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

The rigorous neo-Kraepelinean research criteria of the St. Louis/Iowa and Taylor groups were applied to case record data of 116 first admissions of Schneider-negative schizophrenics--that is, those without first-rank symptoms (FRSs)--hospitalized in a strongly Schneider-oriented German University Psychiatric Clinic from 1962 to 1971. This sample had a total of 45.7% (53 cases) of psychiatric illness diagnosable by research methods. Indeed, only 31% (36 cases) of Schneider-negative schizophrenics turned out to have research-positive Kraepelin-oriented schizophrenia; and of these, 21 fulfilled both sets of research criteria for schizophrenia. It is important that 14.6% (17 cases) of Schneider-negative schizophrenia consisted of research-diagnosable affective disorder, with mania making up 5.2% and depression 9.4% of this figure. The findings suggest that a sample of Schneider-oriented schizophrenia without FRSs as routinely diagnosed in Germany does not seem to represent a clear-cut homogeneous and 'uncontaminated' group of schizophrenics.
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PMID:Kraepelin-oriented research-diagnosable schizophrenia, mania, and depression in Schneider-negative schizophrenics. 70 19

A representative sample of 95 hospitalized bipolar manic-depressive patients was followed up from 1959 to 1975. The mean age of the group at the time of this study was 61 years. It was observed that female bipolar patients demonstrate depression much more frequently than mania, while male patients show a symmetric distribution of both manic and depressive syndromes. The longitudinal occurrence of syndromes remains more or less constant; for instance, individual patients do not tend to go into depression with increasing age. The study shows that even after three episodes 29% of all bipolar patients would still have been misdiagnosed as unipolar depression. An attempt is made to classify bipolar patients into three subtypes, 'preponderantly manic,' 'preponderantly depressed,' and a 'nuclear' type. Male patients belong mainly to the latter with an equal proportion of the first and third subtype. In contrast, female patients belong mainly to the depressed subtype. The findings are discussed assuming either a heterogeneity of bipolar disorders or a threshold model of affective disorders suggested by Gershon et al. (1976).
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PMID:The course of affective disorders. II. Typology of bipolar manic-depressive illness. 70 28

Metabolic compensation appears possible within the serotonergic, folate, purine system and it seems possible that clinical illness may result when the system can no longer compensate. For example, elevated serotonin, induced by stress accumulation of tryptophan, could be compensated by a lowered folate ratio, normalizing the beta-carboline index and preventing hallucinations. Conversely, deficient serotonin, induced by a psychological loss or transport deficit, could be compensated by raising the folate ratio, which would normalize the beta-carboline index and prevent further depression. Increased purine turnover would seemingly lower the folate ratio, compensating perhaps for hallucinatory activity or mania. Several genetic defects of enzymes or transport proteins could seemingly preclude normal compensations within the system.
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PMID:Serotonin, folic acid, and uric acid metabolism in the diagnosis of neuropsychiatric disorders. 73 55

Synthetic salmon calcitonin was administered subcutaneously to 12 inpatients with several primary psychotic diagnoses. Increases in serum total calcium and inorganic phosphorus levels and decreases in CSF calcium level had earlier been observed during periodic psychotic agitation or mania. By contrast, calcitonin, which decreased serum calcium and phosphorus levels and increased CSF calcium level, appeared to produce transient (24-hour) increases in depression and decreases in arousal in this double-blind placebo-controlled trial. Quantitative activity monitoring confirmed the rater's impression that this agent had tranquilizing or depressant effects in such patients. When given in the evening, this polypeptide also appeared to delay sleep onset, as demonstrated both by nurses' 30-minute sleep checks and by the same longitudinal activity record. A decreased hypocalcemic response to calcitonin was noted in the agitated patients, which might explain the increases in serum calcium level described at the "switch".
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PMID:Use of calcitonin in psychotic agitation or mania. 76 Jun 98

A review of all properly controlled studies clearly indicates that lithium carbonate is prophylactic for mania in bipolar patients; it is suggestive of prophylaxis for depression in both bipolar and unipolar patients. Studies are outlined that would clarify lithium carbonate's prophylactic effect for depression in these two patient groups. Continuation therapy with antidepressants reduces incidences of recurrence in unipolar depressives. The only controlled study indicates that tricyclic antidepressants may have prophylactic effect in unipolar patients. This finding needs confirmation. Data are insufficient for conclusions on prophylactic treatment for schizoaffective disorders.
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PMID:Prophylaxis of affective disorders. Current status of knowledge. 76 24

