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

Bipolar manic-depressive illness is a chronic disease in which patients experience recurrent episodes of mania and depression. Patients often change from a nonverbal, retarded depression of many months' duration to a hyperactive, psychotic, manic condition during the switch. The time required for the switch from depression into mania varies from 5 minutes to a couple of days. Just before it happens, pateints experience marked insomnia and decreased rapid eye movement sleep. It is hypothesized that specific changes in brain monoamine metabolism precede the switch. Alterations in neurotransmitter metabolites, as measured in urine and cerebrospinal fluid, may precede and accompany it. The switch into mania can be precipitated by environmental stresses or by drugs that act by increasing functional brain monoamines. Drugs that reverse the manic state all share the common property of affecting biogenic amines. The switch into mania is viewed in the context of a longitudinal cyclic process and may be further studied with specific pharmacologic agents that block drug-induced maniclike states in man.
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PMID:The switch process in manic-depressive psychosis. 2 15

Indirect evidence, mostly pharmacologic, has suggested a role for brain neurotransmitter amines such as norepinephrine in the production of depression or mania. Clinical investigations have supported this concept but also indicate that depression is probably a biochemically heterogeneous group of illnesses. There may be a clinically, biochemically, and pharmacologically definable subtype of depression in which there is a disorder of norepinephrine metabolism or disposition in brain. I review here the experimental data from which this hypothesis is derived.
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PMID:Clinical and biochemical heterogeneity of depressive disorders. 2 35

Genetic factors have been evidenced in the etiology of manic-depressive syndromes through twins, morbidity risk studies, linkage studies with genetic markers such as color blindness and the Xga blood group, as well as through adoption studies. Most genetic studies indicate that there is a genetic and biological heterogeneity in manic-depressive illness. Among these manic-depressive syndromes, one group is consistent with a dominant X-linked transmission of the disease. From the neurochemical point of view, most investigators emphasize the importance of cerebral neurotransmitter substances such as catecholamines and indolamines in the pathogenesis of bipolar depressive states. According with this hypothesis, depression is associated with a functional deficit in brain monoamines while mania may be due to an hyperproduction of monoamines. These neuropharmacological studies are of importance because they also have neuroendocrine implications. Some pituitary hormones are secreted under the control of brain monoamines, and they are also implicated in the pathogenesis of depressive states.
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PMID:[Contribution of biology to nosology of depressive states. Neurochemical, endocrine and genetic factors (author's transl)]. 3 24

This paper reviews the diagnosis and medical treatment of the major affective disorders. Patients with severe mood disturbances are frequently seen by the family physician. The diagnosis may be delayed since the patient may focus predominantly on somatic concerns which may mimic physical illness. The characteristics, course, and differential diagnosis of depression and mania are discussed. Antidepressants and lithium therapy greatly improve the prognosis of these disorders; monoamine oxidase inhibitors and neuroleptics are indicated for special subtypes of depression. Dosage schedules, interactional effects, adverse and toxic effects are reviewed for tricyclic antidepressants and lithium.
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PMID:Primary affective disorders. 3 9

Actions of morphine include analgesia, sleep, euphoria, and depression of respiration. Transmitter or modulator substances in the brain that have actions similar to morphine may control these functions in man. This hypothesis proposes that enkephalin is a controlling neurotransmitter and its binding to opiate receptors determines mood state as well as influencing respiratory and sleep patterns. Lithium may act through modification of the opiate receptor affinity for an endogenous morphine-like substance. The theory predicts blocking action of naloxone in mania and in most drug-induced euphorias. It implies a new chemical pathophysiological basis for the phenomenology of mental illness.
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PMID:Peptide transmitters: a unifying hypothesis for euphoria, respiration, sleep, and the action of lithium. 5 53

