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Parts of the hypotheses of both Babinski and Holmes have been sustained by modern physiologic studies In their analysis of rapid (ballistic) movements, Hallett and colleagues have demonstrated that with cerebellar lesions, there is a prolongation of the interval between the commanded act and the onset of movement More prominently, there is a derangement of the triphasic agonistantagonist-agonist motor sequence, referred to in Chaps 3 and 4; the agonist burst may be too long or too short, or it may continue into the antagonist burst, resulting in excessive agonist-antagonist cocontraction at the onset of movement These ndings explain what has variously been described as asynergia, decomposition of movement, and dysmetria Diener and Dichgans con rmed these fundamental abnormalities in the timing and amplitude of reciprocal inhibition and of cocontraction of agonist-antagonist muscles and remarked that these were particularly evident in pluriarticular movements 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 con ned to discrete functional zones (eg, occulonodular lobe, anterior lobe), it is dif cult 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 Our own observations af rm 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), described in detail in Chap 6; (3) disorders of equilibrium and gait; and (4) diminished muscle tone, particularly with acute lesions Dysarthria, a common feature of cerebellar disease, is probably predicated on a similar incoordination of the muscles of articulation In addition, the stability of eye movements is affected, giving rise to nystagmus Extensive lesions of one cerebellar hemisphere, especially of the anterior lobe, cause hypotonia, postural abnormalities, ataxia, and sometimes mild weakness of the ipsilateral arm and leg 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 sclerotic 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, 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 Incoordination The most prominent manifestations of cerebellar disease, namely, the abnormalities of intended (volitional) movement, are classi ed under the general heading of cerebellar incoordination or ataxia Following Babinski, the terms dyssynergia, dysmetria, and dysdiadochokinesis came into common usage to.

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describe cerebellar abnormalities of movement Holmes s characterization of abnormalities in the rate, range, and force of movement is less confusing, as becomes apparent from an analysis of even simple movements These abnormalities are brought out by nger-to-nose or toe-to- nger movement, running the heel down the opposite shin, or tracing a square in the air with a hand or foot In performing these tests, the patient should be asked to move the limb to the target accurately and rapidly The speed of initiating movement is slowed somewhat in cerebellar disease In a detailed electrophysiologic analysis of this defect, 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 nger or toe approaches its target 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 Or the limb overshoots the mark (hypermetria), due to delayed activation and diminished contraction of antagonist muscles; then the error is corrected by a series of secondary movements in which the nger 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 nger as it approaches its mark tends to assume a rhythmic quality; it has traditionally been referred to as intention tremor, or ataxic tremor, but in reality re ects defective xation at the shoulder (see Chap 6) Gilman and colleagues have provided evidence that more than hypotonia is involved in the tremor of cerebellar incoordination They found that deafferentation of the forelimb of a monkey resulted in dysmetria and kinetic tremor; subsequent cerebellar ablation signi cantly increased both the dysmetria and tremor, indicating the presence of a mechanism as yet unidenti ed in addition to depression of the fusimotor efferent spindle afferent circuit All of 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 ngertip to the thumb The normal rhythm of these movements is interrupted by irregularities of force and speed This is the abnormality that Babinski called adiadochokinesis 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 In addition to intention tremor, there may be a coarse, irregular, wide-range tremor that appears whenever the patient activates limb muscles, either to sustain a posture or to effect a movement It is elicited by having the patient hold the arms out to the sides with elbows bent (wing-beating tremor) Holmes called it rubral tremor, and although the lower part of the red nucleus may be the site of the lesion, the nucleus itself is not involved in this type of tremor Instead, the tremor is due to interruption of the bers of the superior cerebellar peduncle, which traverse the nucleus Also, with certain sustained postures (eg, with arms extended and hands.

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