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The Cerebellum
Clinical Examination
Objectives
To be knowledgeable about the aspects of the neurological examination pertaining to the cerebellum
To understand how to localize lesions within the cerebellum on the basis of clinical findings
To develop a framework about the presentation of nervous system illness
Cerebellar Examination
Midline cerebellar function
Cerebellar hemispheric function
Clinical localization in the cerebellum
For purpose of localization, cerebellum can be viewed as a saggitally-oriented structure containing 3 zones on each side:
Midline Intermediate Lateral
Midline zone
Consists of the anterior and posterior parts of the vermis, fastigial nucleus and associated input and output projections
concerned with posture, locomotion, position of head relative to trunk, control of EOM’s
Cerebellar signs resulting from midline cerebellar disease disorders of stance/gait, truncal postural disturbances, rotated
postures of the head, disturbances of eye movements
Intermediate zone
Consists of paravermal region of cerebellum and interposed nuclei (emboliform, globose)
concerned with control of velocity, force and pattern of muscle activity
Clinical disorders related to disease of this zone not clearly delineated
Lateral zone
cerebellar hemisphere and dentate nucleus on each side
concerned with the planning of movement in connection with neurons in the Rolandic region of the cerebral cortex (fine, skilled)
Lesions result in abnormalities of skilled voluntary movements: hypotonia, dysarthria, dysmetria, dysdiadochokinesia, excessive rebound, impaired check, kinetic and static tremors, past-pointing
Midline Cerebellar Function
Observation
Posture, head position Gait Eye movements
Rhomberg Test Tests of gait- tandem, toe + heel walking, walking backward Hop on each foot
Cerebellar Hemispheric Function
Finger-to-nose test
Rapidly alternating movements
Heel-to-shin test
Cardinal Features of Cerebellar Dysfunction
Hypotonia Ataxia Dysarthria Tremor Ocular Motor Dysfunction
Classic signs of cerebellar damage
Depending on extent, an individual may have one symptom or a combination
In all cases, symptoms from unilateral damage appear on the side ipsilateral to the injury
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
postural instability
delayed initiation and termination of motor actions
inability to perform continuous, repetitive movements
errors in smoothness and direction of a movement
lack of coordingation or synergy of movement, especially complex movements
lack of motor plasticity or learning
Hypotonia
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
Defective timing of sequential contraction of agonist /antagonist muscles
Results in a disturbance in smooth performance of voluntary acts (errors in rate, range, force, duration)
Without cerebellar modulation, skilled movements originating in cerebral cortex are inaccurate, poorly controlled
May affect limbs, trunk, gait (depends on part of cerebellum involved)
usually persists despite visual cues (unlike ataxia due to posterior column disease affecting the spinal cord)
Asynergia= lack of synergy of various muscles while performing complex movements ( movements are broken up into isolated, successive parts-- decomposition of movement)
Dysmetria= abnormal excursions in movement Dysdiadochokinesia= impaired performance of rapidly alternating
movement Past-pointing
Excessive rebound when an opposed motion is suddenly released
Cerebellar Dysarthria
Abnormalities in articulation and prosody (together or independent)
“scanning”, “slurring”, “staccato”, “explosive”, “hesitant”, “garbled”
May result from a generalized hypotonia (disorder of muscle spindle function)
Hemisphere lesions are associated with speech disorders more often than vermal lesions
Posterior Fossa Syndrome
Acute, bilateral injury to both cerebellar paravermal regions, including the dentate, may lead to transient muteness
Seen in up to 20% of posterior fossa tumor resections in children (“cerebellar mutism syndrome”)
May last for several months, with severe dysarthria after return of speech
Cerebellar affective disorder
Impaired executive function, personality, emotional and behavioral changes
Can be seen as part of the mutism syndrome
Tremor
rhythmic, alternating, or oscillatory movements
can be a normal exaggeration of movement, a primary disorder, or a symptom of a cerebellar disorder or Parkinson's disease
Diagnosis is usually clinical
Treatment varies by etiology
Tremor- Framework/ Categories
Trigger: Resting or action-- includes postural tremors and intention tremors (triggered by a purposeful movement)
Cause: Physiologic, essential, parkinsonism, or secondary to drugs or other disorders (including cerebellar disorders)
Amplitude of oscillation: Fine or coarse
Tremor- General features
Resting tremor : maximal at rest, decreases with activity; usually a symptom of Parkinson's disease
Postural tremor : maximal with limb in a fixed position against gravity; gradual onset suggests physiologic or essential tremor; acute onset suggests toxic / metabolic disorder
Intention tremor : maximal during movement toward a target (finger-to-nose testing) ; suggests a cerebellar disorder but may result from other diseases (MS, Wilson’s)
Tremor- Physiologic
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
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) Alcohol and other sedatives usually suppress it
Tremor- Essential tremor
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
may be enhanced by any factor that enhances physiologic tremor (not always required)
Some consider essential tremor a variant of physiologic tremor
Tremor- Cerebellar Disease
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
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)
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
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
Ataxia 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
Gait 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)
Position of Feet Ataxia from spinocerebellar disease is less when the patient
stands on a broad base (feet widely apart)
Eyes open or closed Cerebellar ataxia is not improved by visual orientation; ataxia
from posterior column disease (disordered proprioception) is worsened with the eyes closed
Direction of Falling 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
Normal coordination includes ability to arrest one motor impulse and substitute the opposite
Loss of this = dysdiadochokinesia Characteristic of cerebellar disease
Many simple tests for this:
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
blumenFineFingerTap.rm
blumenRapidlyAltMovements.rm
dysdiadochokinesiamovie
Dysmetria
Finger to nose test 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 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
In general, precise clinical localization is difficult in the cerebellum Some syndromes can be classified anatomically:
Rostral vermis syndrome (anterior lobe)
Caudal vermis syndrome (flocculonodular, posterior lobe)
Hemispheric syndrome (posterior lobe, variably anterior too)
Pancerebellar syndrome
Cerebellar Syndromes- rostral vermis
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
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
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
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
The fourth ventricle is ventral to the cerebellum
Anatomically and clinically important
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 Woodstock15 yr, R-handed ♀ previously healthy from Woodstock
• 3 wk progressive gait unsteadiness, ataxia, dizziness3 wk progressive gait unsteadiness, ataxia, dizziness
• 6 wk H/A, holocephalic, worse when coughing or sneezing, 5/10, 6 wk H/A, holocephalic, worse when coughing or sneezing, 5/10, takes Adviltakes Advil
• 20 lbs weight loss over 3 wks20 lbs weight loss over 3 wks
• admitted to Woodstock Generaladmitted to Woodstock General
• Dx Mono, D/C home,next day H/A 10/10Dx Mono, D/C home,next day H/A 10/10
HR 76, RR 16, BP 135/76 mmHg, T-35.9HR 76, RR 16, BP 135/76 mmHg, T-35.9 Awake, alert, oriented x3, speech OKAwake, alert, oriented x3, speech OK Pupils 4mm bilat., brisk, full EOMPupils 4mm bilat., brisk, full EOM Nystagmus up & lateral gazeNystagmus up & lateral gaze Bilateral papilledemaBilateral papilledema Symetrical facial featuresSymetrical facial features N bulk & tone, full power arms & legs 5/5N bulk & tone, full power arms & legs 5/5 Reflexes symmetric, Plantars equivocalReflexes symmetric, Plantars equivocal Difficulty pointing bilat., dysmetric, past pointing, heel to shin goodDifficulty pointing bilat., dysmetric, past pointing, heel to shin good Broad based gaitBroad 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