Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in cortical blood flow and cerebrovascular activity occurring during and after cortical spreading depression (CSD) were studied in alpha-chloralose-urethan-anesthetized cats. CSD was induced by superficial cortical pinprick, and laser-Doppler velocimetry (LDV) was used to measure cerebral blood flow (CBFLD). CSD resulted in a wave of cortical hyperemia during which there was a 215 +/- 48% peak increase in cortical blood flow that lasted for 2.7 +/- 0.4 min. This hyperemic phase was followed by prolonged cortical oligemia, with a reduction in flow of 20 +/- 4% at 1 h and 28 +/- 4% at 2 h. After CSD, cerebrovascular reactivity to the inhalation of CO2 was abolished and did not fully recover for at least 10 h. Spontaneous vasomotor activity in the cerebral microcirculation was significantly decreased after CSD, and autoregulation of cortical blood flow in response to hypotension was preserved. The abnormal cerebrovascular reactivity seen after CSD in the gyrencephalic cortex of the cat has possible significance for human migraine with aura.
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PMID:Cortical blood flow changes during spreading depression in cats. 185 35

Platelet 5-hydroxytryptamine (5-HT) uptake was measured in asymptomatic headache patients attending a specialist migraine clinic, and in hospital staff who did not suffer from regular or severe headache. Current levels of anxiety and depression were assessed in all subjects using the Hospital Anxiety and Depression (HAD) scale and their possible influence on the uptake kinetics taken into account during the analysis of results. The Michaelis-Menten constant (Km) was significantly raised in common migraine and tension headache compared with controls (p less than 0.001 and p less than 0.01, respectively), but not in classical migraine or cluster headache. The increase remained significant after adjusting for differences in age, sex, presence of anxiety or depression (HAD sub-scale score greater than or equal to 8), drug intake during the week before testing, time elapsed since last attack and time of assay (am or pm). No differences were observed between patients and controls in the maximal rate of uptake (Vmax) or platelet count, and previous reports of a reduction in Vmax in patients experiencing attack within 5 days prior to testing could not be confirmed. The cause and significance of an increased Km are not clear, but plasma factors acting as competitive inhibitors for the uptake site or an alteration in the configuration of the uptake site are possible explanations. If confirmed, the shared biochemical abnormality may suggest that common migraine and tension headache have a common pathogenesis.
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PMID:Kinetics of platelet 5-hydroxytryptamine uptake in headache patients. 188 70

Cortical spreading depression (SD) has been implicated in the pathophysiology of classical migraine headache and cerebral ischemia. A reduction in cerebral blood flow (CBF), mimicking that seen during the aura and headache phase of migraine, is typically observed following SD in the rat. This phenomenon may also play a role in potentiating ischemic brain damage. In the present study, brief cortical exposure to 1 M KCl produced a marked suppression of EEG amplitude which persisted 20 min in the rat. Upon normalization of the EEG, cortical blood flow declined 20-30% and remained low for at least 2 h. Treatment with a 1 mg/kg i.v. dose of the 21-aminosteroid antioxidant tirilazad mesylate (U-74006F), 2 min following KCl application, completely blocked the hypoperfusion while leaving the magnitude and duration of the EEG suppression and mean arterial pressure unchanged. Tirilazad mesylate is a potent inhibitor of oxygen radical-mediated lipid peroxidation both in vitro and in vivo. Thus, based on present results, an oxygen radical hypothesis is proposed to account for the SD-induced cerebral hypoperfusion.
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PMID:The 21-aminosteroid antioxidant tirilazad mesylate, U-74006F, blocks cortical hypoperfusion following spreading depression. 193 84

Previous reports have found an association between coronary vasospasm and migraine. It has been speculated that migraine and variant angina might be manifestations of a generalized vasospastic disorder. To investigate this hypothesis, 74 patients with frequent attacks of migraine were studied using 24-h continuous ambulatory electrocardiography to identify the presence of coronary vasospasm. Control groups consisted of 19 patients with tension headaches, and 38 healthy individuals. All subjects were free of heart disease. One patient in the migraine group and one patient in the control group had symptomless episodes of ST-segment depression not indicative of coronary vasospasm. Our data do not support the hypothesis that migraine and variant angina are components of a generalized vasospastic disorder.
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PMID:Lack of association of migraine with coronary vasospasm. 194 Jul 82

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.
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PMID:Neuroexcitatory plasma amino acids are elevated in migraine. 197 2

