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)

The incidence of the life time history of both maternal migraine and depression were assessed in children with headache, migraine, recurrent abdominal pain and abdominal migraine. An epidemiological survey of 1,104 children registered with a general practice was undertaken. The incidence of maternal migraine and depression agreed with previous estimates. Children with migraine had a greater proportion of mothers with a history of migraine than those who experienced headache alone compared with controls. The survey showed that mothers with depression predisposed their children to headache but not specifically migraine. A history of maternal depression and migraine was significantly more common and proportionately higher in children with abdominal migraine and recurrent abdominal pain.
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PMID:Does a history of maternal migraine or depression predispose children to headache and stomach-ache? 152 67

Many patients with severe migraine remain refractory to the current treatment regimens or cannot tolerate the side effects. Since current research implicates serotonin dysregulation in migraine pathogenesis, we investigated in a double blind, placebo controlled study the prophylactic effect of the serotonergic drug fluoxetine. Sixteen subjects were randomly assigned to 8 week fluoxetine treatment and 16 to the placebo group; nine subjects in each group completed the study. Migraine headache scores were obtained for two weeks prior to commencement of treatment, and then for each successive two week period. Zung depression scores were obtained before and after completion of the study. Fluoxetine caused significant reduction in headache scores starting with weeks 3-4 of treatment; there was no significant change with placebo. Depression scores did not differ between groups before treatment, and did not significantly change with either treatment. Fluoxetine appears to be a safe and effective drug for migraine prophylaxis, and deserves further therapeutic trials with larger groups for longer periods of time.
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PMID:Fluoxetine prophylaxis of migraine. 777 82

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
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PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

The possible use of impedance measurement with scalp electrodes to detect intracranial events non-invasively was investigated by measuring the localised impedance changes during cortical spreading depression (CSD) in anaesthetised rats. Impedance was measured over ipsilateral fronto-parietal cortex by a four electrode method operating at 50 kHz with electrodes spaced 0.5 mm apart. Cortical impedance increased by 39% of the resting level during CSD. With scalp electrodes placed on abraded skin, an unexpected impedance decrease of 0.8% occurred, which correlated spatially and temporally with CSD. CSD was accompanied by a small rise in temperature; when scalp temperature was held constant by warming the scalp, no impedance change greater than baseline variability (+/- 0.1% of the resting impedance level) was observed. The non-invasive detection of CSD in migraine in humans may be possible by measuring the characteristic temperature-related impedance changes with Electrical Impedance Tomography and scalp electrodes.
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PMID:Detection of cortical spreading depression in the anaesthetised rat by impedance measurement with scalp electrodes: implications for non-invasive imaging of the brain with electrical impedance tomography. 156 23

The most important symptoms caused by food additives are urticaria and angioedema, but rhinitis, asthma and gastrointestinal disturbances are also reported. Only seldom food additives have been shown to induce symptoms in other organs such central nervous system or joints and with a sparse objective evidence. In this study, we report two cases of unusual reactions to food additives (tartrazine and benzoates) involving mainly the central nervous system (headache, migraine, overactivity, concentration and learning difficulties, depression) and joints (arthralgias), confirmed with diet and double blind challenge. The possible pathogenetic mechanisms are also discussed.
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PMID:[Unusual reactions to food additives]. 157 15

The recent discovery and characterization of three new 5-HT1 receptor clones and the pharmacological characterization of one orphan receptor (dog RDC4) has revealed a surprising complexity within the 5-HT1D receptor subfamily. This receptor subfamily, which is believed to be the target of the anti-migraine drug sumatriptan and may regulate feeding behavior, anxiety, depression, cardiac function and movement, can now be approached on a molecular level. These cloning discoveries have also taught us an important general lesson about the molecular pharmacology of G protein-coupled receptor genes: species homologues of a gene (the equivalent gene in different species) may be highly homologous in amino acid sequence yet display very different pharmacological properties. Conversely, two different genes in the same species (intraspecies subtypes) that display only moderate degrees of transmembrane amino acid homology can display nearly indistinguishable pharmacological properties. In discussing the implications of these findings for both 5-HT receptors and G protein-linked receptors in general, Paul Hartig, Theresa Branchek and Richard Weinshank approach the question: why have so many receptor subtypes been preserved in the genome? In addition, controversy has been raging for several years over the classification of 5-HT1B receptors (found only in rat brain) and 5-HT1D receptors. Were they different subtypes or simply species homologues of the same receptor? Recent cloning studies have apparently complicated this issue, but the answer to the question is, in fact, becoming clearer.
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PMID:A subfamily of 5-HT1D receptor genes. 158 9

