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At least 19 recordsLinked to original sources
PubMed1977

Neuropsychiatric disorders of alcoholism.

The following neuropsychiatric disorders have been briefly described: alcohol withdrawal syndrome, delirium tremens, alcohol hallucinosis, Wernicke-Korsakow syndrome, seizures, tremor, Marchiafava-Bignami disease, central pontine myelinolysis, alcoholic amblyopia, alcoholic cerebellar degeneration cerebral atrophy, alterations of personality in chronic alcoholics, alcoholic polyneuropathy. The pathogenetical aspects as well as the pathological findings have been reviewed with special emphasis on nutritional factors.

Alcohol Withdrawal Delirium↗
PubMed1978

Evaluation of speech and language in neuropsychiatric disorders.

Changes of language and speech in neuropsychiatric patients are described by use of a quantifying procedure. In the transcript of a standardized interview the following variables are evaluated (by estimation of indices): rate of speech, pauses, indistinct and incomprehensible articulations, aphasic disturbances, subordinate: principal clause ratio, stuttering, neologisms, grammatical mistakes, thought disconnections, perseverations/verbigerations, vague utterances, disturbances of orientation, utterances with unusual though content, euphoric utterances, dysphoric utterances, and change of the affective state. Reliability of these indices is tested by inter-rater comparison. The course of speech-language reorganization during therapy is followed. The present method does not intend to give a detailed psycholinguistic analysis, but it yields an objective measure of clinical impressions on abnormalities of language and speech in neuropsychiatric disorders.

Aphasia↗
PubMed1979

beta-Endorphin-like immunoreactivity in cerebrospinal fluid and plasma of patients with schizophrenia and other neuropsychiatric disorders.

Measurements of beta-endorphin-like immunoreactivity have been performed in CSF and plasma of patients with schizophrenia and other neuropsychiatric disorders. The detection limit of the RIA was between 20--50 pg/ml (6--15 fmole/ml). In CSF the quantity of beta-endorphin-like immunoreactivity ranges up to 65 pg/ml. The data from schizophrenics and other neuropsychiatric patients show no obvious deviation from the results in a control group of medical patients with normal CSF findings. In plasma the immunoreactive beta-endorphin-like material ranges up to 250 pg/ml. There is only a small tendency to higher values in schizophrenic patients, if compared with different types of neuroses and affective and organic psychoses. In a second series of experiments also this tendency could not be reproduced. In 9 electroconvulsive treatments an increase of blood beta-endorphin-like immunoreactivity was observed 7 times. A possible endorphinergic mechanism in the mode of action of electroconvulsion is hypothesized.

Adolescent↗
PubMed1976

[Neuropsychiatric disorders of the diseases of exocrine pancreas (author's transl)].

Neuropsychiatric and psychosomatic disorders occurring the exocrine pancreatic diseases are not rare, nevertheless didn't it seem to be very interesting in research and there exists no summarizing work of this disorders. Therefore we tried to give a comprehensive representation of those neuropsychiatric problems which are connected with the function of this organ. At first we give a description of psychopathology and pathogenesis of the functional pancreatic psychosis. The problematic of the reciprocal relationship of nervous system and pancreatitis, alcoholism and pancreatitis are demonstrated as well as the psychic disorders occurring the pancreas insufficiency, cystes of pancreas and congenital pancreatic diseases. Psychosomatic and mental disorders of pancreas carcinoma and mucoviscidosis are shown in detail. The question of the interrelation between pancreatic function and amyotrophic lateral sclerosis or parathyreotic diseases are discussed just as themes of neuropsychiatric pharmacotherapie and pancreatic function and mental disorders in pancreatic treatment.

Acute Disease↗
PubMed1979

Gilles de la Tourette syndrome. Interactions with other neuropsychiatric disorders.

Gilles de la Tourette syndrome is a neuropsychiatric disease with a childhood onset below age 16, characterized by chronic involuntary movements, obsessions, compulsions, utterances, echolalia, coprolalia and aggressive behavior symptoms. Two unique case histories are described in this report, one with an intercurrent history of primary anorexia nervosa and the other with rheumatic encephalitis. They were successfully treated; the former with chlorimipramine, and the latter with combination of L-tryptophan, nicotinic acid, and pyridoxine HCl. These two cases illustrate the possibility that one neuropsychiatric syndrome may induce another during its evolution when the same anatomo-biochemical loci of the brain are involved.

