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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is considerable similarity between paranoid schizophrenia and psychoses provoked by dopaminergic overstimulation in the central nervous system. The fact that neuroleptics are able to block dopaminergic neural activity has led to the hypothesis that there might exist a common biochemical substrate for schizophrenia and e. g. the amphetamine psychoses. Dopaminergic overstimulation may be elicited by different drugs interacting with the dopamine metabolism e. g. dopamine-beta-hydroxylase inhibition (disulfiram, fusaric acid); monoamine-oxidase-inhibition (phenelzine, tranylcypromine); dopamine release (amphetamine); stimulation of postsynaptic dopamine receptors (bromocriptine, apomorphine). Resulting psychotic symptoms consist of ideas of reference, delusions, visual and acustic hallucinations in a clear setting of consciousness. Psychoses occur usually in subjects, who have suffered from various psychiatric illnesses, which have apparently in common a reduced monoamine-oxidase activity in platelets. It is concluded from various biochemical findings, that psychoses resulting from dopaminergic overstimulation and schizophrenia have different biological substrates.
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PMID:[Psychotropic drugs as tools for clinical research into schizophrenia (author's transl)]. 2 31

In 20 psychotic patients with frequent hallucinations and/or actual delusional experience a possible antipsychotic action of the opiate antagonist naloxone (N-allyl-noroxymorphone) was investigated, using a double-blind placebo-controlled cross-over design. 18 of these patients were not treated with neuroleptic drugs; 13 suffered from an acute episode of schizophrenia. Psychopathological changes were assessed by the use of the IMPS-scale and of a symptom-specific rating scale (VBS). Intravenous injection of naloxone (in most cases 4.0 mg) induced a reduction of psychotic symptomatology (especially hallucinations) in the majority of patients. Compared with placebo this effect reached statistical significance within 2-7 hours after injection. From this result a possible involvement of endogenous ligands of opiate receptors in the pathogenesis of schizophrenia may be concluded.
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PMID:Indication of an antipsychotic action of the opiate antagonist naloxone. 3 Jan 1

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.
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PMID:Psychopharmacological treatment of psychotic children. A survey. 3 38

The antipsychotic drugs have provided effective and relatively safe treatment of schizophrenia, paranoid illnesses, and manic-depressive conditions marked by psychotic features. These agents are sometimes called "neuroleptic," as virtually all produce signs of extrapyramidal neurologic disorders in addition to their antipsychotic actions; in part, evidently, the neuroleptic effects are an artifact of the means of screening of potential new agents. These agents have a strong and selective antagonistic action on synaptic mechanisms in the brain mediated by dopamine as a neurotransmitter. This antidopamine action almost certainly contributes importantly to their parkinsonism effect (basal ganglia) and their prolactin-elevating (hypothalamic) effect; in addition, antipsychotic actions may be mediated by antidopamine effects, possibly in limbic and other forebrain centers.
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PMID:The "neuroleptic" antipsychotic drugs. 1. Mechanisms of action. 3 41

The long-term course or natural history of schizophrenia is correlated with differing diagnostic criteria and commonly agreed upon prognostic variables. A review of 38 long-term followup studies of hospitalized schizophrenics reveals that unspecified or Kraepelinian-type schizophrenia has a much worse prognosis than atypical schizophrenia, schizoaffective psychosis, reactive psychosis, or other good premorbid types. Diagnoses based on longitudinal as well as cross-reactional data are more predictive of outcome than cross-sectionally based diagnoses. Drug and psychosocial treatment results must be evaluated in terms of prognostic variables, many of which are incorporated in some currently employed diagnostic criteria. There is no firm evidence that maintenance medication is indicated in some good prognosis patients. The paucity of long-range followups, the inadequacies of outcome assessments, and diagnostic disagreements limit our understanding of the effects of drug treatment, a treatment which is not without dangerous neurological side effects in many patients.
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PMID:Long-term prognosis and followup in schizophrenia. 3 8

Catastrophe theory is a new mathematical technique relating variables in a novel, discontinuous way. It suggests ways in which neurochemical and environmental influences could interact so that very small changes in either variable may produce rapid changes in intensity of psychosis that are characteristic of schizophrenia. Other behavioural and pharmacological characteristics of schizophrenia previously considered paradoxical may be similarly explicable, and the model predicts factors most likely to generate relapse.
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PMID:Catastrophe theory: a model interaction between neurochemical and environmental influences in the control of schizophrenia. 3 5

