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