Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic administration of amphetamine to cats (twice daily, in doses increasing from 5 to 15 mg/kg over a 10-day period) elicited a number of behaviors, e.g., limb flick and abortive groom, characteristic of the action of hallucinogenic drugs and dependent on a depression of central serotonergic neurotransmission. This drug treatment produced large decreases (-40 to -60%) in central nervous system serotonin (5-HT) and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA), when measured either 6 or 24 hr after the last amphetamine injection. The rate of limb flicking returned to a predrug level approximately 5 days after drug withdrawal, at which time 5-HT and 5-HIAA levels had returned to within 30 to 40% of base line. Both 5-HT and 5-HIAA returned to base-line levels within 14 days after drug withdrawal. Norepinephrine (NE), dopamine (DA) and DA metabolites were decreased 60 to 95% by chronic amphetamine treatment and showed little recovery within the 14 days after drug withdrawal. A second experiment examined the latency to onset of the behavioral and neurochemical changes with a constant dose of amphetamine (7.5 mg/kg, twice daily). Limb flicking was significantly increased above base-line levels following 3 days of amphetamine administration, at which time 5-HT and 5-HIAA levels were decreased 30 to 40%. NE, DA and DA metabolites were decreased approximately 50 to 90% by this treatment regimen. A third experiment examined the effects of a low dose of amphetamine (3.75 mg/kg), injected more frequently (every 6 hr for 6 days), to approximate the administration pattern in human amphetamine abuse. This treatment produced significant increases in limb flicking and abortive grooming on days 5 and 6 and resulted in 30 to 40% depletions of 5-HT and 5-HIAA. NE, DA and DA metabolites were decreased by approximately 50 to 90%. These data are discussed in relation to a role for serotonin in amphetamine psychosis and schizophrenia.
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PMID:Chronic amphetamine administration to cats: behavioral and neurochemical evidence for decreased central serotonergic function. 50 68

Animals treated with high doses of amphetamines have been used as a model of schizophrenia due to the similarities between the psychosis associated with this mental disorder and that induced by chronic amphetamine abuse. When administered to naive rats in high doses, the amphetamine-like CNS stimulant methamphetamine produces drastic alterations in the neurochemical parameters of the neostriatal monoaminergic systems. These alterations are characterized by a decrease in the activities of the rate-limiting enzymes for dopamine and serotonin synthesis, as well as a decrease in the concentrations of both neurotransmitters and their metabolites. However, tolerance develops to these neurochemical effects when drug administration occurs in a pattern similar to that encountered during chronic amphetamine abuse. The results indicate that the neurochemical alterations produced by amphetamines in naive and tolerant animals differ widely. This suggests that the administration of high doses of amphetamine-like central stimulants to naive rats may not be an appropriate model for studying the neurochemical changes associated with psychosis and amphetamine abuse.
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PMID:Methamphetamine-induced depression of monoamine synthesis in the rat: development of tolerance. 257

A series of 33 patients with combined (injurious) sleepwalking, sleep terrors, and rapid eye movement (REM) sleep behavior disorder (viz. "parasomnia overlap disorder") was gathered over an 8-year period. Patients underwent clinical and polysomnographic evaluations. Mean age was 34 +/- 14 (SD) years; mean age of parasomnia onset was 15 +/- 16 years (range 1-66); 70% (n = 23) were males. An idiopathic subgroup (n = 22) had a significantly earlier mean age of parasomnia onset (9 +/- 7 years) than a symptomatic subgroup (n = 11) (27 +/- 23 years, p = 0.002), whose parasomnia began with either of the following: neurologic disorders, n = 6 [congenital Mobius syndrome, narcolepsy, multiple sclerosis, brain tumor (and treatment), brain trauma, indeterminate disorder (exaggerated startle response/atypical cataplexy)]; nocturnal paroxysmal atrial fibrillation, n = 1; posttraumatic stress disorder/major depression, n = 1; chronic ethanol/amphetamine abuse and withdrawal, n = 1; or mixed disorders (schizophrenia, brain trauma, substance abuse), n = 2. The rate of DSM-III-R (Diagnostic and Statistical Manual, 3rd edition, revised) Axis 1 psychiatric disorders was not elevated; group scores on various psychometric tests were not elevated. Forty-five percent (n = 15) had previously received psychologic or psychiatric therapy for their parasomnia, without benefit. Treatment outcome was available for n = 20 patients; 90% (n = 18) had substantial parasomnia control with bedtime clonazepam (n = 13), alprazolam and/or carbamazepine (n = 4), or self-hypnosis (n = 1). Thus, "parasomnia overlap disorder" is a treatable condition that emerges in various clinical settings and can be understood within the context of current knowledge on parasomnias and motor control/dyscontrol during sleep.
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PMID:A parasomnia overlap disorder involving sleepwalking, sleep terrors, and REM sleep behavior disorder in 33 polysomnographically confirmed cases. 945 62

The authors conducted questionnaire surveys utilizing model cases with the aim of investigating the current views of psychiatrists regarding criminal responsibility judgments in forensic psychiatric evaluations. Six model cases-injury by a person with acute schizophrenia, indecent assault by a person with chronic schizophrenia, attempted murder by a woman with depression, arson by an alcohol abuser, burglary by an amphetamine abuser, rape and indecent assault by a person with personality disorder-were presented to 345 psychiatrists, who were asked about criminal responsibility and appropriate treatment for each of the cases. One hundred eighty-five of the psychiatrists responded. In the case of acute schizophrenia with hallucination and delusion, the case of severe depression, and the personality disorder case, there was a high level of agreement between the evaluations of criminal responsibility made by the different respondents, but in the case of chronic schizophrenia, the case of alcohol-induced psychotic disorder, and the case of amphetamine abuse, there were variations in the evaluation of criminal responsibility, with many respondents emphasizing the patient's symptoms and condition at the time of the offense, and relatively few emphasizing whether the disorder was endogenous. Regarding the form of treatment, many of the respondents recommended compulsory hospitalization for the case of acute schizophrenia with hallucination and delusion, while at the same time recommending treatment in a prison environment for the personality disorder case. In contrast, for the case of chronic schizophrenia and the case of alcohol-induced psychotic disorder, opinion was divided as to whether the subject should be handled with a medical or a judicial approach. Regarding treatment for the case of alcohol-induced psychotic disorder and the case of amphetamine abuse, there was a tendency to make a judgment based on the subject's condition at the point of psychiatric evaluation, which was not necessarily linked to the criminal responsibility.
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PMID:[A questionnaire survey on judgment of criminal responsibility]. 1598 19

Amphetamine abuse may lead to a psychotic state, its symptomatology being very similar to what is seen in paranoid schizophrenia. Failure of attentional inhibition of irrelevant information is thought to be associated with the psychotic symptoms in schizophrenia. Negative priming (NP) paradigm is believed to measure this impairment. Several studies have shown impaired NP in schizophrenia. In the present study a spatial NP task was used to assess attentional inhibition in a group of amphetamine-induced psychosis patients. Nineteen patients with amphetamine-induced psychotic disorder and 20 healthy subjects participated in this study. Severity of psychotic symptoms was measured prior to testing using the Brief Psychiatric Rating Scale (BPRS). Patients showed no deficit in NP, and the amount of their NP effect was not significantly different from healthy subjects. Besides, we did not find any correlation between the amount of NP effect and severity of symptoms. Our results may indicate that cognitive mechanisms underlying NP might not be affected in amphetamine psychosis.
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PMID:Negative priming in amphetamine psychosis. 2377 94