Two catecholamine-containing pathways, the locus ceruleus system and the dopamine neurons arising from the ventral mid-brain, may be involved in reward. Dopamine neurons function as a system for energizing the organism's responses and directing them toward significant environmental stimuli, but the functions of the locus ceruleus system remain obscure. It appears increasingly likely that neuroleptic drugs exert their anti-psychotic effects in acute schizophrenia by blocking dopamine receptors, although the time course of the effect suggests that the mechanism is more complex than a simple reversal of a neurohumoral imbalance. Evidence from postmortem studies suggests that, at least in the chronic state, dopamine turnover is not increased, but that there may be an increase in postsynaptic receptor density in some cases, including some patients who apparently had not received medication in the year before death. The evidence is consistent with Olds and Travis' conjecture that "counteraction of positive feedback processes subserving positive reinforcement mechanisms may be a key to control of certain psychotic episodes".
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PMID:Catecholamine reward pathways and schizophrenia: the mechanism of the antipsychotic effect and the site of the primary disturbance. 3 90

Sleep disturbances in psychoses can mean hypo- as well as hypersomnia. In 90% of endogenous depressed patients sleep disturbances were seen, mostly as hyposomnia. In the group of schizophrenic psychotic patients only 30% had sleep disturbances. With polygraphical investigations in endogenous depressed patients a shortening of REM-latency and a disturbed sleep profile, in schizophrenic psychoses a shortened REM-rebound and a reduced amount of stages 3 and 4 were found. The treatment of choice for depressions are antidepressive drugs and sleep deprivation, for schizophrenic psychoses neuroleptic drugs. This treatments improved subjective and objective sleep disturbances with psychopathological remission at the same time. So far, only hypothetical considerations do exist about the relationship between psychopathology and sleep disturbances. It is suspected that etiological relations exist between depression and desynchronization of central sleep mechanisms and between schizophrenia and special disturbances of REM-sleep and stage 3 and 4.
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PMID:[Sleep problems and their treatment in psychosis (author's transl)]. 4 23

The steady rise in the promiscuous use of phencyclidine (PCP) as a "recreational" drug has recently gained nationwide attention because of the numerous violent and/or bizarre incidents caused by the use of this drug. Because the media often exaggerate reports of bizarre and violent behavior to make a "good" story, the potential PCP user may be tempted to ignore the media warnings. In the case of PCP, however exaggerated the story, a real danger does exist. So, despite numerous newspaper, radio and television warnings about the possible consequences of PCP use and abuse, the incidence of toxic reactions continues to climb. In many cases PCP is sold as other drugs, particularly THC, and in various colored capsules, tablets, liquids and crystals which may explain the increased usage despite the numerous warnings against its use. The advances in laboratory techniques and chemical processess have enabled the clandestine chemist to prepare relatively pure PCP and thus eliminate many of the toxic side effects due to impurities in the drug. In addition, 30 or more psychoactive PCP analogues have been developed and are starting to make an appearance on the street. PCP is perhaps the most potent psychotomimetic compound known at the present time and is capable of inducing a psychosis which is clinically indistinguishable from schizophrenia. The psychosis-producing effects of PCP are the most common toxic effects seen in hospital emergency rooms; but as the amount of PCP taken and/or the simultaneous involvement of other drugs, particularly barbiturates, occurs, severe medical problems (e.g., coma, seizures, respiratory arrest) begin to appear. Death from high doses of PCP or PCP plus other drugs does occur, but the principal cause of death from PCP abuse is due to trauma, homicide or suicide (usually of the bizarre or violent form). Young adult males, persons predisposed to mental illness and naive drug users appear to be the most susceptible to the adverse effects of PCP. The fact that chronic PCP users are starting to increase in number is mute testimony that not all users experience "bad trips" with PCP. Unfortunately for the user, however, this does not guarantee that the next trip will not be a bad one. The effects of chronic use seem to be twofold: severe depression with suicidal thoughts and numerous violent, agitated behavioral patterns. Neither seems to be a suitable alternative. At the present time there is not specific antidote for toxic PCP reactions and the prolonged psychosis induced in some cases does not appear to respond to the standard antipsychotic medications as quickly as do the functional psychoses. The major improvement from a medical standpoint is the development of more sensitive laboratory techniques to confirm the presence of PCP in body fluids. This advance has undoubtedly led to the apparent increase in the number of PCP cases reported by hospitals and to the accuracy of clinical diagnosis by medical, drug or law enforcement communities...
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PMID:PCP (phencyclidine): an update. 4 8

The model psychosis associated with amphetamine overdosage is known to bear a close resemblance to acute paranoid schizophrenia. Amphetamine is chemically similar to the endogenous sympathomimetic amine, phenylethylamine, which possess many of its pharmacological properties. It is suggested that some cases of schizophrenia may be associated with an abnormal phenylethylamine response, either from increased concentrations of the amine or from abnormal receptor sensitivity to it.
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PMID:Does phenylethylamine cause schizophrenia? 5 86


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