Transcript The Cerebellum

The Cerebellum
Clinical Examination
Objectives
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To be knowledgeable about the aspects of the neurological
examination pertaining to the cerebellum
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To understand how to localize lesions within the cerebellum on the
basis of clinical findings
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To develop a framework about the presentation of nervous system
illness
Cerebellar Examination
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Midline cerebellar function
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Cerebellar hemispheric function
Clinical localization in the cerebellum
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For purpose of localization, cerebellum can be viewed as a
saggitally-oriented structure containing 3 zones on each side:
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Midline
Intermediate
Lateral
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Midline zone
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Consists of the anterior and posterior parts of the vermis,
fastigial nucleus and associated input and output projections
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concerned with posture, locomotion, position of head relative to
trunk, control of EOM’s
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Cerebellar signs resulting from midline cerebellar disease
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disorders of stance/gait, truncal postural disturbances, rotated
postures of the head, disturbances of eye movements
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Intermediate zone
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Consists of paravermal region of cerebellum and interposed
nuclei (emboliform, globose)
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concerned with control of velocity, force and pattern of muscle
activity
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Clinical disorders related to disease of this zone not clearly
delineated
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Lateral zone
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cerebellar hemisphere and dentate nucleus on each side
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concerned with the planning of movement in connection with
neurons in the Rolandic region of the cerebral cortex (fine,
skilled)
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Lesions result in abnormalities of skilled voluntary movements:
hypotonia, dysarthria, dysmetria, dysdiadochokinesia, excessive
rebound, impaired check, kinetic and static tremors, pastpointing
Midline Cerebellar Function
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Observation
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Posture, head position
Gait
Eye movements
Rhomberg Test
Tests of gait- tandem, toe + heel walking, walking backward
Hop on each foot
Cerebellar Hemispheric Function
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Finger-to-nose test
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Rapidly alternating movements
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Heel-to-shin test
Cardinal Features of Cerebellar Dysfunction
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Hypotonia
Ataxia
Dysarthria
Tremor
Ocular Motor Dysfunction
Classic signs of cerebellar damage
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Depending on extent, an individual may have one symptom or a
combination
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In all cases, symptoms from unilateral damage appear on the side
ipsilateral to the injury
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Ascending spinocerebellar pathways are uncrossed and descending
corticoopontocerebellar fibers are crossed; thus motor deficits from
cerebellar damage are ipsilateral to the lesion whereas motor
deficits from damage to motor areas of the cerebral cortex are
contralateral to the lesion
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postural instability
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delayed initiation and termination of motor actions
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inability to perform continuous, repetitive movements
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errors in smoothness and direction of a movement
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lack of coordingation or synergy of movement, especially complex
movements
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lack of motor plasticity or learning
Hypotonia
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usually accompanies acute hemispheric lesions
Interestingly less often seen in chronic lesions
Ispilateral to the side of a cerebellar lesion
More noticeable in upper limbs and proximal muscles
(beware of increased tone with a cerebellar lesion—may reflect
compression of brainstem/corticospinal tracts)!!
Probably due to  fusimotor activity, secondary to cerebellar injury
(especially the dentate), with a  response to stretch in muscle
spindle afferents
Ataxia
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Defective timing of sequential contraction of agonist /antagonist
muscles
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Results in a disturbance in smooth performance of voluntary acts
(errors in rate, range, force, duration)
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Without cerebellar modulation, skilled movements originating in
cerebral cortex are inaccurate, poorly controlled
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May affect limbs, trunk, gait (depends on part of cerebellum
involved)
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usually persists despite visual cues (unlike ataxia due to posterior
column disease affecting the spinal cord)
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Asynergia= lack of synergy of various muscles while performing
complex movements ( movements are broken up into isolated,
successive parts-- decomposition of movement)
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Dysmetria= abnormal excursions in movement
Dysdiadochokinesia= impaired performance of rapidly alternating
