The essential disturbance in cerebellar disease is dyssynergia. Normally, there is harmonious, coordinated action between the various muscles involved in a movement so that they contract with the proper force, timing, and sequence of activation to carry out the movement smoothly and accurately. Cerebellar disease impairs the normal control mechanisms that organize and regulate the contractions of the different participating muscles and muscle groups to insure smooth, properly coordinated movement. There is a lack of speed and skill in performing movements that require the coordinated activity of several groups of muscles or of several movements. The cerebellum is instrumental in timing the activation of the different muscles involved in a movement. Lack of integration of the components of the act results in decomposition of movement—the act is broken down into its component parts and carried out in a jerky, erratic, awkward, disorganized manner. The cerebellum is particularly important in coordinating multi-joint movements.

Dysmetria refers to errors in judging distance and gauging the distance, speed, power, and direction of movement. Cerebellar dysfunction leads to loss of the normal collaboration between agonist and antagonist. When reaching for an object 50 cm away, the hand shoots out 55 cm, overshooting the target (hypermetria), or fails to reach the target (hypometria). Hypermetria is more common. The movement may be carried out too slowly or too rapidly with too much or too little force. The patient with dysmetria does not make a movement along a straight line between two points, but erratically deviates from the intended track.

A disturbance in reciprocal innervation results in a loss of the ability to stop the contraction of the agonists and rapidly contract the antagonists to control and regulate movement. Impairment of the ability to carry out successive movements and to stop one act and follow it immediately by
its diametric opposite causes dysdiadochokinesia, loss of checking movements, and the rebound phenomenon. Dysdiadochokinesia (or adiadochokinesia) is a clumsy term (coined by Babinski) that means inability to make rapid repetitive or rapid alternating movements (RAMs). The patient with impaired RAMs has difficulty with such tests as patting the palm of one hand alternately with the palm and dorsum of the other hand, rapid tapping of the fingers, tapping out a complex rhythm, or tapping the foot in steady beat. Inability to rapidly reverse an action also causes impairment of the check response, producing the Holmes rebound phenomenon (see section on Impaired Check and the Rebound Phenomenon).

The most common type of cerebellar tremor is an intention (active, kinetic, or terminal) tremor that is not present at rest but becomes evident on purposeful movement. In the upper extremity, when the patient reaches to touch an object there are irregular, to-and-fro, jerky movements perpendicular to the path of movement that increase in amplitude as the hand approaches the target. A postural tremor of the outstretched limbs may also occur, without the patient reaching for a target. Cerebellar tremor often involves the proximal muscles. When severe, cerebellar tremor may involve not only the extremities, but also the head or even the entire body. Severe cerebellar tremor may at times take on an almost myoclonic character; some conditions cause both cerebellar ataxia and myoclonus. The tremors and other movements probably result from disease involving the cerebellar efferent pathways or their connections with the red nucleus and thalamus (dentorubraI and dentothalamic pathways, or superior cerebellar peduncle), and are sometimes referred to as a cerebellar outflow tremor. A rubral tremor is present at rest but worsens with action, and probably results from a lesion involving the cerebellar outflow tracts.

Hypotonia, or muscle flaccidity, with a decrease in resistance to passive movement, is often seen in cerebellar disease. Cerebellar dysfunction results in a decrease in the tonic output of the cerebellar nuclei, causing loss of cerebellar facilitation to the motor cortex. The muscles are flabby and assume unnatural attitudes; the parts of the body can be moved passively into positions of extreme flexion or extension. The stretch reflexes are normal or diminished in disease limited to the cerebellum. Occasionally, the tendon reflexes are “pendular.” Tapping the patellar tendon with the foot hanging free results in a series of to-and-fro movements of the foot and leg before the limb finally comes to rest. Pendular reflexes are caused by muscle hypotonicity and the lack of normal checking of the reflex response. The superficial reflexes are unaffected by cerebellar disease. Cerebellar disease may also cause a characteristic position of the extended hand, probably because of hypotonia. The wrist is flexed and arched dorsally, with the fingers hyperextended, and a tendency toward overpronation. The hand is similar to that seen in Sydenham chorea. A cerebellar lesion may cause a decrease in the normal pendular movement of the affected arm when walking. A decreased arm swing may also occur with extrapyramidal disorders and with mild hemiparesis. In the shoulder-shaking test, a cerebellar lesion causes an increase in the range and duration of swinging of the involved arm, although the movements may be irregular and nonrhythmic.

Cerebellar disease often affects speech. Articulation may be slow, ataxic, slurred, drawling, jerky, or explosive in type, because of dyssynergy of the muscles of phonation. A scanning type of dysarthria is particularly characteristic of cerebellar disease. The scanning speech of multiple sclerosis and the staccato speech of Friedreich ataxia are probably the result of cerebellar dysfunction.

Nystagmus and other disturbances of ocular motility may occur with lesions of the cerebellum. Nystagmus often indicates involvement of vestibulocerebellar pathways. The ocular abnormalities often result from involvement of the connections of the cerebellum with other centers rather than actual cerebellar dysfunction. Cerebellar disease may cause gaze paretic nystagmus. The patient is unable to sustain eccentric gaze and requires repeated saccades to gaze laterally. With a lesion of one hemisphere the eyes at rest may be deviated 10 degrees to 30 degrees toward the unaffected side. When the patient attempts to gaze elsewhere, the eyes saccade toward the point of fixation with slow return movements to the resting point. The movements are more marked and of greater amplitude when the patient looks toward the affected side. When a tumor of the cerebellopontine angle is present, the nystagmus is coarse on looking toward the side of the lesion and fine and rapid on gaze to the opposite side (Bruns nystagmus). Other ocular motility disturbances seen with cerebellar disease include skew deviation, ocular dysmetria, ocular flutter, opsoclonus, and saccadic intrusions. Rebound nystagmus is a type of nystagmus that may be unique to cerebellar disease; the fast component is in the direction of lateral gaze, but transiently reverses direction when the eyes come back to primary position.

Abnormalities of posture and gait with abnormal attitudes and spontaneous deviation of the head and parts of the body may be seen in cerebellar disease. In unilateral cerebellar disease there may be deviation of the head and body toward the affected side, with past pointing of the extremities toward the affected side. When standing, there is an inclination to fall, and when walking a tendency to deviate, toward the side of the lesion. The outstretched extremities deviate laterally, toward the affected side. There may be a decrease or absence of the normal pendular movement of the arm in walking. In midline, or vermis, lesions the patient may not be able to stand erect and may fall either backward or forward. The gait is staggering, reeling, or lurching in character, without laterality.