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Biomedical subjects

F K Goodwin

Publications and source records attributed to F K Goodwin.

At least 73 records · Page 4Linked to original sources
PubMed1989

The biology of recurrence: new directions for the pharmacologic bridge.

Recurrence is a fundamental reality of the major affective disorders and must be considered in treatment planning. Historically, however, information regarding the pathophysiology and neurobiology of affective disorders was not gained from studies on recurrence, but rather from research utilizing drugs classified on the basis of their effect on acute manic and/or depressive states. Though such cross-sectional strategies were critical in developing the original amine hypotheses, they also were inherently limited. Today, accumulating information regarding differential drug effects on cycle length calls for reexamining the pharmacologic bridge from the perspective of the nascent neurobiology of recurrence of affective disorders. This presentation considers the array of drugs now used in treating mood disorders and reviews recent data relating to the role of acute and maintenance treatments on the occurrence of manic and hypomanic reactions in bipolar patients. In addition, emerging data on the impact of longitudinal treatments on the natural course of bipolar illness are used to develop a model for examining the effects of treatment on recurring unipolar illness.

Antidepressive Agents↗
PubMed1988

Clinical and biochemical manifestations of depression. Relation to the neurobiology of stress (2)

Thousands of studies have been conducted of the functioning of the many neurotransmitter systems in order to explore the biologic basis of major depressive disorder. Instead of reviewing this literature exhaustively, we have attempted to propose a model that accommodates the clinical observation that chronic stress early in life in vulnerable persons predisposes them to major depression with contemporary observations of the potential consequences of repeated central nervous system exposure to effectors of the stress response. This model accords with current clinical judgment that major depression is best treated with a combination of psychopharmacologic agents and psychotherapy. Accordingly, whereas psychopharmacologic intervention may be required to resolve an active episode of major depression and to prevent recurrences, psychotherapy may be equally important to lessen the burden of stress imposed by intense inner conflict and counterproductive defenses.

Animals↗
PubMed1988

The NIMH Depression Awareness, Recognition, and Treatment Program: structure, aims, and scientific basis.

Unrecognized, untreated, and undertreated depressive disorders extract an inordinate human and economic cost, despite the availability of an extensive array of effective clinical interventions. To enhance the availability and quality of care, the National Institute of Mental Health launched the Depression Awareness, Recognition, and Treatment Program, a multiphase information and education program designed to alert health professionals and the general public to the fact that depressive disorders are common, serious, and treatable. The authors review the development of this program, describing the professional education efforts it supports in anticipation of increased demand for services, the public education campaign launched in May 1988, and highlights of the scientific advances that make the program feasible and timely.

Catchment Area, Health↗
PubMed1988

Neuroanatomical studies of major affective disorders. A review and suggestions for further research.

Interest in the long-neglected neuropathology of major affective disorders has recently been rekindled, partly because of the emergence of brain-imaging techniques. We review the literature suggesting that attention be given to the neuroanatomy and neuropathology of primary and secondary affective disorders. Computerised tomography studies show that patients with affective disorders tend to be similar to schizophrenic patients and significantly different from normal control subjects in ventricle:brain ratio, sulcal widening, and cerebellar vermian atrophy. As yet, there are few neuropathological investigations of the brains of patients with primary affective disorders. Suggestions for further research in the neuropathology of affective disorders are offered.

Affective Disorders, Psychotic↗
PubMed1987

Cerebrospinal fluid monoamine metabolite levels in male arsonists.

Cerebrospinal fluid (CSF) monoamine metabolite levels were studied in 20 arsonists, 20 habitually violent offenders, and ten healthy inpatient volunteers. The arsonists and violent offenders had been in prison an average of six months before the study. Both the raw data and data adjusted by analysis of covariance for group differences in age, height, sex, and season of the lumbar puncture showed significantly lower concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA) in the arsonists than in the other groups. The finding remained the same when arsonists with violent suicide attempts were excluded from the analysis. Although CSF concentrations of MHPG or 5-HIAA did not correlate with the severity of repeated fire-setting behavior, low blood glucose nadir in the oral glucose tolerance test (a measure of the tendency toward hypoglycemia) did. These results support the hypothesis that poor impulse control in criminal offenders is associated with low levels of certain CSF monoamine metabolites and with a hypoglycemic tendency.

Adolescent↗
PubMed1987

Can antidepressants cause mania and worsen the course of affective illness?

Several investigators have recently challenged the belief that antidepressants can precipitate mania or rapid cycling between mania and depression. With one exception, there appear to be no placebo-controlled studies of switches into mania in bipolar patients during antidepressant treatment. Patients most likely to switch into mania during antidepressant therapy have probably been excluded from maintenance treatment studies and are probably overrepresented in studies at special research facilities. On balance, the available evidence suggests that some bipolar patients become manic, and a few experience rapid cycling, when they are treated with antidepressants. The prevention of these responses will require further research on risk factors and on the antimanic efficacy of coadministered lithium or other mood stabilizers.

Antidepressive Agents↗
PubMed1986

Diazepam-binding inhibitor. A brain neuropeptide present in human spinal fluid: studies in depression, schizophrenia, and Alzheimer's disease.

Diazepam-binding inhibitor is a novel peptide purified to homogeneity from rat and human brain. Diazepam-binding inhibitor is present, though not exclusively, in gamma-aminobutyric acid (GABA)-containing neurons where it is believed to inhibit GABAergic neurotransmission mediated by GABA by binding to the benzodiazepine-GABA receptor complex. Since an impairment of central GABAergic tone has been postulated to be associated with a number of neuropsychiatric disorders, we measured human diazepam-binding inhibitor immunoreactivity in the cerebrospinal fluid (CSF) of patients suffering from endogenous depression, schizophrenia, and dementia of the Alzheimer's type. Patients with major depression had significantly higher concentrations of human diazepam-binding inhibitor immunoreactivity in CSF when compared with age- and sex-matched normal volunteers, while no difference in CSF diazepam-binding inhibitor immunoreactivity was found in schizophrenics or patients with dementia of the Alzheimer's type when compared with controls. The possibility is discussed that the increased CSF human diazepam-binding inhibitor immunoreactivity observed in depressed patients may represent a functional disinhibition of GABAergic neurotransmission associated with depression.

Adult↗