movement
Past-pointing
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Excessive rebound when an opposed motion is suddenly released
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Cerebellar Dysarthria
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Abnormalities in articulation and prosody (together or independent)
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“scanning”, “slurring”, “staccato”, “explosive”, “hesitant”, “garbled”
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May result from a generalized hypotonia (disorder of muscle spindle
function)
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Hemisphere lesions are associated with speech disorders more
often than vermal lesions
Posterior Fossa Syndrome
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Acute, bilateral injury to both cerebellar paravermal regions,
including the dentate, may lead to transient muteness
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Seen in up to 20% of posterior fossa tumor resections in children
(“cerebellar mutism syndrome”)
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May last for several months, with severe dysarthria after return of
speech
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Cerebellar affective disorder
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Impaired executive function, personality, emotional and
behavioral changes
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Can be seen as part of the mutism syndrome
Tremor
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rhythmic, alternating, or oscillatory movements
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can be a normal exaggeration of movement, a primary disorder, or a
symptom of a cerebellar disorder or Parkinson's disease
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Diagnosis is usually clinical
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Treatment varies by etiology
Tremor- Framework/ Categories
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Trigger: Resting or action-- includes postural tremors
and intention tremors (triggered by a purposeful
movement)
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Cause: Physiologic, essential, parkinsonism, or
secondary to drugs or other disorders (including
cerebellar disorders)
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Amplitude of oscillation: Fine or coarse
Tremor- General features
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Resting tremor : maximal at rest, decreases with activity; usually a
symptom of Parkinson's disease
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Postural tremor : maximal with limb in a fixed position against
gravity; gradual onset suggests physiologic or essential tremor;
acute onset suggests toxic / metabolic disorder
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Intention tremor : maximal during movement toward a target (fingerto-nose testing) ; suggests a cerebellar disorder but may result
from other diseases (MS, Wilson’s)
Tremor- Physiologic
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Physiologic tremor: present normally -- usually so slight that it is
noticeable only under certain conditions ; predominantly postural,
fine and rapid (8 to 13 Hz)
most visible when hands are outstretched
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Amplitude may be increased (enhanced) by
 Anxiety
 Stress
 Fatigue
 Metabolic disorders (eg, hyperadrenergic states such as alcohol
or drug withdrawal or thyrotoxicosis)
 Certain drugs (eg, caffeine, other phosphodiesterase inhibitors,
β-adrenergic agonists, corticosteroids)
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Alcohol and other sedatives usually suppress it
Tremor- Essential tremor
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benign hereditary tremor, senile tremor
coarse or fine, medium frequency (4 to 8 Hz); min or absent at rest
usually bilateral
can affect the hands, head, voice
tends to increase with aging
In 50% of patients, inheritance is autosomal dominant
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may be enhanced by any factor that enhances physiologic tremor
(not always required)
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Some consider essential tremor a variant of physiologic tremor
Tremor- Cerebellar Disease
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an intention tremor; no effective drug available; physical measures
(eg, weighting the affected limbs or teaching patients to brace the
proximal limb during activity) sometimes helps
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Asterixis: not a tremor; muscle tone lapses when wrist extension is
attempted, resulting in repetitive, nonrhythmic, non-oscillatory wrist
flexion; a sign of chronic renal or liver failure (differentiate from
tremor)
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3-5 Hz
Usually bilateral
Can be a sign of hepatic encephalopathy (inability of liver to metabolize
ammonia to urea)
Patient is usually drowsy or stuporous
Oculomotor dysfunction
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Nystagmus frequently seen in cerebellar disorders
Gaze-evoked nystagmus, upbeat nystagmus, rebound nystagmus,
opticokinetic nystagmus may all be seen in midline cerebellar
lesions
Other ocular lesions seen include opsoclonus, skew deviation,
ocular bobbing
Most of the disorders giving rise to these affect brainstem structures,
too: cerebellar role in their onset not well-defined
Overall, most “cerebellar” eye signs cannot be localized to specific
areas of the cerebellum
Features to Examine
Gait
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Ataxia
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In cerebellar disease, the walk is staggering/lurching/wavering
Not benefitted by patient’s view of his surroundings
Lesion in mid-cerebellum: movements are in all directions
Lesion in lateral cerebellum: staggering/falling are toward the side of the
lesion
Somewhat steadied by standing or walking on a wide base
(ataxia secondary to vestibular disease may appear similar)
Gait
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Gait
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have patient walk across room under observation
