The speed of initiating movement is slowed somewhat in cerebellar disease. In a detailed electrophysiologic analysis of this defect mentioned earlier, Hallett and colleagues noted, in both slow and fast movements, that the initial agonist burst was prolonged and the peak force of the agonist contraction was reduced. Also, there is irregularity and slowing of the movement itself, in both acceleration and deceleration. These abnormalities are particularly prominent as the finger or toe approaches its target. All the foregoing defects in volitional movement are evident in acts that require alternation or rapid change in direction of movement, such as pronation–supination of the forearm or successive touching of each fingertip to the thumb. The normal rhythm of these movements is interrupted by irregularities of force and speed. Even a simple movement may be fragmented (“decomposition” of movement), each component being effected with greater or lesser force than is required. These movement abnormalities together impart a highly characteristic clumsiness to the cerebellar syndromes, an appearance that is not simulated by the weakness of upper or lower motor neuron disorders or by diseases of the basal ganglia.
Normally, deceleration of movement is smooth and accurate, even if sharp changes in the direction of a limb are demanded, as in following a moving target. With cerebellar disease, the velocity and force of the movement are not checked in the normal manner. The excursion of the limb may be arrested prematurely, and the target is then reached by a series of jerky movements. In contrast, the limb may overshoot the mark (hypermetria) because of delayed activation and diminished contraction of antagonist muscles; then the error is corrected by a series of secondary movements in which the finger or toe sways around the target before coming to rest, or moves from side to side a few times on the target itself. This side-to-side movement of the finger as it approaches its mark tends to assume a rhythmic quality; it has traditionally been referred to as intention tremor, or ataxic tremor. The tremor is mainly perpendicular to the trajectory of movement and mostly in the horizontal plane (the reason for the latter is not known). The term “intention” as applied to cerebellar tremor, while embedded in neurologic parlance, does not fully capture the necessity for the limb to be in action rather than for the patient to “intend” a movement for the tremor to be manifest. “Action tremor,” however, has been used for an entirely different category of oscillations, as discussed in Chap. 4 so that “ataxic tremor” or “goal directed action tremor” may be preferable terms.
In addition to intention tremor, there may be a coarse, irregular, wide-range tremor that may be present whenever the patient activates limb muscles, either to sustain a posture or to effect a large amplitude proximal movement. It is traditionally elicited by having the patient hold the arms out to the sides with elbows bent (“wing-beating tremor”). Holmes called it rubral tremor; however, although the red nucleus may be the site of the lesion, the nucleus itself is not necessarily involved in this type of tremor. Instead, it is a result of interruption of the fibers of the superior cerebellar peduncle, which traverse the nucleus, for which reason it may be more properly called “cerebellar outflow tremor.” Also, with certain sustained postures (e.g., with arms extended or hands on knees), the patient with cerebellar disease may develop a rhythmic oscillation of the fingers having much the same tempo as a parkinsonian tremor. A rhythmic tremor of the head or upper trunk (3 to 4 per second) called titubation, mainly in the anteroposterior plane, often accompanies midline cerebellar disease, but may also be a manifestation of essential tremor (see further on).