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)

Five hundred and seventy nine Chinese patients with schizophrenia who met DSMIV criteria for the disorder were genotyped for alleles epsilon 2,3,4 of apolipoprotein E (APOE) gene. All were recruited from inpatients and outpatients attending a large mental health centre in Shanghai. Results were compared to APOE data on 1528 controls drawn from the same area. Major differences in APOE genotype ratios and allele frequencies were observed between the patients and controls. The patients with schizophrenia had highly significantly (p<0.0001) increased epsilon 4/-genotypes and allele frequencies, and decreased epsilon 3/3 genotypes and epsilon 3 allele frequencies compared to controls. The effect was independent of sex and/or age of onset of illness, but strongly influenced by date of birth. Significant differences were restricted to individuals with schizophrenia born either before 1949 or during the period 1958-1967. Both were times of severe food shortages and malnutrition. We suggest that APOE may operate as an additional risk factor for schizophrenia in individuals subjected to fetal and/or early postnatal malnutrition.
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PMID:Association of APOE gene with schizophrenia in Chinese: a possible risk factor in times of malnutrition. 1283 18

The diagnosis of schizophrenia likely encompasses a heterogeneous group of disorders, complicating the search for its causes. Studies of deficit schizophrenia represent an attempt to reduce this heterogeneity by identifying biologically distinct subgroups. Supplementing clinical phenotypes with biological markers of risk (e.g., eye-tracking and sensory-gating deficits) have also been used to reduce disease heterogeneity. In this study, we examined smooth pursuit eye movements in healthy controls (n = 37), and deficit (n = 18) and nondeficit (n = 32) patients with schizophrenia to determine what aspects of abnormal smooth pursuit are associated with the two patient groups, and which, if any, specifically mark the deficit phenotype. A small sample of relatives of deficit (n = 12) and nondeficit (n = 35) patients was also examined. Positive symptoms were equally present in deficit and nondeficit patients. Subtle, psychotic-like positive traits were also equally present in the relatives of both deficit and nondeficit probands, whereas negative symptoms were significantly more prevalent among the relatives of deficit probands. Deficits in predictive pursuit were present in both patient groups and both groups of relatives. Deficit patients showed significantly lower initiation acceleration. A similar pattern of results was seen in our pilot sample of relatives of deficit patients. These findings suggest that predictive smooth pursuit abnormality is associated with positive symptoms in schizophrenia, and that initiation abnormalities may be associated with the deficit syndrome.
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PMID:Components of the smooth pursuit function in deficit and nondeficit schizophrenia. 1289 56

Twenty-nine patients with DSM-IV diagnoses of schizophrenia were categorized into deficit syndrome (n=14) and non-deficit syndrome (n=15) subgroups on the basis of the Schedule for the Deficit Syndrome. The patients, who had all been free of antipsychotic medication for at least 3 weeks, and 17 sex- and age-matched normal controls were studied with single-photon emission computed tomography with Tc-99m HMPAO. Age at onset, Brief Psychiatric Rating Scale (BPRS) total scores, BPRS positive symptom subscores and duration of illness were similar between the two schizophrenic subgroups. As expected, the deficit patients had more negative symptoms than the non-deficit patients. There were no statistically significant correlations between clinical parameters and regional cerebral blood flow (rCBF) values. The deficit syndrome subgroup showed diminished rCBF in the frontal regions bilaterally, right parietal regions and right superior temporal region compared with the control groups. Deficit patients showed significantly lower rCBF perfusion ratios in the right superior and inferior frontal cortex than did the non-deficit patients. No differences were detected between the controls and the non-deficit schizophrenic patients in terms of rCBF perfusion indices. The results of the present study confirm previous reports of different patterns of rCBF in deficit vs. non-deficit schizophrenic subgroups.
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PMID:A Tc-99m HMPAO SPECT study of regional cerebral blood flow in drug-free schizophrenic patients with deficit and non-deficit syndrome. 1292 8

The aim of this study was to reexamine and compare the characteristics of the deficit and nondeficit schizophrenic patients. This cross-sectional study consisted of 62 in- and out-patients, 18-65 years of age, diagnosed with schizophrenia according to DSM-IV. The sociodemographic variables, premorbid adjustment, clinical course and general functioning level in the past five years were evaluated by utilizing the appropriate sections of Comprehensive Assessment of Symptoms and History (CASH). In addition, GAF, the Schedule for the Deficit Syndrome (SDS), Positive and Negative Syndrome Scale (PANSS), Montgomery Asberg Depression Scale (MADRS), the Neurological Evaluation Scale (NES) and the Simpson Angus Extrapyramidal Side Effects (EPS) Rating Scale, Trail A and B, Verbal Fluency, Stroop, Block Design and Finger Tapper tests were administered. Using the SDS, 19 patients (30.6 %) were categorized as deficit; 43 (69.4 %) were categorized as nondeficit. The deficit patients were worse on the Functioning During Past Five Years score of CASH. The PANSS and MADRS mean scores were not significantly different between the two groups, except a higher level of negative symptoms observed in the deficit group. NES scores were also significantly higher in the deficit group. However, sociodemographic and other clinical variables, neurocognitive measures and EPS symptoms did not show any significant difference between the two groups. Our findings suggest that the deficit schizophrenia is a distinct subgroup comprised of patients who have more negative symptoms, neurological impairment and poor functioning which may have a common underlying pathology.
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PMID:Reexamination of the characteristics of the deficit schizophrenia patients. 1450 90