Characteristic personality profiles of patients suffering from either migraine headache (MH) or tension type headache (TTH) have been described in the light of Minnesota Multiphasic Personality Inventory (MMPI). In the present study we evaluated personality profile changes following modifications of the painful symptoms after treatment, through the administration of the MMPI to MH and TTH patients. In TTH patients with no clinical improvement the depression scale scores were higher after 6 months of treatment, whereas in MH patients similar scores were observed before and after therapy, thus suggesting a primary role of depression in the onset of pain in the latter patients. Computerized EMG recording of the neck muscle activity showed different patterns of muscle contraction in resting condition and during stress or maximal muscular activity in patients suffering from TTH as compared to MH patients and normal subjects.
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PMID:Tension type headache: a neuropsychological and neurophysiological study. 160 32

Changes in cerebral cortical perfusion (CBFLDF), local cerebral blood flow (lCBF) and local cerebral glucose utilization (lCGU) elicited by unilateral cortical spreading depression (SD) were monitored and measured in separate groups of rats anesthetized with alpha-chloralose. CBFLDF was recorded with laser Doppler flowmetry, while lCBF and lCGU were measured by the quantitative autoradiographic [14C]iodoantipyrine and [14C]-2-deoxyglucose methods, respectively. SD elicited a wave of hyperemia after a latency of 2 to 3 min followed by an oligemic phase. Ninety minutes following the onset of SD cortical (frontal, parietal and occipital) lCBF and lCGU were essentially the same as on the contralateral side and in sham-treated rats. However, alteration in the lCBF and lCGU in upper and lower brainstem persisted. The present results demonstrate, for the first time, that long-lasting cerebrovascular and metabolic alterations take place within the subcortical regions following SD. These regions provide an attractive site to integrate observations in man concerning spreading depression and the aura of migraine with the other features of the syndrome.
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PMID:Subcortical cerebral blood flow and metabolic changes elicited by cortical spreading depression in rat. 162 7

Gamma-aminobutyric acid (GABA) levels in platelets were measured in 19 patients with migraine (7 males and 12 females, average age: 36.5 years) and 27 patients with chronic tension-type headache (TH; 9 males and 18 females, average age: 48.9 years). Twenty-one normal healthy volunteers composed the control group (11 males and 10 females, average age 34.9 years). The GABA levels in platelets were determined using high performance liquid chromatography with fluorescent detection (HPLC-FC). The GABA levels in platelets were 30.8 +/- 11.7 pmol/10(9) platelets (mean +/- S.D.) in the patients with migraine, 43.1 +/- 11.8 pmol/10(9) platelets in the patients with TH and 34.7 +/- 8.1 pmol/10(9) platelets in the healthy controls. The platelet GABA levels in the patients with TH were significantly higher than in the migraine patients and the healthy controls (p less than 0.05). The possible role of GABA in headache is discussed. We consider that TH may be a state of neuronal hyperexcitability similar to migraine and that GABA in the platelets of patients during TH attacks may be elevated to counterbalance it. Alternatively, we suggest that the rise of GABA levels in platelets is related to emotional factors, such as depression, in the TH patients. Further studies must be undertaken concerning the relationship between platelet GABA levels and headache.
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PMID:Platelet gamma-aminobutyric acid levels in migraine and tension-type headache. 162 59

The drugs used in migraine therapy can be divided into two groups: agents that abort an established migraine attack and agents used prophylactically to reduce the number of migraine attacks. Both groups have drugs that are specific for migrainous headaches and that are non-specific, and are used to treat the accompanying headache (analgesics), vomiting (anti-emetics), anxiety (sedatives and anxiolytics), or depression (antidepressants). The main drugs with specific action on migraine include ergot alkaloids (ergotamine, dihydroergotamine), agonists (sumatriptan) or partial agonists (methysergide) at a specific subtype of 5-HT1-like receptors, beta-adrenoceptor antagonists (propranolol, metoprolol), calcium antagonists (flunarizine) and anti-inflammatory agents (indomethacin). The pharmacological basis of therapeutic action of several of these drugs is not well understood. In the case of the ergot alkaloids and 5-HT1-like receptor agonists, however, it is likely that the antimigraine effect is related to the potent and rather selective constriction of the large arteries and arteriovenous anastomoses in the scalp and dural regions. In addition, these drugs inhibit plasma extravasation into the dura in response to trigeminal ganglion stimulation, but it is possible that this effect is related to the selective vasoconstriction in the extracerebral vascular bed. The selectivity of the pharmacological effects of these antimigraine drugs (constriction of the extracerebral arteries and arteriovenous anastomoses, poor penetration into the central nervous system and the absence of an antinociceptive effect even after intrathecal administration) strongly suggests that excessive dilatation in the extracerebral cranial vasculature, probably initiated by a neuronal event, is an integral part of the pathophysiology of migraine.
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PMID:Pharmacology of antimigraine drugs. 164 88


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