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At least 361 records · Page 20Linked to original sources
PubMed1990

Methamphetamine. Stimulant of the 1990s?

During the past several years, the use of a smokable form of methamphetamine hydrochloride called "ice" has increased rapidly. The heaviest use has occurred on the West Coast and in Hawaii. Many regional emergency departments treat more methamphetamine users than cocaine-intoxicated patients. The ease of synthesis from inexpensive and readily available chemicals makes possible the rampant abuse of a dangerous drug that can produce a euphoria similar to that induced by cocaine. Clinicians should be familiar with the medical effects and treatment of acute methamphetamine toxicity.

Central Nervous System Diseases↗
PubMed1987

[Preventive effect of dipropylacetamide in bipolar manic-depressive psychoses].

Dipropylacetamide (DEPAMIDE) was administered to 60 patients with bipolar manic-depressive psychoses. The dosage was 900 mg per day, administered orally. In 5 (8%) of the patients gastrointestinal disorders were observed. Administration of lithium carbonate results in undesirable side-effects in 50% of the cases. Our clinical experience shows dipropylacetamide to have a considerably slighter toxic effect on the human organism than lithium carbonate. We regard Dipropylacetamide (DEPAMIDE) as a valuable and significant addition in the prophylaxis of affective disorders, notably bipolar manic-depressive psychoses.

Anticonvulsants↗
PubMed1979

[Pharmacotoxic psychoses in patients with neurological disorders during old age (author's transl)].

23.3 per cent out of 180 old patients (age above 60 years, 71 y in the mean) suffering from chronic cerebral disorders (3 large groups of disease) developed pharmacotoxic psychoses. This relative high percentage can be explained by psychotoxic side effects of the modern antiparkinson-therapy. The incidence to psychotoxicity of combined L-Dopa seems to be less marked in patients without Parkinson's disease when compared to patients with progredient nigrostriatal degeneration. Toxic delirium as a result of treatment with antidepressants, diuretics and digitalis was observable only in a few percentage. This occurance was even less pronounced in comparison to acute developing exogene psychoses in the same group of patients when drugs were not administered.

Aged↗
PubMed1975

[Etiology of childhood psychoses].

When studying etiology of childhood psychosis, causes may be divided in biological and psychodynamic. The present paper focuses on the first, which are divided in infectious, toxic, neurologic, endocrine, biochemical and genetic; these last include chromosomic alterations and hereditary factors. The relevant bibliography is reviewed. In spite of a growing list of research work, a single etiologic factor has not been found. It is probable that brain disorder in the psychotic child is psychological, mediated by chemical disturbance and with environmental correlates.

Child↗
PubMed1987

On organically based hallucinatory-delusional psychoses.

In an investigation of 70 chronically mentally ill patients in a district psychiatric hospital, 11 cases were discovered which had been diagnosed up to now as schizophrenia, but could now be diagnosed as being of organic origin. In group 1 (cases 1-6) there are dementive states after toxic, inflammatory or early childhood brain damage and familial epileptic malady with slowly progressive brain atrophy. They were easy to recognize clinically in their organic psychosyndromes, dementia, neurological symptoms and CT findings showing extensive, massive brain damage. In group 2 (cases 7-11), in contrast, there are patients with chronic psychoses of remittent course, with brain findings indicative of centrencephalic damage. On superficial examination they give a schizophrenic picture, but can be differentiated from this by the absence of schizophrenic personality changes and thought disturbances, and also by the form of the hallucinations. These are distinguished by their plastic character, and show the criteria which Schröder had already pointed out 60 years ago for the differentiation of exogenous and endogenous hallucinations.

Aged↗
PubMed1995

Interference with nitric oxide production and action potentiates the antiseizure efficacy of flurazepam.

The effect of inhibiting "downstream" consequences of NMDA receptor stimulation with 7-nitroindazole, an inhibitor of the neuronal form of nitric oxide synthase (NOS), and methylene blue, an inhibitor of the nitric oxide (NO)-sensitive soluble guanylyl cyclase, on electrically precipitated tonic hindlimb extension in mice was studied. Moreover, the abilities of these compounds to potentiate the antiseizure efficacy of flurazepam were also examined. When administered alone, 7-nitroindazole (10.0-100 mg/kg) and methylene blue (1.0-100 mg/kg) did not share the ability of MK-801 (0.1 to 1.0 mg/kg) to antagonize electrically precipitated tonic hindlimb extension. However, doses of MK-801 (0.18 mg/kg), 7-nitroindazole (100 mg/kg), and methylene blue (10.0 and 100 mg/kg) that were devoid of apparent antiseizure efficacy by themselves potentiated the ability of flurazepam to antagonize electrically precipitated seizures. NMDA receptor antagonists cause neuronal toxicity, interfere with acquisition of spatial memory and induction of long-term potentiation in the hippocampal CA1 region, and precipitate psychoses in susceptible individuals. Thus, the development of both open-channel blockers of the NMDA receptor complex that can be administered in lower doses, and inhibitors of the "downstream" consequences of NMDA receptor-gated transient elevations of intraneuronal calcium ions as potential adjunctive antiseizure medications should be considered. Moreover, administration of these compounds with benzodiazepines may attenuate some of the neurotoxicity that may result from NMDA receptor antagonism.

Analgesics↗