Cerebellar lesions commonly give rise to a disorder of speech, which may take one of two forms: either a slow, slurring dysarthria, or a scanning dysarthria with variable intonation, so-called because words are broken up into syllables, as when a line of poetry is scanned for meter. The typical cerebellar speech simulates the abnormality of limb movements in that the rhythm and amplitude of phonation and articulation are irregular, imparting a pattern that is distinguishable from spastic and extrapyramidal speech and may be so severe as to be incomprehensible. The scanning pattern of speech disorder is uniquely cerebellar; in addition to its scanning quality, speech is slow, and each syllable, after an involuntary interruption, may be uttered with less force or more force (“explosive speech”) than is natural. The scanning and slurred patterns may, of course, be combined. Urban and associates deduced from cases of cerebellar infarction that the articulatory muscles are controlled from the rostral paravermian area of the anterior lobe, and this area is affected in most cases with dysarthria.
Ocular movement may be altered as a result of cerebellar disease, specifically if vestibular connections are involved (Thach and Montgomery). Patients with cerebellar lesions are unable to hold eccentric positions of gaze, resulting in a special type of nystagmus and the need to make rapid repetitive saccades to look eccentrically (saccadic substitution). Conjugate voluntary gaze can be accomplished only by a series of jerky movements. Smooth pursuit movements are slower than normal and require that the patient make small “catch-up” saccades in an attempt to keep the moving target near the fovea. On attempted refixation to a target, the eyes overshoot the target and then oscillate through several corrective cycles until fixation is attained. It will be recognized that these nystagmoid abnormalities, as well as those of speech, resemble the abnormalities of ataxic movements of the limbs. Skew deviation (vertical displacement of one eye), vertical nystagmus, ocular flutter, and ocular myoclonus (opsoclonus) may also be the result of cerebellar disease; these abnormalities and other effects of cerebellar lesions on ocular movement are discussed in Chap. 13.
Disorders of Equilibrium and Gait
The patient with cerebellar disease has variable degrees of difficulty in standing and walking, as described more fully in Chap. 6. Standing with feet together may be impossible or maintained only briefly before the patient pitches to one side or backward. Closing the eyes may worsen this difficulty slightly. The Romberg sign (which signifies impaired proprioceptive input), however, is not dramatically evident in cerebellar disease if the patient is allowed to steady himself before closing his eyes. In walking, the patient’s steps are uneven and placement of each foot is inconsistent, resulting in unexpected lurching, sometimes most apparent during turns.
Careful clinicoanatomic correlation studies indicate that the disequilibrium syndrome with normal movements of the limbs corresponds more closely with lesions of the anterior vermis than with those of the flocculus and nodulus (essentially, the posterior vermis). This statement is based in part on the study of cerebellar degeneration in alcoholics (see Chap. 41). In such patients, the cerebellar disturbance is often limited to abnormal stance and gait and the pathologic changes are restricted to the anterior parts of the superior vermis. In more severely affected patients, who also manifest impaired coordination of the limbs, the changes are found to extend laterally from the vermis, involving the anterior portions of the anterior lobes when the legs are affected and more posterior portions of the anterior lobes when the arms are affected.