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George E. Carvell, PhD, PT   University of Pittsburgh
A classical picture of cerebellar dysfunction comes from the study of head wounds of soldiers injured in WWI. Cerebellar lesion signs and symptoms were systematically documented by Gordon Holmes, an Irish Neurosurgeon in the British Armed Forces. G. Holmes used observation, and simple instrumentation to document the acute and subacute effects of posterior fossa lesions that involved the cerebellum. While some of the details have been questioned by more recent studies that precisely localize the lesion, there is general agreement for the broad strokes of Holmes portrait of cerebellar deficits. The following is a list that approximates G. Holmes’ list from the early 1900s (see G. Holmes, The Cerebellum of Man (Hughling-Jackson Lecture), Brain  62:1-30, 1939.) Collectively, the deficits are called cerebellar ataxia. The location of the lesion determines the site of the deficits. A lesion of the midline produces (bilateral) truncal ataxia and typically includes vestibular and eye movement defects. If the anterior lobe is involved an ataxic gait is obvious. A lesion of the paramedian cerebellum produces an ipsilateral limb ataxia. A dysarthric speech pattern (scanning speech) may develop with a bilateral lesion. A lesion restricted to the most lateral portion of the cerebellar hemisphere in the posterior lobe may produce few typical cerebellar signs but does result in a deterioration of skilled movements. These deficits are obvious to the subject if not to the clinician. Often the screening clinical exam uses tests that are insensitive to the more subtle clumsiness recognized by the subject. The skilled actor must now slow down and consciously attend to formerly automatic tasks as errors creep into performance. Holmes and more recent investigators point out that if the lesion is restricted superficially to the cerebellar cortex one can expect greater recovery than if the lesion includes the deep cerebellar nuclei. See W. T. Thach, Cerebellar Ataxia. IN: Encyclopedia for Neuroscience, G. Adelman (ed). Boston: Birkhauser, pp. 83-86, 1987.
•  Delays in initiation of movement (slow reaction time) and delays in termination of movements (rebound test)
•  Delays in rapidly alternating movements (dysdiadochokinesia)
•  Movement errors: direction, velocity and range (dysmetria)
•  Errors in Joint Synergy (dyssynergia)
•  Hypotonia (pendular deep tendon reflex) and asthenia (functional weakness despite normal strength using manual muscle test)
•  Intention tremor (~ 3-5 Hz)