To investigate systemic serotonin (5-HT) metabolism in migraine, we determined platelet and platelet-free plasma concentrations of 5-HT, its precursors tryptophan and 5-hydroxytryptophan, and its main metabolite 5-hydroxyindoleacetic acid (5-HIAA), as well as the activities of the platelet enzymes monoamine oxidase and phenolsulfotransferase in classic and common migraineurs. Between attacks, migraineurs had lower plasma 5-HT and higher 5-HIAA levels than did healthy controls and patients with tension headache. During migraine attacks, plasma 5-HT levels were substantially higher than during attack-free periods, while 5-HIAA concentrations and platelet enzyme activities were lower. Platelet 5-HT was reduced only during common, but not classic, migraine attacks. We hypothesize that systemic 5-HT metabolism is enhanced in migraineurs during headache-free periods and transiently decreases during attacks, presumably due to a fall in enzymatic degradation. Furthermore, platelet behavior differs during migraine attacks with and without aura, and release of platelet 5-HT cannot (exclusively) be held accountable for the rise of plasma 5-HT during migraine attacks.

To investigate the role of glutamic (Glu) and aspartic acid (Asp) in migraine, we measured the plasma amino acids in migraine patients with and without aura, between and during attacks, and compared the profiles with the plasma amino acid profiles of tension headache patients and healthy controls. Between attacks, migraineurs (notably with aura) had substantially higher plasma Glu and Asp levels than did controls and tension headache patients. In addition, patients with migraine without aura showed low plasma histidine levels. During migraine attacks, Glu (and to a lesser extent Asp) levels were even further increased. The results suggest a defective cellular reuptake mechanism for Glu and Asp in migraineurs, and we hypothesize a similar defect at the neuronal/glial cell level, predisposing the brain of migraineurs to develop spreading depression.

The age at onset and duration of illness were studied in patients with Huntington's disease in the Leiden Roster which at 1 July 1990 contained 2787 patients. Of 1106 patients, 800 deceased and 306 alive, the age at onset was known. The median duration was 16-2 (range 2-45) years. In contrast to the current opinion, the median duration was independent of the age of onset. The median duration in juvenile Huntington's disease was 17'1 years, which is much longer than reported in the literature, and comparable with the categories for the age of onset of 20-34 and 35-49 years. Only in the group where onset was over 50 years of age was the median duration somewhat shorter (15.6 years), which can be ascribed to unrelated causes of death. As age of onset and duration of illness are not related, at least two mechanisms to determine the clinical course have to be postulated: one for age of onset and another for duration of illness. Duration was shorter for males, especially for those with an affected father. ( Neurol Neurosurg Psychiatry 1993;56:98-100)

We analysed the clinical, imaging, electrophysiological, laboratory findings, course and prognostic factors in 31 patients with acute transverse myelitis (20 men and 11 women; mean age, 30 years; range, 18-51 years). All patients were assessed for maximal clinical deficit 'deficit score'; pattern-shift visual, auditory and somatosensory evoked potentials were measured, CSF was examined, and neuroimaging of the spinal cord and brain (MRI or CT myelography) was carried out. The myelitis was preceded by febrile illness in 25 (81%) of the patients. The site of the lesion was cervical in 11 (36%), upper thoracic in two (6%), lower thoracic in 16 (52%). MRI of the spinal cord was abnormal in 10 out of the 20 patients examined (50%); in the remaining 11 patients, only CT was carried out and it was normal in all of them. Somatosensory evoked potentials were abnormal in 19 (61%), while pattern-shift visual and brainstem auditory evoked potentials were normal in all patients. CSF was abnormal in 94% of patients with pleocytosis, increased protein or both. Eighteen patients (58%) had good outcome. All patients had monophasic illness. Three variables have emerged as being associated with significant worsening of the outcome: (i) abnormal somatosensory evoked potentials; (ii) abnormal imaging and (iii) high 'deficit score' at onset. Acute transverse myelitis affects a complete segment of the spinal cord, is monophasic and represents a localized form of postinfectious acute encephalomyelitis.

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