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The current view of drug induced tremors in general is that an increase in the gain of the muscle receptors and spinal reflex loops leads to an enhancement of the oscillations in peripheral physiological tremor. This has been studied, for instance, for [beta]-adrenergic agents 1 2 and thyroid hormones. 3 However, many drugs that can induce tremor mainly act within the CNS. One example of such a drug is amitriptyline, 4 5 which can cause a sometimes disabling postural tremor of the hands when used as an antidepressant drug or analgesic. Although this is a well known clinical phenomenon 4-7 its physiological basis has never been studied. Although there are also peripheral side effects 8 it cannot be inferred that the tremor found under amitriptyline shares the same peripheral mechanisms with the other so far described drug induced postural tremors. A second well established component of physiological tremor which is independent of the periphery and peripheral reflex loops 9 has been termed "central" and was postulated to arise from an oscillator within the CNS. 10 11 It seems plausible to hypothesise an enhancement of this central component as the mechanism of postural tremors occurring under centrally acting drugs such as amitriptyline. However, amitriptyline induced tremor has never been analysed physiologically and it has never been shown, so far, that the central component of physiological tremor can be enhanced by drugs at all. We used accelerometry and EMG before and after amitriptyline intake to characterise this tremor and to define its relation to normal physiological tremor. It will be shown for the first time that in parallel to the increase in tremor amplitude a synchronisation of motor units between different muscles in the 7-15 Hz band develops indicating an enhancement of the common central rhythmic input that is the central component of physiological tremor.
Preliminary results of this study have been published in abstract form. 12
Methods
PATIENTS
Fifteen patients (six male, nine female) were analysed before amitriptyline intake (T0), 1 week after the beginning of amitriptyline treatment (T1), and after the individually effective dose was reached (T2). In one of the patients the final dosage was reached already at T1 so the analysis at T2 was not performed. Fourteen of the patients were treated for...