The symptoms produced in animals by ablation of discrete anatomic or functional zones of the cerebellum bear only an imperfect relationship to the symptoms of cerebellar disease in humans. This is understandable for several reasons. Most of the lesions that occur in humans do not respect the boundaries established by experimental anatomists. Even with lesions that are more or less confined to discrete functional zones (e.g., flocculonodular lobe, anterior lobe), it is difficult to identify the resultant clinical syndromes with those produced by ablation of analogous zones in cats, dogs, and even monkeys, indicating that the functional organization of these parts varies from species to species.
Clinical observations affirm what was stated above—that lesions of the cerebellum in humans give rise to the following abnormalities: (1) incoordination (ataxia) of volitional movement; (2) a characteristic tremor (“intention,” or ataxic tremor, by which is meant a side-to-side oscillation as movement approaches a target), described in detail in Chap. 4; (3) disorders of equilibrium and gait; and (4) diminished muscle tone, particularly with acute lesions. (5) Dysarthria, a common feature of cerebellar disease, is probably predicated on a similar incoordination of the muscles of articulation. (6) In addition, the stability of conjugate eye movements is affected, giving rise to impaired ocular pursuit, inaccurate saccades, and pathological nystagmus.
Extensive lesions of one cerebellar hemisphere, especially of the anterior lobe, cause hypotonia, postural abnormalities, ataxia, and mild weakness of the ipsilateral arm and leg, the last of these perceived mostly by the patient. Lesions of the deep nuclei and cerebellar peduncles have the same effects as extensive hemispheral lesions. If the lesion involves a limited portion of the cerebellar cortex and subcortical white matter, there may be surprisingly little disturbance of function, or the abnormality may be greatly attenuated with the passage of time. For example, a congenital developmental defect or an early life cortical atrophy of half of the cerebellum may produce no clinical abnormalities. Lesions involving the superior cerebellar peduncle or the dentate nucleus cause the most severe and enduring cerebellar symptoms, which manifest mostly as ataxia in the ipsilateral limbs. Disorders of stance and gait depend more on vermian than on hemispheral or peduncular involvement. Damage in the inferior cerebellum causes vestibulocerebellar symptoms—namely, dizziness, vertigo, vomiting, and nystagmus—in varying proportions. These symptoms often share with disturbances of the vestibular system the feature of worsening with changes in head position.
The most prominent manifestations of cerebellar disease, the abnormalities of intended (volitional) movement, are classified under the general heading of cerebellar incoordination, or ataxia. Following Babinski, the terms dyssynergia, dysmetria, and dysdiadochokinesis came into common usage to describe cerebellar abnormalities of movement. Holmes’s characterization of abnormalities in the rate, range, and force of movement, as mentioned earlier, is less confusing, as becomes apparent from an analysis of even simple movements. These signs are brought out by standard neurologic tests, including finger-to-nose and toe-to-finger movement, running the heel down the opposite shin, or tracing a square in the air with a hand or foot. In performing these maneuvers, the patient should be asked to move the limb to the target accurately and rapidly.