astrocytomas, in contrast to astrocytomas of other locations,
are associated with a good prognosis.

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 Astrocytomas arise from glial cells located within the
substance of the brainstem
• result in a Brainstem or Pontine Glioma
• involve either the base or the tegmentum and are usually
associated with progressive (often bilateral) symptoms of cranial
nerve, motor, and sensory dysfunction.
• If the reticular formation is affected = altered consciousness
• Certain tumors arise outside the parenchyma of the brainstem
(extra-axial tumors), often from the meninges (meningiomas)
or the supporting cells in the cranial nerves.
Extra-axial tumors
• Alter cranial nerve function and secondarily affect brainstem
function by compression or direct invasion.
• The most common tumor is the Vestibular Schwannoma
(Acoustic Neuroma).
Vestibular Schwannoma (Acoustic Neuroma)
• Arises from Schwann cells in the vestibular division of cranial
nerve VIII in virtually all cases.
• The tumors frequently are bilateral in central, or type II,
neurofibromatosis.
• Early signs are unilateral tinnitus, decreased hearing, and
disequilibrium.
• As the tumor enlarges, ipsilateral facial paresis, loss of the
corneal reflex, and ipsilateral limb ataxia occur.
• With further increase in size, additional signs of brainstem
compression and increased intracranial pressure may
develop.
• These tumors are usually visualized
• with CT-scan and when very small, MRI.
Figure 15. Minimally Invasive Surgery for Giant Vestibular Schwannoma
Herniation of the Brain
• Changes in shape and position that occur from intracranial
mass lesions
• Because cranial cavity is a closed space and cannot
accommodate changes in intracranial volume, presence of a
supratentorial or posterior fossa mass increases intracranial
pressure. With further expansion, this causes herniation of the
brain
See Appendix. Table 11.
1. Uncal Herniation
• Clinical sign in compression of:
→ Cranial nerve III - ipsilateral palsy of cranial nerve III,
usually beginning with dilatation of the
→ Contralateral cerebral peduncle against the free edge of
the tentorium - hemiparesis and the Babinski sign
ipsilateral to the expanding lesion.
→ Midbrain - affects the ascending reticular activating
system, causing progressive loss of consciousness.
→ Posterior cerebral artery - infarction of the occipital lobe
producing homonymous hemianopia.
Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System)
2. Central or Transtentorial Herniation
• Clinical signs
→ oculomotor paresis, progressive alteration of
consciousness, and decerebrate posturing.
• Because mass lesions are rarely directly in the midline, some
degree of lateral shift and uncal herniation nearly always
accompanies transtentorial herniation.
• Duret hemorrhages
→ Caudal displacement of the basilar artery (which is
attached to the circle of Willis by the posterior cerebral
arteries) does not occur to the same degree, resulting in
stretching and shearing of paramedian perforating
vessels, with secondary infarction and hemorrhage in the
brainstem
3. Tonsillar or Foramen Magnum Herniation
• As a result of an expanding mass in the posterior fossa or
further progression of uncal or transtentorial herniation, the
cerebellar tonsils herniate downward through the foramen
magnum and compress the medulla
• Signs:
→ neck pain and stiffness, the result of stretching and irritation
of the lower cranial nerves supplying the neck muscles
→ progressive loss of consciousness from involvement of the
ascending reticular activating system
→ generalized flaccidity
→ alteration of vital signs, with slowing of the pulse and
vasomotor instability
→ periodic or irregular respirations from involvement of visceral
centers in the medulla.
On additional information:
• Dysarthria is a motor speech impairment that may result
from impairment of any portion of the motor system.
• Coma may result from a posterior fossa lesion that involves
the ascending reticular activating system.
• Decorticate posturing is due to damage of the rostral
brainstem (rostral to the red nucleus) and results in
increased flexor tone in the upper extremities and increased
extensor tone in the lower extremities.
• Decerebrate posturing occurs with lesions at or caudal to the
red nucleus but above the vestibular nuclei and results in
increased extensor tone in all four limbs.
• Acute onset and focal neurologic deficits are likely to
represent a vascular cause of dysfunction. Vascular lesions
of the posterior fossa present with specifically recognizable
syndromes
VI. NEUROLOGIC EXAMINATION OF THE POSTERIOR
FOSSA LEVEL
A. THE OCULAR MOTOR SYSTEM AND CRANIAL
NERVES III, IV, AND VI
• Size and bilateral symmetry of the palpebral fissures
• Size, shape, and symmetry of the pupils
• Pupillary light reflex and near reflex
• Position, alignment, and stability of the eyes when the patient
attempts to gaze straight ahead (primary position) are
observed
→ Abnormalities include inability to maintain the primary position
because of conjugate deviation, misalignment of the eyes
because of monocular deviation, and spontaneous nystagmus
• Eye movement test and subtle muscle weakness test
• Look especially for ptosis and nystagmus
9 of 15
 Figure 18. Test the Corneal Reflex (tested by asking the patient to
look to one side while the cornea is gently touched with a wisp of
cotton, brought toward the cornea from the opposite direction)
B. CRANIAL NERVE VII
• Observe facial expressions and facial symmetry
• Specific muscle groups to be examined:
→ Frontalis muscle
Figure 16: 1st image: near reaction; 2nd image: extraocular movement tests ▪ tested by asking the patient to wrinkle the forehead;
strength can be assessed by attempting to smooth the
wrinkles on each side
→ Orbicularis oculi
▪ tested by asking the patient to close the eyes tightly and
then to try opening them
→ Lower facial muscles
▪ tested by asking the patient to smile or show the teeth
→ Taste is not examined unless a peripheral facial nerve lesion
is suspected
▪ Taste test: tested by having the patient protrude the tongue
and then asking him or her to identify sugar, salt, or other
substances applied to the side of the tongue

C. THE AUDITORY AND VESTIBULAR SYSTEMS

AND CRANIAL NERVE VIII
• Audiometry- the best means of examining hearing
• Auditory acuity of one side is compared with that of the other
• Weber and Rinne tests
Figure 17: 1. to the patient’s extreme right; 2. to the right and upward; and 3. down Refer to Table 2.
on the right; then 4. without pausing in the middle, to the extreme left, 5. to the left
and upward, and 6. down on the left.

