primidone, botulinum toxin
during passive movement, some authors have suggested that the postural tremor and cogwheel phenomenon have similar pathophysiologies (Fig. 3) (54).
The biochemical defect underlying either resting or postural parkinsonian tremor is unknown. Bernheimer et al. (55) showed that the severity of tremor paralleled the degree of homovanillic acid reduction in the pallidum. In contrast, bradyki-nesia correlated with dopamine depletion in the caudate nucleus. In an experimental monkey model of parkinsonian tremor, a pure lesion in the ascending dopaminer-gic nigrostriatal pathway is not sufficient to produce the alternating rest tremor (56). Experimental parkinsonian tremor requires nigrostriatal disconnection combined with a lesion involving the rubrotegmentospinal and the dentatorubrothalamic pathways. A typical PD tremor is observed in humans and animals exposed to MPTP, which presumably affects, rather selectively, the nigrostriatal dopaminergic system (57,58). However, the cerebellorubrothalamic system has not been examined in detail in this MPTP model. Furthermore, in MPTP subjects, a prominent action tremor was more typically seen than a tremor at rest.
In early studies, mechanical and optic devices were used to record tremor (59). EMG recordings and accelerometers, assisted by computer analysis, have been utilized to measure the characteristics of tremor. However, most accelerometers record tremor in a single plane. By using computed triaxial accelerometry, the distortion of the normal motion characteristics in patients with PD and ET during voluntary arm abduction-adduction movement was recorded (24). There was a good correlation between the reduction in the distortion and the clinical improvement in response to medications. However, the quantitative recordings of tremor, although accurate, are time-consuming, costly, and influenced by the emotional state of the patient. Moreover, it is questionable whether such recordings provide a reliable index of a meaningful therapeutic response.
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