Animal studies have revealed two important aspects of vasopressin function which make this peptide a suitable candidate for involvement in complex behavioural syndromes: (1) vasopressin deficiency produces deficits of behaviour which are reversed by vasopressin; (2) well-developed systems exist for the distribution of vasopressin throughout the central nervous system (C.N.S.) via either peptidergic neurons or the cerebrospinal fluid (C.S.F.) and provide the means by which vasopressin may regulate cells controlling behavioural or physiological processes. Among the processes which vasopressin can influence are several of significance in the symptom-complex of affective illness, including alterations in memory, changes in pain sensitivity, synchronisation of biological rhythms, the timing and quality of R.E.M. sleep, and the regulation of fluid and electrolyte balance. In addition, vasopressin is functionally linked to monoamine neurotransmitter systems and, like them, is altered by pharmacological agents which affect mood. Some of the pharmacological and clinical data suggest that vasopressin function is diminished in depression and augmented in mania; sometimes, however, alterations in vasopressin function may be detectable only during crucial periods of the manic-depressive cycle. The hypothesis that vasopressin plays a role in disorders of human behaviour, particularly manic-depressive illness, can now be directly tested by radioimmunoassays of vasopressin in C.S.F. and plasma and by the administration of specific vasopressin analogues and inhibitors.
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PMID:Vasopressin in affective illness. 7 97

Serum-cortisol response to the 1 mg overnight dexamethasone suppression test was investigated in 86 patients with unipolar primary depressive illness and 80 non-depressed controls (45 with mania and 35 with schizophrenia). The depressed patients were assigned to one of three genetic subtypes according to the family psychiatric history. Resistance to suppression of serum-cortisol by dexamethasone was found in 37 of 86 (43%) depressives and none of the 80 controls. Non-suppression distinguished the three genetic subtypes of depression, being found in 23 of 28 (82%) patients with familial pure depressive disease (F.P.D.D.), 13 of 35 (37%) patients with sporadic depressive disease (S.D.D.), and 1 of 23 (4%) patients with depression spectrum disease (D.S.D.). The three genetic subtypes were further distinguished by the age of onset, with S.D.D. the oldest, and by the number of previous depressive episodes, with F.P.D.D. the most. Severity of depression did not separate the three subtypes. This is the first report of a distinct neuroendocrine abnormality which supports an objectively defined classification of unipolar primary depressive illness. It is suggested that unipolar primary depressive illness is three or more separate illnesses, each with a potentially distinctive mode of inheritance, pathophysiology, neurochemistry, clinical course, and treatment response.
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PMID:Genetic subtypes of unipolar primary depressive illness distinguished by hypothalamic-pituitary-adrenal axis activity. 8 87

Acetylcholinesterase (AChE) was measured in the cerebrospinal fluid (CSF) of patients with a diagnosis of Huntington's disease, depression, schizophrenia, or mania and also in the CSF of normal subjects. No significant differences in CSF AChE were found between any diagnostic group and normal subjects. Furthermore, the administration of choline chloride, physostigmine, or probenecid did not significantly alter CSF AChE. No diurnal variation in CSF AChE activity was apparent. These findings, combined with the unclear relationship of brain AChE to CSF AChE, suggest that this measurement does not reflect the relative cholinergic underactivity presumed to exist in some neuropsychiatric conditions.
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PMID:Cerebrospinal fluid acetylcholinesterase in neuropsychiatric disorders. 15 94

Narrow definitions of schizophrenia increase homogeneity at the expense of leaving unclassified many patients with shizophrenic symptoms. Family history and follow-up studies indicate that many such patients ought to be classified with those having affective disorders. This study determines morbid risks for affective disorder and schizophrenia in first degree relatives of patients with chart but not research diagnoses of schizophrenia. Comparisons with morbid risk figures for relatives of individuals satisfying research criteria for depression, mania or schizophrenia indicate that the 'non-Feighner schizophrenia' group is probably too heterogenous to be classified entirely as affective disorder or as schizophrenia.
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PMID:Should 'non-Feighner schizophrenia' be classified with affective disorder? 16 80

Biochemical and electrophysiological factors were studied longitudinally in a rapidly cycling manic-depressive patient. Slow changes in mood, motor activity, sleep, and urinary norepinephrine levels during the course of each depressed and manic episode are reported, as well as rapid alterations in many variables at the time of mood switch. Urinary concentrations of norepinephrine and its metabolite, 3-methoxy-4-hydroxyphenyl glycol (MHPG) were significantly lower in depression than in mania; norepinephrine but not MHPG excretion increased prior to the switch. We postulate that the slow behavioral and biological changes preceding switches in this patient are an important manifestation of the cyclic process in manic-depressive illness.
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PMID:Alterations in motor activity, sleep, and biochemistry in a cycling manic-depressive patient. 19 69


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