Cerebellar Motor Examination

Eye Movements. Cerebellar lesions produce unsteady ocular fixation in primary position, microsaccadic oscillations, square wave jerks, ocular flutter, ocular bobbing, and opsoclonus. Pursuit eye movements show saccadic intrusions—jerkiness following a moving target. Volitional gaze (saccades) is hypermetric (overshoot) or hypometric (undershoot/catch-up). Gaze-evoked, direction-beating nystagmus has a fast phase in the direction of eccentric gaze and slow phase in the opposite direction. Downbeat nystagmus in primary gaze points to lesions of the cervicomedullary junction, upbeat nystagmus to midline lesions or drug toxicity.

The vestibulo-ocular reflex (VOR) maintains visualized image stabilization on the retina during head movement. With passive trunk and head rotation while focusing on his or her own hand, the patient’s eyes should not move relative to the head. Failure of this VOR cancellation from lesions of the vestibulocerebellum manifests as saccadic eye movements.

Slowing of eye movements leading to ophthalmoplegia occurs in spinocerebellar ataxias and mitochondrial disorders. Patients with oculomotor apraxia cannot direct gaze voluntarily and perform head thrusts to initiate these movements.

Speech/Swallowing. Cerebellar dysarthria is described as “scanning speech.” Syllables are poorly articulated, cadence is slowed and irregular, and rapid or alternating buccal, palatal, and lingual consonants are degraded. Dysarthria is compounded by deficient volume control. Ataxic respiration affects quality of speech. Impaired control of muscles of deglutition leads to dysphagia and aspiration risk.

Motor Control. Resting tone in pure cerebellar disease is generally decreased, or hypotonic. There may be a spastic catch or frank spasticity when spinal cord pathology is also present in some inherited ataxic disorders. Cerebellar lesions do not produce weakness, but there may be slowed initiation and generation of force. Truncal ataxia occurs with midline lesions, including titubation, that is, oscillations of the head and trunk. The patient has a widened stance and is unable to stand in tandem position or on one foot. Cerebellar ataxic gait is staggering, uneven, irregular, and veers from side to side. Unilateral lesions cause stumbling toward the affected side.

Coordination of Arms and Legs. Dysmetria (Greek dys, and metron [measure]) is the disordered ability to regulate, judge, and control behavior, both with motor and cognitive domains (see Plate 8-15). The cerebellar motor syndrome causes difficulty judging distances, trajectory of intended movements, and force required for movements. Compound movements (across more than one joint) are particularly affected. Visual guidance improves outcome minimally.

Postural tremor is assessed with arms extended in pronated position. Rebound is tested by the examiner displacing the arm downward, observing for overshoot above the starting point. Dysmetria characteristics include end-point tremor, overshooting targets (hypermetria) or undershooting (hypometria), and oscillation at the elbow. These are assessed with finger-to-nose testing; the patient brings the index finger to his/her nose and then to the examiner’s finger held steady at arm’s length. Tremor increases with proximity to the target; tremor direction is generally perpendicular to direction of movement. The finger chase/mirror test measures overshoot/undershoot. The patient points to the examiner’s finger held at arm’s length, following his/her sequential moves horizontally and vertically. Dysdiadochokinesia is degradation of rapid alternating movements, tested by forearm pronation/supination. Tapping the index finger on the crease of the thumb assesses fine motor control. Dysrhythmia is an inability to generate normal rhythms, assessed by rapidly tapping the hand on a surface or the heel on the ground.

The heel-to-shin test, performed with the patient supine, assesses leg coordination. The heel is placed on the opposite knee and moved down the shin. In wheelchair-bound patients, the heel is brought to the knee of the opposite leg held parallel to the ground. Proximal overshoot occurs as the heel is placed on the knee, and tremor occurs as the heel is maintained in that position. Slowing, jerking, or side-to-side movements are noted as the heel moves down the shin. In the draw-a-circle test, the supine patient traces a circle in the air; decomposition manifests as irregular or chaotic motions.

Cerebellar tremor is large amplitude, 2 to 3 Hz, and may involve many body parts. Rubral tremor from red nucleus lesions and its connections involves multiple joints, direction changes, and is frequently rotatory. Palatal tremor is slow and semirhythmic, resulting from Guillain-Mollaret myoclonic triangle lesions of this neuronal brainstem/cerebellum network (dentate nucleus to red nucleus and inferior olivary nucleus).

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