Watch for normal posture + coordinated arm movements
ask patient to walk heel-to-toe across room, walk on toes to test
for plantar flexion weakness, and on heels to test for dorsiflexion
weakness
Abnormalities in heel to toe walking: ethanol intoxication,
weakness, poor position sense, vertigo -- exclude before poor
balance is attributed to a cerebellar lesion
elderly patients have difficulty with tandem gait (heel to toe
walking) -- general neuronal loss impairs combination of position
sense, strength, coordination
blumentandemgait
blumenTipToeGaitandHopping
impairedTandemGait.flv
CerebGait.flv
Testing of Station (equilibratory
coordination)
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Position of Feet
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Eyes open or closed
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Ataxia from spinocerebellar disease is less when the patient
stands on a broad base (feet widely apart)
Cerebellar ataxia is not improved by visual orientation; ataxia
from posterior column disease (disordered proprioception) is
worsened with the eyes closed
Direction of Falling
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Disease of lateral lobe of cerebellum causes falling to ispilateral
side
Lesions of midline/vermis cause indiscriminate falling,
depending on initial stance of the patient
blumenRhombergTest
Diadochokinesia
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Normal coordination includes ability to arrest one motor impulse and
substitute the opposite
Loss of this = dysdiadochokinesia
Characteristic of cerebellar disease
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Many simple tests for this:
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Alternating movements (pronate and supinate forearm + hand
quickly): in cerebellar disease, movements overshoot, undershoot
be irregular or inaccurate
Rapidly tap fingers on table
Open and close fists
Stewart-Holmes rebound sign
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blumenFineFingerTap.rm
blumenRapidlyAltMovements.rm
dysdiadochokinesiamovie
Dysmetria
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Finger to nose test
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With eyes open, have pt partially extend elbow and rapidly bring tip of
index finger in a wide arc to tip of his nose
In cerebellar disease, the action may have an intention tremor
With eyes closed, sense of position in the shoulder and elbow is tested
Heel to Shin test
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Pt places one heel on opposite knee and slides heel down the tibia with
foot dorsiflexed
Movement should be performed accurately
In cerebellar disease, the arc of the movement is jerky/wavering
The slide down the shin has an action tremor
blumenFingerNoseTest.rm
Coordinationwithpuppets.mp4
Cerebellarintentiontremor.mp4
Heelshintest.mp4
Heelshinabnormal.mp4
Checkreflexmovie.mp4
Checkreflexabnorvideo.mp4
Spasticspeech.flv
Cerebellar Syndromes
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In general, precise clinical localization is difficult in the cerebellum
Some syndromes can be classified anatomically:
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Rostral vermis syndrome (anterior lobe)
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Caudal vermis syndrome (flocculonodular, posterior lobe)
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Hemispheric syndrome (posterior lobe, variably anterior too)
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Pancerebellar syndrome
Cerebellar Syndromes- rostral vermis
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Wide-based stance and gait
Ataxia of gait, proportionally little ataxia on heel-shin with pt lying
down
Normal or slightly impaired arm cooordination
Infrequent hypotonia, nystagmus, dysarthria
alcoholics (restricted form of cerebellar cortical degeneration)
Cerebellar Syndromes- caudal vermis
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Axial dysequilibrium, staggering gait
Little or no limb ataxia
Sometimes spontaneous nystagmus
Rotated postures of head
Seen in diseases that damage the flocculonodular lobe (esp
medulloblastoma in children)—as tumor grows, a hemispheric
cerebellar syndrome may be superimposed
Need to also consider other signs of  ICP (obstruction of CSF)
Cerebellar Syndromes- hemispheric
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Incoordination of ipsilateral limb movements
More noticeable with fine motor skills
Incoordination affects most noticeably muscles involved in
speech and finger movements
Etiologies include infarcts, neoplasms, abscesses
Cerebellar Syndromes- pancerebellar
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Combination of all the other syndromes
Bilateral signs of cerebellar dysfunction involving trunk, limbs,
cranial musculature
Etiologies usually infectious/parainfectious processes,
hypoglycemia, paraneoplastic disorders, toxic-metabolic disorders
Cerebellum: 4th ventricle
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The fourth ventricle is ventral to the cerebellum
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Anatomically and clinically important
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Mass lesions located in the cerebellum, or swelling of the
cerebellum (eg. Edema from an infarct) can compress the 4th
ventricle and result in obstructive hydrocephalus
My patient: Tamra
• 15 yr, R-handed ♀ previously healthy from Woodstock
• 3 wk progressive gait unsteadiness, ataxia, dizziness
• 6 wk H/A, holocephalic, worse when coughing or sneezing, 5/10,
takes Advil
• 20 lbs weight loss over 3 wks
• admitted to Woodstock General
• Dx Mono, D/C home,next day H/A 10/10
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HR 76, RR 16, BP 135/76 mmHg, T-35.9
Awake, alert, oriented x3, speech OK
Pupils 4mm bilat., brisk, full EOM
Nystagmus up & lateral gaze
Bilateral papilledema
Symetrical facial features
N bulk & tone, full power arms & legs 5/5
Reflexes symmetric, Plantars equivocal
Difficulty pointing bilat., dysmetric, past pointing, heel to shin good
Broad based gait
Cerebellar dysarthria video clip
Nystagmus video clip
Finger to nose- Tamra
Heel to shin- Tamra
Lower extremity ataxia- Tamra
Upper extremity ataxia- Tamra