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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although decreased CBF has now been reported during the prodrome of migraine, the cause of the decreased flow is still unknown. It is particularly unclear whether these phenomena are related to vasospasm and "steal" between the extracranial and intracranial circulation or to the spreading depression of Leao and the accompanying metabolic depression. In the present paper, metabolic changes in the brain during ischemia and reperfusion are reviewed and compared with CNS biochemical changes during migraine attack. In addition, the technique of Topical Magnetic Resonance (TMR) as applied to the in vivo study of energy phosphate metabolism in extracranial tissues and brain is described and the potential of this technique to evaluate shifts in energy metabolism and pH in stroke and migraine is discussed.
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PMID:Biochemical effects of cerebral ischemia: relevance to migraine. 286 8

There are some evidences to propose blood platelets as a model of bioaminergic neurons. Similarities between platelets and neurons are particularly important with respect to serotonin metabolism but now it is possible to extend this model to other neurotransmitters such as dopamine, GABA, glutamate... The reason for these similarities may be due to the common embryonic origin of these two very different cell types. Some changes of platelet functions are observed in psychiatric syndromes. For example: serotonin uptake, bioamine storage, enzymatic activities are modified in different types of depression and schizophrenia, infantile autism, neurologic diseases (migraine, chorea, Down syndrom). Furthermore, psychotropic drugs also alter the platelet functions. Recently, the discovery of neuro-endocrine disorders in psychiatric diseases has led to the proposal of platelets as a model in neuro-endocrinology. Some arguments can be developed to support this hypothesis. In biological psychiatry, the platelet model seems actually useful essentially in the classification of psychiatric diseases, the management of treatments and the study of new psychotropic drugs. However methodologic difficulties still presently limit the development of this model.
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PMID:[Blood platelets: neuronal model in psychiatric disorders]. 286 6

Spreading depression (SD) is a severe but transient disruption of neural activity in the brain, which spreads like waves in a pond in which a stone has been cast. It propagates to normal tissues and is accompanied by flux of Na+, Ca++, and Cl- ions into the cells, resulting in a brief burst of action potentials followed by electrical silence. Its rate of spread correlates almost exactly with the observed spread of the aura of classical migraine. It is accompanied in animal experiments by changes in regional cerebral blood flow which closely simulate changes observed in man during the migraine aura. There are serious difficulties in extrapolating from SD in animals to migraine in man, but the possibility of SD as the initiating event accords with the notion of migraine as a cerebral (neural) disorder and encourages further investigation in man.
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PMID:Is migraine explained by Leao's spreading depression? 286 94

Spreading depression is a reversible response of brain tissue to a local insult. It has been postulated to be the physiological substrate for the aura phase of classic migraine. The properties and mechanisms of spreading depression were studied in the parietal neocortex of the alfentanil-anesthesized rat, by using a cup electrode that provided close control of the electrical stimulus while allowing specific ion (K+) and potential recordings to be made directly beneath the cathode, the region of origin of the stimulus-induced spreading depression. Cathodal stimulation caused the extracellular K+ concentration to rise, and spreading depressions were observed when this concentration exceeded 8-12 mM in the upper 100-200 microns of cortex. In some experiments extracellular [K+] continued to increase for 5-10 sec after termination of the stimulus, without detectable after-discharge in the potential record, before subsiding. While spreading depression could easily be induced by pressure on the cortex, local damage incidental to opening the dura rarely induced spreading depression. This suggests that a local (1-mm2) neurovascular injury is not likely to induce spreading depression--at least in normal cortex--and so is probably not the source of the spreading depression postulated to generate the aura of classic migraine. Mechanisms of spreading depression, and drugs that influence spreading depression, are reviewed, and possible uses of spreading depression in the pharmacology of the central nervous system are considered.
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PMID:Spreading depression and central nervous system pharmacology. 289 9