This article explores the hypothesis that migraine with aura is associated with a state of central neuronal hyperexcitability. The authors propose that this central neuronal hyperexcitability involves overactivity of the excitatory amino acids, glutamate, and possibly aspartate. Stimuli that activate the migraine attack evoke neuronal depolarization, slow depolarization shifts, and spreading suppression of spontaneous neuronal activity possible by glutamate and K+ dependent mechanisms. A low brain Mg2+ and consequent reduced gating of glutamatergic receptors may provide the link between the physiologic threshold for a migraine attack and the mechanisms of the attack itself by promoting glutamate hyperactivity, neuronal hyperexcitability, and susceptibility to glutamate-dependent spreading depression.
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PMID:The concept of migraine as a state of central neuronal hyperexcitability. 197 55

"Whole body composition" was investigated in 30 people subject to alcohol-induced migraine. The control group was 30 people matched for age, sex, height and weight, who were not subject to migraine and who consumed moderate amounts of alcohol. The following were evaluated: anthropometric data, alcohol intake in grams per day, total body water, fat-free mass, fat mass, and body mass index (kg/m2). Two methods of measurement were used: skin fold thickness evaluation, and bioelectric impedance assay (BIA). BIA is a non-invasive method based on the principle that lean tissues conduct a low frequency alternating current of electricity better than do fatty tissues. Body mass index was increased in the alcohol-induced migraine patients (p less than 0.04), as was fat mass, (p less than 0.03) as evaluated by skin fold measurements. Bioelectric impedance assay demonstrated a slight total body water increase in alcohol-induced migraine patients (p less than 0.07). Possibly, if this total body water increase was reflected at the neuronal level, the bioelectric properties of the migrainous brain may be altered, thus creating a hypothetical link with the phenomenon of spreading depression.
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PMID:Bioelectrical impedance assay (BIA) of total body composition in alcohol-induced migraine patients. Preliminary report. 201 67

Psychological factors, such as psychological stressors, personality style, conditioning, and psychodynamic issues, play a role in the etiology of chronic migraine and muscle contraction headaches. Psychiatric disorders, such as depression, anxiety, personality disorders, conversion, and hypochondriasis, may accompany and complicate headache. Psychiatric diagnosis and treatment add a useful and important dimension to the medical care of the patient. This article presented a useful conceptual model for discriminating between different kinds of psychological influencing factors and guidelines for selecting the appropriate form of psychiatric treatment.
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PMID:Psychiatric aspects of headache. 202 Feb 24

The effects of 5-HT are varied and widely distributed throughout the human body. At this time, 5-HT research is a field ripe for "plucking." Not only is there a great demand for more selective agonists and antagonists, but there is more than enough work needed in receptor binding studies to keep pharmacologists employed for years to come. The clinical benefits of 5-HT receptor pharmacology are just starting to be developed and explored. Novel treatments for hypertension, migraine headaches, anxiety, and depression using 5-HT are just the beginning. It will be exciting to see what the future holds for 5-HT clinically.
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PMID:Serotonin receptor subtypes: functional, physiological, and clinical correlates. 202 90

Studies of regional cerebral blood flow (rCBF) are rapidly increasing our understanding of migraine mechanisms. In the early phase of an attack, migraine with aura (previously classic migraine) is associated with posterior focal hypoperfusion in one hemisphere. This spreads forward, usually to involve the posterior one-third to one-half of a hemisphere. Hypoperfusion persists into the headache phase and is associated with partial or complete vasoparalysis. From patient to patient, it varies in severity, ranging from almost normal to well below the usual ischemic threshold. After 1 h to several hours, the formerly hypoperfused areas becomes hyperperfused. The headache begins while rCBF is decreased and relates topographically to the area affected by rCBF changes. There is no association with hyperperfusion, which usually begins long after headache onset and often outlasts headache. In migraine without aura, there are no focal rCBF abnormalities but a dispute as to whether flow is globally increased. For a number of reasons, pain mechanisms, however, are likely to be the same as in migraine with aura, just initiated by something else. Extracranial blood flow is unchanged during migraine attacks but the superficial temporal artery on the side of the headache is dilated and recent transcranial Doppler studies have been interesting although difficult to interpret. These results will stimulate further studies of large arteries. The migrainous aura is probably the clinical manifestation of a cortical spreading depression. The resulting ionic and neurotransmitter changes are by way of local irritation of pial perivascular nerves, the most likely mechanism of migraine headache.
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PMID:Cerebral and extracranial circulatory disturbances in migraine: pathophysiological implications. 203 98


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