Several recent data indicate the blood-brain transport of amino acids as a critical factor in the synthesis of monoamines. The complex, peripheral and central regulation of TP transport plays an essential role sine TP-hydroxylase is not a saturated enzyme. The hydroxylated derivatives 5-HTP and dopa are probably transported into the brain by similar mechanisms as their precursors TP and tyrosine, respectively. The maic-depressive patients show an increased uptake of administered L-5-HTP in the depressive phase, whereas L-dopa uptake is enhanced in the manic phase. Heuristically, we propose a biochemical model of manic-depressive psychosis in which an increased TP uptake causes alternation in the balance of monoaminergic system activity. Depression is possibly characterized by a hyperserotonergic and a relative hypocatecholaminergic activity. In contrast, mania is possibly determined by a hypercatecholaminergic (NA and DA) and a relative hyposerotonergic activity. The data offered by the physiology of monoamines, the semeiology and the biological alterations of the manic-depressive psychosis, as well as the monoaminergic and the electrolyte theory of manic-depressive psychosis. A diminution of the transport of TP with consequent increase of that of tyrosine represents a possible biochemical model of schizophrenia which may be well explained by a hyposerotonergic-hyperdopaminergic activity, with or without noradrenergic insufficiency. This model is compatible with our knowledge on the monoamine physiology, the biological alterations of schizophrenia, the therapeutical results as well as with the classical clinical notions (typology, intermediate syndromes and crossed heritance).
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PMID:The common pathophysiology of monaminergic psychoses: a new hypothesis. 77 59

The thymoleptics potentiate and modify the behavioral effects of apomorphine (probably the most specific dopaminergic agonist) as well as those of Dopa. The effect of the thymoleptics is not abolished by emptying of amine stores, and this together with other evidence suggests that these drugs facilitate the access of apomorphine to the dopamine receptors. The effects of thymoleptics on elements of animal behavior that can be associated with brain dopamine appear interesting on the background of a considerable body of evidence indicating an association of brain dopamine with depression and mania (references).
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PMID:Effects of thymoleptics on behavior associated with changes in brain dopamine. II. Modification and potentiation of apomorphine-induced stimulation of mice. 82

A distinctive pattern of clinical change during eight affective episodes is reported in a rapidly cycling manic-depressive patient. After a rapid switch to near maximal intensity of affective symptoms, slow changes in symptomatology were documented by significant slopes and correlation coefficients over the course of each episode. Decreases in depression, anxiety, drowsiness, helplessness/hopelessness, anger, and sadness preceded the switches into mania; decreases in mania, euphoria, seeking others, and talking preceded the switches into depression. Psychologically important events appeared to regularly precede rapid mood switches. It is suggested that the consistent, slow clinical changes which occur during affective episodes may reflect part of an underlying rhthmic biological process and that environment events may be capable of triggering a final common pathway for the mood switch during a vulnerable period.
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PMID:Slow and rapid psychobiological alterations in a manic-depressive patient: clinical phenomenology. 83 12

A patient with unusually regular and rapid switches from mania to depression was studied for 113 consecutive days through five switches. Average evoked responses (AERs) to four intesities of light were recorded from vertex and occipital leads; telemetered activity records and behavioral ratings were also collected. Late AER components (P200) tended to change amplitude synchronously with the switches, vertex P200 amplitude decreased and occipital P200 amplitude increased in mania. Urinary MHPG changes paralleled the changes in P200 amplitude. Early AER components (P100) and especially the amplitude/intesity slope measures for P100 decreased about 8-10 days before a switch from depression to mania. Cross-spectral and linear regression analysis helped confirm these observations. The results, taken together with AER data in recent L-dopa studies, were consistent with catecholamine potentiation prior to the switch process from depression into mania.
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PMID:Average evoked responses in a rapidly cycling manic-depressive patient. 83 24

Bipolar affective disorder (manic-depressive disease) is a mental disturbance characterized by phases of both depression and mania. Mania is essential to the diagnosis and is characterized by elevated mood, flight of ideas, and increased psychomotor activity. Current psychiatric literature not only shows that this disease is familial but has also demonstrated, through linkage studies, that an X-linked dominant mode of inheritance adequately explains the strong prevalence of bipolar affective disorder in some families. The family discussed here shows many of the known clinical aspects of bipolar affective disorder. It serves as an example consistent with the X-linked dominant mode of inheritance. Knowledge of the genetic background of this disease aids the family physician by helping to identify members of the family likely to have acquired this condition. The family physician can then look for future problems in them and in their offspring, leading to earlier diagnosis and more effective management. Thus, a member of a bipolar family with supposed unipolar illness (depression only) might be better served with the prophylactic use of lithium carbonate because of his likelihood of possessing a bipolar genotype. The prophylactic use of this drug has been shown effective in reducing the frequency, duration, and intensity of both manic and depressive mood swings.
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PMID:Genetic aspects of manic-depressive disease in family practice. 84 63


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