Although therapeutic responsiveness to tricyclic antidepressants has been primarily associated with the affective disorders, clinical investigations in the last decade have suggested that non-affective disorders such as panic disorder, obsessive-compulsive disorder, anxiety disorder, bulimia, enuresis, migraine, and the chronic pain syndrome may also respond to tricyclics and other antidepressants. This therapeutic responsiveness may sometimes be related to improvement in secondary depressive symptoms, but may also clearly occur in the absence of secondary depression; in particular, improvement in the core symptoms of at least some of these disorders may occur without a change in mood. Furthermore, many patients with these disorders display psychobiologic abnormalities that show many similarities, but also some differences, compared to those observed in patients with affective disorders, despite the frequent absence of affective symptoms. While an improvement in subclinical or "masked" depression remains one hypothesis linking tricyclic responsiveness and shared biological abnormalities in this diverse group of diagnostic entities, an alternative hypothesis (the "ven disorder" hypothesis) is presented, suggesting the possibility that tricyclic and other antidepressant-responding patients have a core disorder with common psychobiologic abnormalities but multiple clinical and diagnostic presentations. An alternative hypothesis (the "shotgun" hypothesis) suggests that the multiple actions of tricyclics (e.g. on adrenergic receptors vs. muscarinic receptors vs. serotonin system changes) may each be differentially important in the therapeutic outcome in patients with specific or predominant problems in one or another of these areas. An examination of both the similarities and differences among the non-affective, tricyclic-responsive disorders and the affective disorders may provide clues about the important psychobiologic elements in these disorders, and to the mode of action of tricyclic antidepressants and related drugs across the psychiatric disorder spectrum.
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PMID:Therapeutic responses to tricyclic antidepressants and related drugs in non-affective disorder patient populations. 298 99

This review of the effects of sex steroids and oral contraceptives (OCs) on neurologic function in health and disease covers the following: sex steroids and their interaction with neural tissues; the human menstrual cycle and OCs; and sex hormones and OCs in human neurologic disease, i.e., stroke (thromboembolic cerebral infarction, subarachnoid hemorrhage, vascular malformations, and cerebral venous thrombosis), migraine, movement disorders, nervous system neoplasm, and the peripheral nerve. The various sex hormones may exert their effects on the nervous system directly or undergo conversion to more active metabolites. Interactions of sex hormones with neural substrates subserve numerous activities essential to both the well-being and perpetuation of the individual and the species. These interactions are key to the sexual differentiation of the brain, control of the brain-pituitary-gonad axis, and to the establishment of normal patterns of sexual and aggressive behavior in both sexes. Additionally, they play a role in temperature regulation (progesterone), caloric homeostasis (estrogen), and possibly sensory discrimination. The potent influences exerted by sex steroids on catecholamine and indoleamine turnover and the colocalization of labeled E2 within catecholamine and luteinizing hormone-releasing hormone (LHRH) positive perikarya suggest that many of the physiologic effects of sex steroids are mediated by modulation of specific monoaminergic and peptidergic pathways. Estrogens and aromatizable androgens also induce irreversible structural alterations in the rodent hypothalamus during the neonatal and peripubertal periods that are predominantly synaptogenic. In adult mammals, estrogens induce pathologic changes in the hypophysiotropic hypothalamus that may contribute to reproductive senescence in some species. Data from a series of retrospective and prospective studies have implicated OC use as an independent risk factor for the development of hemorrhagic and nonhemorrhagic stroke. Hormonal changes accompanying the pregnant state and the estrogen (and possibly progestogen) content of OCs may be predisposing factors in thromboembolic cerebral infarction, subarachnoid hemorrhage, cerebral venous thrombosis, and bleeding from intracranial and spinal vascular malformations. There are well-documented temporal associations of migrainous headache with specific phases of the menstrual cycle and the modifying influences of pregnancy, the menopause, and OC use. Also well established are relationships between endogenous and exogenous sex hormones and chorea. Fluctuating sex steroids also influence neuropsychiatric states, such depression and neuroendocrine disorders.
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PMID:Neurology of sex steroids and oral contraceptives. 302 81

