Abstract
This paper defines the nature of parkinsonian tremor, illustrates its relationship to cerebellar intention tremor, and demonstrates a cerebellar mechanism in the production of the so-called resting tremor of parkinsonism. Actually the tremor of parktasonism does not occur at absolute rest but is a postural tremor superimposed upon tonically contracted muscles. Cerebellar tremor does not require active motion or intention for its production but is initiated and maintained by tonic postural muscular contraction. Thus, both are postural tremors. Therefore, it was hypothesized that 5-per-sec. "resting" tremor could be produced by superimposing excessive gamma motoneuron drive in muscles clinically at rest in patients known to have brachium conjunctivum lesions. Such patients ordinarily demonstrated muscular hypotonia and absence of tremor at rest. By means of the Jendrassik method and other maneuvers which excite gamma motoneuron drive in resting muscles, 5-per-sec. postural tremor was produced in patients with dentatofugal pathology. This postural tremor was indistinguishable from parkinsonian tremor. A conflict of abnormal pallidothalamic sensory communication, which is ordinarily productive of excessive muscular tone, and abnormal cerebellothalamic sensory communication, which singly would result in decreased muscular tone, can produce parkinsonian tremor. The thalamic lesion which denies this abnormal sensory communication access to the cerebral cortex destroys the tremorogenic mechanism and abolishes tremor. The site of tremorogenesis is within that portion of ventrolateral thalamus in which the dentatofugal and rubrofugal pathways terminate.