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At least 19 recordsLinked to original sources

[Mechanism of action of lithium in manic-depressive psychoses: current research results].

The mechanism of action lithium in the treatment of manic-depressive illness is far from being known. A great progress will be achieved when it is known wherther lithium has an actual anti-depressive action, which implies to determine whether all the "endogenous" depressive states belong to the same pathogenic group. Lithium salts have a real therapeutic action on manic states which may be put together with the decrease of available Norepinephrine that lithium salts bring about on cerebral receptors. This decrease concords with the aminergic theory of affective disorders. Many actions of lithium salts on the physiologic systems have been brought to evidence but the uncertainties that remain concerning their interactions prevent us to formulate any coherent assumption.

Acetylcholine↗

[Manic-depressive psychoses. Chronic treatment with tricyclic antidepressive agents].

Long-course Tricyclic anti-depressing treatment affonds clinical healing--i.e. abolition of the recurrences--in melancolic unipolary periodic depressions. This treatment--T.A.T.C.--allows a good prevention of melancolic recurrences in bipolar periodic patterns of psychosis. For the authors Lithium and/or Dipropylacétamide are not sufficient protection for melancolic or maniac recurrences in this patterns. It seems to be three patterns in fact: pure melancolic, pure maniac, and maniaco-depressive. Therapeutic and psychopathologic considerations.

Adult↗

Psychopharmacological treatment of psychotic children. A survey.

Controlled investigations on the psychopharmacological treatment of psychotic children are reviewed. Children with infantile autism might benefit from psychopharmacological medication when they grow older, e.g. above the age of 7 years. Learning might be facilitated when the psychoactive medication is able to inhibit psychotic preoccupations and idiosyncratic reactions. Schizophrenic and manic-depressive psychoses are rarely seen in childhood. A subgroup of the children with infantile autism might develop schizophrenic symptoms. Schizophrenia and manic-depressive psychosis in children are treated as in adults. Special caution must be paid to the toxic effects of imipramine.

Antipsychotic Agents↗

[The time-structure of a manic-depressive psychosis (author's transl)].

Some ideas about the desynchronisation and the restabilisation of the diurnal time-structure in the mood-and-drive system are the background for some hypotheses about the determination of the course and the theory of mixed states of manic-depressive psychoses. A model given in graphs is compared with empiric material from a typical casus, which could be shown with its prodrom and some weeks of its course. The structure of dimensionality was studied by factor-analysis, the time structure was studied by autocorrelation technique. A development of the chronobiological theory seems to be of interest.

Bipolar Disorder↗

Genetic and other factors in schizophrenic, manic-depressive, and schizo-affective psychoses.

The major psychoses have been investigated for genetic and environmental etiological factors for over two centuries. Recent emphasis has been placed on a genetic (diathesis) environmental stress model. For schizophrenia, manic-depressive, and schizo-affective psychoses, research evidence from psycho-biological studies, family, pedigree, twin, and adoptee studies has provided sufficient data from diagnostic and follow-up studies and new psychopharmacological research that for these three major psychoses a strong necessary but not sufficient basis for genetic causation exists. This review attempts to summarize existing data into a hypothesis that suggests that two separate gene pools of polygenic nature relate to the development of schizophrenia and manic-depressive illness and that schizo-affective illness may result from genetic transmission from each of these separate gene pools. The hypothetical model for each psychosis proposes that polygenetic inheritance affects different central nervous system neuroanatomical sites in the human which are in homeostasis as to catecholamine neurotransmitter regulation of the psyche. With sufficient environmental stress, an "imbalance" occurs in the neural integrative systems which produces phenotypically the three separate psychotic behavioral syndromes of schizophrenia, manic-depressive psychosis, and schizo-affective psychosis.

Adoption↗

[Physiopathology of endogenous psychoses].

Metabolic theories of manic-depressive psychosis and schizophrenia are reviewed and constructivist models are presented which attempt to integrate biochemical, neurophysiological and clinical findings.

Antidepressive Agents↗

[Latent endogenous depressions in adolescents].

A clinico-catamnestical study of 200 adolescents with depressive conditions in endogenous psychoses revealed 28 patients who suffered from schizophrenia and manic-depressive psychosis with manifestations of larvate depressions. It was established that larvate depressions in adolescents in the majority of the cases proceed with disorders of behaviour and poor school progress. The clinical picture is characterized by diverse somatic complaints in the absence of actual somatical pathology. Larvate depressions in adolescents differ significantly from similar states in adults, inasmuch as poor progress in school is due to disorders of cognitive activity during the disease.

Bipolar Disorder↗

Diagnosis in schizophrenia and manic-depressive illness: a reassessment of the specificity of 'schizophrenic' symptoms in the light of current research.

Present clinical and research methods of differential diagnosis of schizophrenia and affective psychoses rely very heavily on presenting symptoms and signs, especially in acute psychosis. We have reviewed studies bearing on this issue, including studies of the phenomenology of psychotic illness, outcome, family history, response to treatment with lithium carbonate, and cross-national and historical diagnostic comparisons. We conclude that most so-called schizophrenic symptoms, taken alone and in cross section, have remarkably little, if any, demonstrated validity in determining diagnosis, prognosis, or treatment response in psychosis. In the United States, particularly, overreliance on such symptoms alone results in overdiagnosis of schizophrenia and underdiagnosis of affective illnesses, particularly mania. This compromises both clinical treatment and research.

Bipolar Disorder↗

Mixed affective states and the natural history of manic-depressive psychosis.