Adolescent↗
PubMed1979

The neuropsychiatric disorder in systemic lupus erythematosus: evidence for both vascular and immune mechanisms.

As part of a prospective survey of systemic lupus erythematosus (SLE) a detailed collaborative study of the clinical, psychiatric, and laboratory features in 15 patients with nonfocal neuropsychiatric disease has been undertaken. In addition to conventional clinical and psychometric evaluation, electroencephalograph, and cerebrospinal fluid analysis, the study included the assessment of cerebral blood flow with oxygen-15 brain scans and serological testing for the presence of antineuronal and lymphocytotoxic antibodies. Of the 15 patients 12 had psychiatric manifestations, while 13 had various neurological abnormalities. All except 2 episodes of cerebral disease were transient. Striking abnormalities in cerebral blood flow and metabolism were seen in 12 patients, even in the presence of subtle clinical features. Sequential scans showed that improvement in clinical features was accompanied by a reversal of scan abnormalities. All sera contained brain-reactive antibody, either antineuronal IgG antibody (13) or lymphocytotoxic IgM antibody (12) or both (10), though there was an inconsistent association between clinical features and antibody titre. It is suggested that transient disturbances of cerebral vascular function in SLE might allow brain-reactive antibodies from the circulation access to cerebral tissue. In this way the nature of the neuropsychiatric abnormalities would depend on both vascular and immunopathogenic mechanisms.

Adolescent↗
PubMed1979

Cerebrospinal fluid acetylcholinesterase in neuropsychiatric disorders.

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.

Acetylcholinesterase↗
PubMed1975

Pathologic axons and synapses in human neuropsychiatric disorders.

Ultrastructural studies of cerebral biopsy specimens from patients with various forms of psychomotor retardation and dementia have disclosed pathologic changes in axons and presynaptic or postsynaptic processes. The clinical disorders with lesions in axons and presynaptic terminals are reviewed. Three basic abnormalities have been detected: proliferation of tubulovesicular structures which probably originate from the smooth endoplasmic reticulum, "abnormal" mitochondria, and proliferation of 80 to 100 A filaments. Understanding of the pathogenesis of human disorders associated with axonic or "synaptic" lesions will probably depend on progress in areas of basic biomedical research concerned with the synthesis and turnover of biological membranes and the packaging and secretion of neurotransmitters, elucidation of mechanisms of cytoplasmic streaming and axoplasmic flow, and biophysical and biochemical characteristics and functions of "fibrous" proteins (neurotubules, neurofilaments, pathologic fibrous proteins). In several cases of mental retardation of unknown etiology, abnormal dendritic spines of cortical neurons have been observed with the use of the Golgi method. These dendritic (postsynaptic) disorders have been attributed to defective development ("dysgenesis"). The knowledge provided by ultrastructural analysis of brain tissue from the human disorders of mental retardation or dementia is "still formless, incomplete, lacking the essential threads of connection," and only future developments in lacking neurobiology will make possible the dissection of the primary phenomena from the secretory and probably irrelevant findings.

Animals↗
PubMed1979

[Epidemiologic-rehabilitation aspect of borderline neuropsychiatric disorders in students].

The prevalence, treatment and rehabilitation of students with border-line neuropsychic disturbances were studied in higher educational establishments. The intensive indices of the morbidity and incidence of border-line states amounted to 6.9 and 19.3 per 1000 students. Among the students of humanitarian faculties the number of the patients with border-line states was 6 times as great as compared to technical students and 3 times as great as compared to the students of biomedical and physico-mathematical departments. The authors recommend that the main attention in the rehabilitation of students with border-line neuropsychic disturbances should be attached to the outpatient programmes as they are the most effective for this group of patients. It is also recommended to organize specialized rooms of mental hygiene for students.

Adult↗
PubMed1978

Serotonin, folic acid, and uric acid metabolism in the diagnosis of neuropsychiatric disorders.

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.

Adolescent↗