• Sensory function test: ability to perceive pinprick and light

touch applied to the skin
• The corneal reflex (also involves cranial nerve VII) using
wisp of cotton
→ The normal response is prompt, bilateral blinking.
• Motor function is tested by having the patient open the jaw
→ unilateral pterygoid weakness: jaw deviates to the weak side
→ The patient is also asked to bite firmly while the examiner
palpates the masseter and temporalis muscles

• Jaw jerk test

→ tested by placing the examiner’s forefinger on the relaxed
jaw and by striking the finger with a reflex hammer
▪ substances applied to the side of the tongue

Figure 19. Weber Test

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 10 of 15

 E. CRANIAL NERVE XI
• Sternocleidomastoid muscle
→ Ask the patient to turn the head to the side, against resistance
applied by the examiner to the patient’s jaw.
→ Contracting muscle (on the side opposite the turn of the head)
can be observed and palpated.
• Trapezius muscle
→ examined by having the patient elevate the shoulders against
resistance applied by the examiner.

Figure 20. Rinne Test (bone conduction test)

Figure 22. Test Sternocleidomastoid strength

Figure 21. Rinne Test (air conduction test)

• Vestibular function ordinarily is not examined unless disease of
cranial nerve VIII, sensory ataxia, or brainstem disease is Figure 23. Test Trapezius Strength
suspected.
• Caloric testing F. CRANIAL NERVE XII
→ convenient means of testing vestibular function • Patient is asked to protrude the tongue in the midline and then
to wiggle it from side to side.
→ usually is reserved for comatose patients.
→ UMN lesions: slowing of the alternate motion rate of the
→ Irrigating the outer ear canal with cold water and observing
tongue.
for nystagmus, conjugate deviation of the eyes, or subjective
vertigo → Unilateral lower motor neuron weakness: ipsilateral atrophy
and fasciculations develop and the protruded tongue
D. CRANIAL NERVES IX AND X
deviates toward the side of the lesion.
• The glossopharyngeal and vagus nerves are often tested
together
→ Soft, breathy voice- nasal escape of air is suggestive of G. SPEECH
weakness in the oropharynx • Verbal communication- cognitive and motor skills.
→ hoarse or husky voice- lesion of the nerve supply to the larynx • Cognitive aspects- considered language
→ listening to the patient talk and inquiring about difficulty in • Some motor speech disorders may result from disease of:
speaking or swallowing → brainstem and cranial nerves (flaccid dysarthria)
• Ask the patient to open the mouth and say “ah.” → cerebellum (ataxic dysarthria)
→ Normally, palate rises in the midline • Spastic, hypokinetic, and hyperkinetic dysarthrias- disease at the
→ Unilateral palatal weakness causes the uvula to deviate supratentorial level
toward the intact side • Speech can be evaluated by
→ listening to spontaneous speech
• Gag reflex
→ have the patient repeat the syllables
→ examined by touching the back of the throat with a tongue
→ pa-pa-pa (facial muscle and nerve function)
blade and noting the contraction of the pharyngeal muscles.
Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 11 of 15
 → ta-ta-ta (tongue and hypoglossal nerve function)
→ ka-ka-ka (pharyngeal muscle and cranial nerve IX and X
function)
→ pa-taka-pa-ta-ka test cranial muscle coordination (cerebellar
function)
• Tests for disorders of speech, the dysarthrias, are commonly
administered at the same time as the testing of cranial nerve
function

VII. REFERENCES
• Reporter’s PPT and Lecture
• Benarroch, E. E., Daube, J. R., Flemming, K. D., & Westmoreland,
B. F. (2008). Mayo clinic medical Neurosciences. Organized by
Neurologic Systems and Levels.

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 12 of 15

 VIII. APPENDIX

Table 6. Location of Control Cells for Horizontal and Vertical Conjugate Eye
Movements

Table 7. Systems Controlling Conjugate Gaze

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 13 of 15

Table 8. Types of Nystagmus

Table 9. Levels of Brainstem Involvement in Patients With Coma

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 14 of 15

 Infarction results in… Due to the involvement of the…

ipsilateral sixth nerve palsy axons arising in the abducens nucleus

ipsilateral facial weakness facial nerve as it passes around the abducens nucleus
PARAMEDIAN AREA OF
THE PONS contralateral hemiparesis corticospinal tracts in the basis pontis
contralateral impairment of conscious medial lemniscus
proprioception
ipsilateral facial paralysis facial nucleus
impairment of touch, pain, & temperature main sensory nucleus and descending nucleus and tract
on the same side of the face of cranial nerve V

LATERAL AREA OF THE

loss of pain and temperature sensation on spinothalamic tract
PONS the contralateral side of the body
Ipsilateral deafness nuclei of cranial nerve VIII
ipsilateral Homer syndrome descending sympathetic fibers
ipsilateral cerebellar signs middle cerebellar peduncle

Table 10. Paramedian Area of the Pons and Lateral Area of the Pons

Table 11. Types of Herniation of the Brain

Trans # 11 Posterior Fossa Level (Cerebellar, Auditory and Vestibular System) 15 of 15