Since neither the unipolar nor the bipolar theories of manic-depressive psychosis explain all its features, an alternative model was tested. The hypotheses are that mixed affective psychoses represent a superimposition on hypomania of a second type of depression which can sometimes develop from the depressive phase of manic-depressive psychosis, and that schizophrenia occurring in the course of a manic-depressive illness is an alternative to mixed affective psychosis. From an examination of the clinical histories of a random sample of people with bipolar manic-depressive psychosis, evidence was found to support both ideas.

Adult↗

An amphetamine model of manic depressive illness.

Many features of manic-depressive illness can be mimicked in man by the use and withdrawal of amphetamines. In higher doses these drugs induce a syndrome virtually indistinguishable from paranoid schizophrenia. In this paper, some of the biochemical and physiological effects of the amphetamines are examined with the hope of clarifying the nature of the biological changes in these two major functional psychoses. The actions of the amphetamines are shown to reveal the operation of specific homeostatic or adaptive nervous mechanisms. These appear likely also to operate in adaptation to psychological stress. Evidence is presented that these mechanisms are malfunctioning in manic-depressive and acute schizophrenic states and that this accounts for many of the clinical features of these conditions.

Adaptation, Psychological↗

Manic depressive illness in adolescence and childhood: review and case report.

The literature on this topic from its inception by Kraepelin is reviewed. While Kraepelin and the French school always recognized juvenile mania, the Anglo-American school has no such unanimity of opinion. Less than 100 cases are described in the world literature. In Canada affective psychoses are rarely diagnosed under age 10 and of all affective psychoses admitted to institutions less than 5% are under age 20. The differences between child and adult mania are outlined. It is proposed that manic-depressive illness occurs in children but is not diagnosed more often because of its dissimilar presentation to the adult form and doubts about its existence in childhood. The case history of a 14 year old boy who presented in a hypomanic state is described. There was a strong family history of affective disorder. Both his parents and his half-sister were already on lithium for manic-depressive illness.

Adolescent↗

Psychoses precipitated by psychotomimetic drugs. A follow-up study.

Fifteen patients who developed prolonged psychotic reactions following psychotomimetic drug use (probably primarily LSD) were followed up 1.9 to 5.8 years later. Two patients had committed suicide. Approximately half of the patients had a relatively good outcome and half did poorly. Aspects of the initial clinical picture that correlated with outcome measures are discussed. The possibility is considered that vulnerability to a prolonged psychotic reaction following psychotomimetic drug use may be related to a genetic vulnerability to illnesses in the manic-depressive/schizo-affective spectrum. In some instances this vulnerability may implicate central serotonergic neuronal systems.

Adolescent↗

Linkage between an X-chromosome marker (deutan color blindness) and bipolar affective illness. Occurrence in the family of a lithium carbonate-responsive schizo-affective proband.

Studies with X-chromosome markers in mental illness have been limited to the diagnostic concept of primary affective disorders. The present study is the first to our knowledge to demonstrate statistically measurable linkage between color blindness and manic-depressive illness in a family identified by a schizo-affective proband. Linkage data and lithium carbonate response in the proband suggest that the schizophreniform-affective spectrum in members of the pedigree may reflect a genetically distinct disorder. The use of a genetic marker as a heuristic diagnostic criterion in a subgroup of heredofamilial psychoses with unclear diagnostic boundaries is proposed.

Adult↗

[Cerebral embolism and psychosis with special reference to cardiac surgery (author's transl)].

Cerebral embolism can manifest itself in certain cases as pure psychosis. In the absence of neurological symptoms it might be mistaken for schizophrenia or manic-depressive psychosis. Cardiac disease and cardiac surgery involve a high risk of embolism. Microembolism plays a special role with extracorporal circulation. There is a significant increase of postoperative psychosis in cases with E.C.C. in comparison to closed heart surgery. Immediately post-operatively there occurs what has been described as the "catastrophic reaction" or "immobilization syndrome". This reaction is in fact an akinetic, parkinsonian-like state for which there is good evidence that it is due to transient microembolism of the basal ganglia ("striatum apoplexy"). After its disappearance around the 3rd--5th day "cardiac psychoses" (cardiac delirium) may manifest themselves. Patients who develop these "late" psychoses have a significantly higher correlation with endogenous psychoses in their family histories. On the psychopathological level--in the absence of disturbances of consciousness and orientation--it is not possible to differentiate between "exogenous" and "endogenous" psychosis. A special type of psychopathological reaction is dependent, as in neurological disease, on the severity of brain damage, its localization and on hereditary factors.

Basal Ganglia↗

Clinical response and plasma levels: effect of dose, dosage schedules, and drug interactions on plasma chlorpromazine levels.

Plasma chlorpromazine (CPZ) levels of 50 psychotic inpatients were measured by gas liquid chromatography; the clinical progress of 29 of these patients with acute psychoses was also assessed. CPZ levels of 50-300 ng/ml were usually associated with clinical improvement; there was also a relationship between CPZ levels and increases in certain symptoms. The 50-300 ng/ml level was best attained by doses of 400-800 mg/day. Trihexyphenidyl decreased plasma CPZ by a mean of 44.7% in 12 of 15 patients. A single 400-800-mg dose of CPZ at bedtime produced steady states equal to or better than those achieved with multiple doses. Those patients who failed to attain CPZ levels of more than 70 ng/ml despite doses of 400-1000 mg/day were receiving lithium throughout the study and had discharge diagnoses of manic-depressive psychosis, manic type, and schizo-affective schizophrenia--a finding with implications for future research.

Acute Disease↗