Clinical Abnormalities of the Cerebellum
An important feature of clinical cerebellar abnormali-ties is that destruction of small portions of the lateral cerebellar cortex seldom causes detectable abnormali-ties in motor function. In fact, several months after as much as one half of the lateral cerebellar cortex on one side of the brain has been removed, if the deep cere-bellar nuclei are not removed along with the cortex, the motor functions of the animal appear to be almost normal as long as the animal performs all movementsslowly. Thus, the remaining portions of the motorcontrol system are capable of compensating tremen-dously for loss of parts of the cerebellum.
Therefore, to cause serious and continuing dysfunc-tion of the cerebellum, the cerebellar lesion usually must involve one or more of the deep cerebellar nuclei—thedentate, interposed, or fastigial nuclei.
Dysmetria and Ataxia. Two of the most important symp-toms of cerebellar disease are dysmetria and ataxia. As pointed out previously, in the absence of the cerebel-lum, the subconscious motor control system cannot predict how far movements will go. Therefore, the movements ordinarily overshoot their intended mark; then the conscious portion of the brain overcompen-sates in the opposite direction for the succeeding com-pensatory movement.This effect is called dysmetria, and it results in uncoordinated movements that are called ataxia. Dysmetria and ataxia can also result from lesions in the spinocerebellar tracts because feedback informa-tion from the moving parts of the body to the cerebel-lum is essential for cerebellar timing of movement termination.
Past Pointing. Past pointingmeans that in the absenceof the cerebellum, a person ordinarily moves the hand or some other moving part of the body considerably beyond the point of intention. This results from the fact that normally the cerebellum initiates most of the motor signal that turns off a movement after it is begun; if the cerebellum is not available to do this, the movement ordinarily goes beyond the intended mark.
Therefore, past pointing is actually a manifestation of dysmetria.
Dysdiadochokinesia. When the motor control systemfails to predict where the different parts of the body will be at a given time, it “loses” perception of the parts during rapid motor movements. As a result, the suc-ceeding movement may begin much too early or much too late, so that no orderly “progression of movement” can occur. One can demonstrate this readily by having a patient with cerebellar damage turn one hand upward and downward at a rapid rate. The patient rapidly “loses” all perception of the instantaneous position of the hand during any portion of the movement. As a result, a series of stalled attempted but jumbled move-ments occurs instead of the normal coordinate upward and downward motions. This is called dysdiadochokine-sia.
Dysarthria. Another example in which failure of pro-gression occurs is in talking because the formation of words depends on rapid and orderly succession of indi-vidual muscle movements in the larynx, mouth, and res-piratory system. Lack of coordination among these and inability to adjust in advance either the intensity of sound or duration of each successive sound causes jumbled vocalization, with some syllables loud, some weak, some held for long intervals, some held for short intervals, and resultant speech that is often unintelligi-ble. This is called dysarthria.
Intention Tremor. When a person who has lost the cere-bellum performs a voluntary act, the movements tend to oscillate, especially when they approach the intended mark, first overshooting the mark and then vibrating back and forth several times before settling on the mark. This reaction is called an intention tremor or an action tremor, and it results from cerebellar overshoot-ing and failure of the cerebellar system to “damp” the motor movements.
Cerebellar Nystagmus. Cerebellar nystagmusis tremor ofthe eyeballs that occurs usually when one attempts to fixate the eyes on a scene to one side of the head. This off-center type of fixation results in rapid, tremulous movements of the eyes rather than steady fixation, and it is another manifestation of failure of damping by the cerebellum. It occurs especially when the flocculonodu-lar lobes of the cerebellum are damaged; in this instance it is also associated with loss of equilibrium because of dysfunction of the pathways through the flocculonodu-lar cerebellum from the semicircular ducts.
Hypotonia. Loss of the deep cerebellar nuclei, particu-larly of the dentate and interposed nuclei, causes decreased tone of the peripheral body musculature on the side of the cerebellar lesion. The hypotonia results from loss of cerebellar facilitation of the motor cortex and brain stem motor nuclei by tonic signals from the deep cerebellar nuclei.
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