In order to evaluate the relationships between endogenous opioid activity and premenstrual complaints, we subjected three groups of patients in the mid (days 8-12 prior to menses) and late (days 1-5 prior to menses) luteal phases of the cycle to a naloxone test and some of the patients to a luteinizing-hormone-releasing hormone (LHRH) test. The premenstrual syndrome (PMS) group was composed of nine patients complaining of dizziness, irritability and depression close to menses for at least three years. The menstrually related migraine (MM) group was composed of 15 patients complaining of premenstrually related migraine. The common migraine (CM) group was made up of 16 women suffering from common migraine for years whose attacks occurred independently of menstrual cycle events. A group of seven fertile women served as controls. Every two days the patients filled out the Menstrual Distress Questionnaire for evaluation of their complaints. After the evaluation of spontaneous LH pulsatility for one hour, 4 mg of naloxone was injected as a bolus, and samples were collected every 15 minutes for 2 hours. Both estradiol (E2) and progesterone (P) were measured in basal samples from each naloxone test. LH responsiveness to LHRH was similar in the mid and late luteal phases and did not change between groups. In the mid luteal phase the LH response to naloxone in PMS and MM patients was similar to that in normal subjects, while CM patients had impaired LH secretion. In the premenstrual phase only the controls maintained an LH responsiveness similar to that observed in the mid luteal phase, while both PMS and MM lost the naloxone-induced LH release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transient failure of central opioid tonus and premenstrual symptoms. 305 71

This article serves as a summary of the principles of prescription, hormone content, minor side effects, prescriptions for atypical individuals and significant drug interactions for oral contraceptives. There are 5 principles for prescribing oral contraceptives: the lowest possible dose should be given that is effective and produces the least side effects: adequate instructions should be given about the mode of action, taking the medication and possible side effects; adequate instructions about managing missed pills should be given; adequate supervision and explanations should be given if side effects occur; remember that each woman is different and idiosyncratic reactions to different formulations can occur. Possible side effects include: breakthrough bleeding, amenorrhoea, dysmenorrhoea, breast fullness and tenderness, nausea, chloasma, depression, acne, migraines and weight gain. Certain individuals such as epileptics, diabetics, women over 35 and women who have recently given birth need special care. Rifampicin, the phenytoins and barbiturates can all decrease the effectiveness of oral contraceptives. Oral contraceptives may effect the action of anticoagulants, antidiabetic agents and imipramine.
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PMID:Choosing an oral contraceptive. 307 12

The purpose of the present study was to characterize the initial vascular events accompanying cortical spreading depression (CSD) of the rat brain. Regional cerebral blood flow (rCBF) was measured during the first 1-2 min of CSD using 14C-iodoantipyrine autoradiography. The material included a reference group, and 4 groups where rCBF was altered by indomethacin treatment, hypo- or hypercapnia, or one previous episode of CSD. rCBF did not change prior to, or during the onset of CSD. Thirty seconds later, rCBF increased depending on the pre-existing level of blood flow, i.e. the rise of rCBF was pronounced at depressed flow levels, but small or absent at normal or high flow levels. The prevalent view that CSD is intimately associated with vasodilatation was accordingly not supported. The activated rCBF in normocapnic rats ranged between 93 and 175 ml/100g/min, supranormal values were the exception rather than the rule. The rCBF rise, when present, probably succeeds a period of brain hypoxia, and should be classified as a reactive hyperfusion. The results together with earlier clinical and experimental findings, support that CSD may serve as experimental migraine model.
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PMID:Regional cerebral blood flow during cortical spreading depression in rat brain: increased reactive hyperperfusion in low-flow states. 310 34

One hundred epileptic patients were questioned about their headaches. Post-ictal headaches occurred in 51 of these patients and most commonly lasted 6-72 hours. Major seizures were more often associated with post-epileptic headaches than minor attacks. Nine patients in this series of 100 also had migraine: in eight of these nine a typical, albeit a mild, migraine attack was provoked by fits. The post-ictal headache in the 40 epileptics who did not have migraine was accompanied by vomiting in 11 cases, photophobia in 14 cases and vomiting with photophobia in 4 cases. Furthermore, post-epileptic headache was accentuated by coughing, bending and sudden head movements and relieved by sleep. It is, therefore, clear that seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics. It is proposed that post-epileptic headache arises intracranially and is related to the vasodilatation known to follow seizures. The relationship of post-epileptic headache to migraine is discussed in the light of current ideas on migraine pathogenesis, in particular the vasodilation which accompanies Leao's spreading cortical depression.
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PMID:Post-epileptic headache and migraine. 311 78


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