[Catecholamine metabolism in essential tremor]

The pathogenesis of essential tremor (ET) is evidently very complicated and involves various biochemical and pathophysiological mechanisms. The pathology of cerebral adrenergic systems is attributed a high value in the development of the disease. The general catecholamine (CA) metabolic indices were investigated in 40 ET patients. CA excretion was considerably decreased, especially that of norepinephrine, while the urinary level of a CA precursor DOPA was essentially normal. The excretion of a major epinephrine and norepinephrine metabolite vanillylmandelic acid also tended to decrease. Contrarily to the CA excretion, their blood levels did not change considerably. The data are supposed to point to a reduction of the general CA body pool, especially of norepinephrine. This yields the shift of relationship between lepinephrine and norepinephrine toward the latter, that can provide another mechanism for ET. Possible deterioration of noradrenergic neurotransmission as a pathogenic factor of ET, and adrenergic receptors hypersensitivity in particular, are still pending. Major genetically predetermined biochemical defect in ET leading to impaired control of complicated mechanisms behind the regulation of synchroneous activity of spinal motor structures, is believed to be closely related to CA systems modifying ET in response to various impacts and involving the mechanisms of central action alcohol.