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At the turn of the last century, Flourens and Luciani in animals and Babinski and Holmes in humans described behavioral deficits caused by focal cerebellar lesions, and they speculated about the causal mechanism. Perhaps most influential were the studies of Gordon Holmes, who meticulously documented the movement deficits associated with cerebellar gunshot wounds in World War I.1,2 He insisted that these deficits may be attributed to cerebellar disease only in patients who have normal strength and somesthesis. Yet even he accepted that weakness/“asthenia” may sometimes occur transiently and acutely.
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Ataxia is a condition that involves lack of coordination between movements of body parts. The term is often used in referelnce to gait or movement of a specific body part, as in “ataxic arm movements.”
Dysmetria is an inability to make a movement of the appropriate distance. Hypometria is undershooting a target, and hypermetria is overshooting a target. Patients with cerebellar damage tend to make hypermetric movements when they move rapidly and hypo metric movements when they move more slowly and wish to be accurate.
Dysdiadochokinesia is an inability to make rapidly alternating movements of a limb. It appears to reflect abnormal agonist-antagonist control.
Asynergia is an inability to combine the movements of individual limb segments into a coordinated, multisegmental movement.
Hypotonia is an abnormally decreased muscle tone. It is manifest as a decreased resistance to passive movement, so that a limb swings freely upon external perturbation. Hypotonia often limited to the acute phase of cerebellar disease.
Nystagmus is an involuntary and rhythmic eye movement that usually consists of a slow and a fast phase. In a unilateral cerebellar lesion, the fast phase of nystagmus is toward the side of the lesion.
Action tremor, or intention tremor, is an involuntary oscillation that occurs during limb movement and disappears when the limb is at rest. Cerebellar action tremor is generally of high amplitude and low frequency (3–5 Hz). Titubation is a tremor of the entire trunk during stance and gait. Lesions of cerebellar target structures (e.g., the red nucleus and the thalamus) often result in cerebellar outflow tremor, or postural tremor. Most prominent when a limb is actively held in a static posture, postural tremor attenuates during limb movement and disappears when the limb is at rest.
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As to the mechanism for these deficits, both Luciani and Holmes ascribed to a theory of deficient cerebellar tonic excitatory reinforcement of targets in spinal cord, brain stem, and (via thalamus) cerebral cortex. This thinking was followed by Derek Denny-Brown, and in turn by Sid Gilman.3 In this view, the signature clinical feature is hypotonia, which is fundamental to all the other deficits.4 Nonetheless, all of the aforementioned accepted that, given time, even hypotonia may di-minish. This in turn was interpreted as an indication that “cerebellar deficits are compensated for, to a considerable extent, by other structures in the brain if sufficient time is given.5
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