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)

Electroconvulsive therapy (ECT) in the treatment of schizophrenia was evaluated in a double-blind trial; the clinical change after ECT was compared with that after a treatment procedure identical to it but for two exceptions--no electricity was used and no convulsion was induced. All patients had paranoid schizophrenia according to Present State Examination criteria and all received standard doses of neuroleptics for at least 2 weeks before random assignment to the two groups. 20 patients completed the trial: 10 had ECT and 10 were in the control group. Treatment was given three times a week, with a minimum of eight treatments and a maximum of twelve. Clinical change was assessed by the Comprehensive Psychiatric Rating Scale. Both groups improved but the improvement of patients receiving ECT was significantly greater than that of controls both after six treatments (p=0.02) and at the end of treatment (p=0.004). Thus the group receiving ECT gained a clear and early advantage compared with the control group, although by 16 weeks there was little difference between the two groups. Possible reasons for this are discussed.
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PMID:ECT for schizophrenia. 610 72

Tryptamine (Try), 5-methoxytryptamine (5MeOT), N-methyltryptamine (N-Met), 5-methoxy-N,N-dimethyltryptamine (5MeODMT) and N,N-dimethyltryptamine (DMT) are metabolites of the neurotransmitter 5-hydroxytryptamine (5HT). The cisternal cerebrospinal fluid (CSF) is probably a suitable biological material for investigating the problem of indolamine metabolism in schizophrenic patients. As part of a biological research programme on schizophrenia we have investigated concentrations of cisternal CSF indolamines in a group of acute paranoid patients in comparison with psychiatrically healthy controls. The concentrations of indolamines in the cisternal CSF reveal that psychotomimetic indolamines like 5MeODMT, 5MeOT and DMT and the indolamines N-Met and Try are present in psychological and pathological states. The patients suffering from acute paranoid schizophrenia have high or very high levels of the investigated indolamines in comparison with healthy controls, but there are significant individual differences in the group of these patients. The search for correlations between the level of a single indolamine and individual psychopathological symptoms could provide more specific information for diagnosis or treatment.
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PMID:[Methylated and unmethylated indolamine in the cisternal fluid in acute endogenous psychoses]. 614 8

When amphetamines are administered to humans every few hours for several days, either during the 'speed runs' of addicts or in controlled laboratory settings, the psychosis which reliably results is similar to paranoid schizophrenia in a number of important aspects. This unique regimen of drug intake, which involves the continuous presence of stimulants over a prolonged period of time, can be simulated in animals using subcutaneously implanted slow-release silicone pellets containing d-amphetamine base. Monkeys and rats implanted with these pellets develop stages of behavioural alterations which are somewhat similar in sequence to those observed in humans who have received frequent doses of amphetamine. An initial period of hyperactivity and exploratory behaviour is followed by the gradual development of motor stereotypies which become virtually incessant. A period of relative inactivity then appears which is followed, at 4-5 days after pellet implantation, by a late stage. This final stage is characterized by 'wet-dog' shakes, parasitotic-like grooming episodes, and a variety of other forms of hallucinatory-like behaviour. At about the same time there are distinctive and partially irreversible alterations in dopaminergic innervations of the caudate nucleus, but not in mesolimbic dopamine innervation of the nucleus accumbens or in several other neurotransmitter systems. Continuous amphetamine administration may reproduce some aspects of the prolonged excitation which accompanies an acute psychotic episode and may be a fruitful model for the clarification of the dopamine theory of schizophrenia.
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PMID:Continuous amphetamine intoxication: an animal model of the acute psychotic episode. 632 Feb 47

Recently, increased brain and spinal fluid (CSF) norepinephrine (NE), and a decreased cAMP response to prostaglandin E1 (PgE1) stimulation of platelet NE sensitive adenylcyclase were observed in some schizophrenic patients. Low CSF dopamine-beta-hydroxylase (DBH) activity was related to brain atrophy, whereas high plasma DBH was associated with tardive dyskinesia. Increased NE (in brain and CSF) and 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels and decreased plasma DBH activity in the brain were associated with a diagnosis of paranoid schizophrenia. Impaired NE transmission in schizophrenia may relate to disturbances in the autonomic nervous system, deficits in attention and information processing and to an impaired ability to deal with stress. Although pharmacological studies have suggested a major role for dopamine (DA) in schizophrenic psychosis, this review indicates the need for further exploration of the NE system. Future studies should address the relationship with DA, the autonomic nervous system (ANS), cerebral blood flow, brain metabolism, stress response, negative and prodromal symptoms.
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PMID:Impaired noradrenergic transmission in schizophrenia? 632 3

Studies of the segregation of major psychiatric disorders in families are consistent with multiple threshold polygenic models rather than with major locus transmission. This does not however rule out the possibility of identifying major locus traits that correlate with disease susceptibility. One approach has been to ascertain the degree of association between well characterized genetic markers and psychiatric disorders. The theory and methodology of such association and linkage studies are reviewed. The results of such studies lead to the conclusion that the association of ABO and HLA subtypes with affective disorders and schizophrenia is extremely variable, although there may be an association between HLA A9 and paranoid schizophrenia. The alternative strategy has been to identify specific genetically transmitted traits which are associated with disorders, and so could represent potential etiological factors. A review of these studies points to the potential usefulness of cholinergic and GABA markers for susceptibility to affective disorders. CT scan traits and attentional variables appear to be the most promising indicators of susceptibility to schizophrenia. cDNA probes in restriction enzyme digests for regularly spaced polymorphisms, and restriction fragment length polymorphisms offer the promise of a radical expansion in the number of markers available for linkage studies.
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PMID:Association and linkage studies of genetic marker loci in major psychiatric disorders. 637 2

