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PATHOGENESIS OF VASCULAR HEADACHE OF THE MIGRAINOUS TYPE: THE ROLE OF IMPAIRED CENTRAL INHIBITION

O. Appenzeller
Published 1975 · Medicine

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5-HT HAS BEEN demonstrated in brain.1 The functional role of 5-HT in the central nervous system is not entirely clear, but abnormalities of brain 5-HT metabolism have been postulated in some neurologic disorders. 5-HT levels are decreased in the brain of patients with Parkinson's disease but the administration of a 5-HT precursor L-5-hydroxytryptophan (L-5HTP) to patients with Parkinsonism does not improve their clinical state. Defects in brain 5-HT metabolism have also been postulated in Huntington's chorea and Down's syndrome and in these disorders the administration of L-5HTP is also ineffective.2,3 L-5HTP, improves however post-anoxic myoclonic jerks.4 In animals the injection of L-5HTP has produced brief repetitive movements reminiscent of myoclonus. L-5HTP has been found effective recently in the treatment of intention myoclonus resulting from cerebral anoxia when given with a decarboxylase inhibitor.5 In patients with intention myoclonus the concentration of CSF 5-hydroxyindoleacetic acid (5-HIAA) a metabolite of 5-HT was found to be low and this was increased by the administration of L-5HTP. This increase in CSF 5-HIAA concentration coincided with marked clinical improvement. These observations suggest that in post-anoxic intention myoclonus, there might be a deficiency of brain 5-HT. It has been proposed that myoclonus is a release phenomenon which arises from an irritable focus of discharge because of removal of higher center control.6 The therapeutic effect of the postulated elevation of brain 5-HT by L-5HTP in patients with intention myoclonus has been attributed to a suggested central inhibitory synaptic neurotransmitter activity of 5-HT. The absence of central inhibition due to impaired 5-HT function causes intention myoclonus in response to lesions of the central nervous system.
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