Neurology
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Changes in estrogen levels at menarche, menstruation, pregnancy, and menopause may trigger or change the prevalence of migraine. The fall in estrogen that occurs with menstruation is the trigger for menstrual migraine, whereas the sustained high estrogen levels during pregnancy frequently result in headache relief. Estrogen produces changes in prostaglandins, hypothalmic opioids, and prolactin secretion, which may in part account for genesis of headache. The treatment of menstrual migraine and migraine associated with menopause and the use of oral contraceptives is discussed, focusing on standard headache treatment and hormonal manipulation.
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Recent evidence suggests that migraine may not be due to vasoconstriction followed by reactive vasodilation, and tension-type headache may not be due to excess muscle contraction. The prodromes of migraine may have a hypothalamic origin, and the aura and changes in cognition may have a cortical neuronal origin. The pain of migraine and tension-type headache may be generated centrally or enhanced or generated by neurogenic inflammation. Drugs used to treat headache frequently interact with serotonin receptor subtypes: abortive drugs at the 5-HT1 receptor and preventive drugs at the 5-HT2 receptor.
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Clinical Trial Controlled Clinical Trial
Deprenyl effects on levodopa pharmacodynamics, mood, and free radical scavenging.
Clinical evidence suggests that deprenyl may slow progression of Parkinson's disease, although mechanisms underlying this putative neuroprotective action remain poorly understood. To address this issue, we studied deprenyl in 12 parkinsonian patients using a single-blind, placebo-controlled, crossover design. After 1 month, deprenyl (10 mg/d) decreased the optimal levodopa requirement by 24% (oral) and 16% (intravenous). ⋯ There was no change in activities of circulating glutathione peroxidase, glutathione reductase, glutathione transferase, superoxide dismutase, and catalase, nor in levels of lipid peroxide and vitamin E. Deprenyl also failed to modify CSF levels of total glutathione and activities of glutathione peroxidase or superoxide dismutase. These effects on levodopa pharmacodynamics and mood complicate the interpretation of available investigations of deprenyl's neuroprotective action and increase the risk of adverse effects of levodopa.
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Ornithine transcarbamylase is a mitochondrial urea cycle enzyme. Women with heterozygous ornithine transcarbamylase deficiency may have no symptoms or have episodic, symptomatic hyperammonemia, which can be fatal. ⋯ Symptomatic hyperammonemia during valproate therapy may indicate ornithine transcarbamylase deficiency. Since valproate inhibits ureagenesis and can be toxic to mitochondria, it should be used extremely cautiously, or not at all, in ornithine transcarbamylase-deficient patients.
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Case Reports
Spontaneous intracranial hypotension: report of two cases and review of the literature.
We report two patients with spontaneous intracranial hypotension. In addition to the cardinal features of a postural headache and a low CSF pressure, the patients also had subdural fluid collections demonstrated by head MRI. In both patients, radionuclide cisternography revealed a CSF leak along the spinal axis and rapid accumulation of radioisotope in the bladder. ⋯ Associated symptoms, including tinnitus and vertigo, and subdural fluid collections are presumably from hydrostatic changes among intracranial fluid compartments that occur at low CSF pressures. Methods of treatment are identical to those for post-dural puncture headaches. Epidural blood patches and epidural saline infusions have rapidly ameliorated the symptoms of spontaneous intracranial hypotension.