The Syndrome Check List (SCL) as detailed by Wing et al. (1) was used on patients belonging to various cultural groups admitted to a London hospital. On the basis of combined Catego diagnosis of schizophrenia and paranoid schizophrenia the frequency of patients with first rank symptoms (FRS) for each group was calculated. It was found that the frequencies of FRS showed cultural differences and that these differences were less when groups were relatively culturally similar. These findings are compared with findings elsewhere. The clinical dilemma presented by these findings is discussed.
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PMID:A cross-cultural study of the frequencies of Schneider's first rank symptoms of schizophrenia. 652 19

Sixty-two Dutch patients with the diagnosis paranoid schizophrenia (SCH) were HLA-A-, -B- and -C-typed. An increase in the frequencies of A9 (P = 0.02, relative risk 1.8) and B5 (P = 0.04, relative risk 1.9) was found. Although these correlations do not remain significant after correction for the number of antigens tested, both findings confirm other data from the literature, including the first published report from a population in Sweden. From all hitherto published literature data, the combined relative risks for A9 and B5 is significantly increased. These data strongly indicate that the distribution of HLA antigens among SCH patients is different from the control population.
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PMID:A search for association of HLA antigens with paranoid schizophrenia. A9 appears as a possible marker. 657 23

In a genetic study of the first-degree relatives of 77 patients with delusional (paranoid) psychoses, the morbidity risks for schizophrenia, affective disorders, and atypical psychoses were evaluated using ICD-9 criteria. The prevalence of schizophrenia was 3.10 percent (4.12 percent with age correction to 40 years and 4.94 percent with age correction to age 60), which is higher than in investigations of paranoid psychoses, but lower than in studies of paranoid schizophrenia. The prevalence figure for affective disorders (age-corrected 3.04 percent for unipolar plus bipolar patients) is also intermediate to those for relatives of paranoid schizophrenics and paranoid psychotics. When the 77 index delusional patients were subdivided into axial syndromes (endogenomorphic-schizophrenic, endogenomorphic-cyclothymic, and organomorphic axial syndromes), two very homogeneous subgroups emerged. The endogenomorphic-schizophrenic subgroup showed high rates of schizophrenic secondary cases, whereas the endogenomorphic-cyclothymic subgroup showed high rates of affectively disordered secondary cases. The third organomorphic subgroup showed a high prevalence of atypical psychoses among first-degree relatives. Thirty-seven of the 77 index patients could not be assigned to any axial syndrome; their first-degree relatives had an increased prevalence of schizophrenia, but affective disorders were no more frequent than in the normal population. These data suggest that the heterogeneous group of paranoid psychoses can be meaningfully subdivided by use of axial syndromes which are viewed as representing "basic" disturbances underlying delusional symptomatology.
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PMID:The genetics of delusional psychoses. 665 92

The results of experimental psychological examinations of the activating and protective functions of the level of ambitions in three groups of subjects (70 patients with moderately progressive shift-like and paranoid schizophrenia with a pronounced defect, 70 patients suffering from schizophrenia with an unmarked defect and 70 healthy controls) are presented. The study demonstrated that in schizophrenic patients with a marked defect as compared with healthy subjects and schizophrenics without any prominent defect, there is a decrease in the activating and an increase in the protective function of the level of ambitions which is considered as one of the mechanisms and signs of adynamia.
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PMID:[Experimental psychological study of the functions of the aspiration level of schizophrenic patients]. 666 59

A lateral deficit explanation of schizophrenic cognition maintains that a left hemisphere deficit is characteristic of nonparanoid schizophrenia whereas right hemispheric deficits may be common in paranoid schizophrenia. An alternate explanation postulates an interhemispheric deficit in schizophrenic functioning. A major piece of evidence for this position is Beaumont and Dimond's oft-cited experiment matching pairs of stimuli presented to left, right, and both hemispheres (Beaumont, J. G., and Dimond, S. J. Brain disconnection and schizophrenia. Br. J. Psychiatry, 123: 661-662, 1973). We expanded upon this study and found left hemisphere deficits and interhemisphere deficits in schizophrenics. However, the type of deficit seemed directly related to the distinction of a paranoid-nonparanoid schizophrenic diagnosis. Paranoids match stimuli in all hemisphere conditions as well as control groups. Nonparanoid schizophrenics, on the other hand, had their greatest problem on all stimuli in the left hemisphere. Their right hemisphere performance was not different from other groups. The nonparanoid also exhibited problems in interhemispheric matching, but this seemed due to an impaired left hemisphere. Results, therefore, did not support an interhemisphere transfer deficit. A discussion of prior work suggests that the nonparanoid schizophrenic has a problem in serial processing in the left hemisphere.
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PMID:Brain disconnection, schizophrenia, and paranoia. 682 51


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