Clinical and experimental evidence suggest an involvement of dopamine systems, mainly the mesocorticolimbic one (MCL), in Attention-Deficit Hyperactivity Disorder (ADHD). However, it remains to be ascertained whether the systems are hyper- or hypo-functioning, for the implications of the functional state. Indeed, differential functional states of the MCL branches are suggested to be the neural substrate of different ADHD variants. This review covers published and unpublished data from the Naples-High Excitability (NHE) rat, an animal model of ADHD, featuring its main aspects, with no hypertension. Therefore, a multiple approach based on morphological studies of dopamine, norepinephrine, glutamate, acetylcholine and GABA systems, synaptic (Calcium/Calmodulin kinase II) and extrasynaptic (chondroitin sulphates) environments, and molecular biology and pharmacological studies on the dopamine system has been carried out. Morphological findings suggest dopamine neurons in the Ventral Tegmental Area (VTA) to be hypertrophic in NHE rats. The mesostriatal and mesolimbic dopamine branches appear to be normal in basal conditions. However, the striatal interface is probably defective following activation. Conversely, the prefrontal cortex, which represents the second main target of VTA dopamine neurons, has many alterations at the basal level. Therefore, the emerging picture is the association of a hyperinnervating and hyperfunctioning mesocortical branch of the dopamine system. Thus, the evidence gathered so far might improve our understanding of the neural substrates of neuropsychiatric disorders such as ADHD, schizophrenia and drug addiction.
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PMID:Behavioural, pharmacological, morpho-functional molecular studies reveal a hyperfunctioning mesocortical dopamine system in an animal model of attention deficit and hyperactivity disorder. 1462 12

The deficit syndrome is a promising distinction within schizophrenia that requires further validation. This study examined the replicability of differences in clinical symptoms, neurocognitive functioning, affect perception, and social functioning previously reported among deficit (n=15) and nondeficit syndrome (n=30) schizophrenia patients classified according to the Schedule for the Deficit Syndrome (SDS; Psychiatry Res. 30 (1989) 119) and nonpatient controls (n=41). Additionally, participants completed self-report affective trait measures of positive affectivity, negative affectivity, and social anhedonia to examine the deficit syndrome concept of diminished emotional range. We were able to replicate symptom profiles and neurocognitive and social functioning impairments in deficit vs. nondeficit patients, but did not find more severe affect perception impairment in deficit vs. nondeficit patients as previously reported. Regarding range of subjectively experienced emotion, deficit patients reported lower trait positive affectivity and marginally higher social anhedonia than nondeficit patients and controls, but also reported elevations in negative affectivity that were similar to nondeficit patients as compared to controls. While replication of patterns of impairment across multiple domains of functioning supports the validity of the deficit syndrome, results also suggest that SDS-defined deficit patients may be characterized by a relative reduction in the tendency or ability to experience positive emotions, rather than a pervasive diminution in the range of emotional experience.
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PMID:Neurocognitive, social, and emotional dysfunction in deficit syndrome schizophrenia. 1463 Mar 5

Epidemiological studies suggest that prenatal malnutrition increases the risk of developing schizophrenia. Animal models indicate that prenatal protein deprivation (PPD) affects many aspects of adult brain function. We tested the hypothesis that PPD in rats would alter prepulse inhibition (PPI), which is an operational measure of sensorimotor gating that is deficient in schizophrenia patients. Additionally, we examined dopaminergic and glutaminergic receptor binding in the striatum and hippocampus, which have been suggested to play a role in the etiology of schizophrenia. Rat dams were fed normal (25%) or low (6%) protein diets beginning 5 weeks prior to, and throughout pregnancy. The pups were tested at postnatal days (PND) 35 and 56 for PPI. Striatal and hippocampal NMDA receptor, and striatal dopamine receptor binding were quantified post-mortem in a subset of these rats. Female rats exposed to PPD had reduced levels of PPI at PND 56, but not PND 35, suggesting the emergence of a sensorimotor gating deficit in early adulthood. Striatal NMDA receptor binding was increased in PPD females. A decrease in initial startle response (SR) was also observed in all PPD rats relative to control rats. These results suggest that PPD causes age- and sex-dependent decreases in PPI and increases in NMDA receptor binding. This animal model may be useful for the investigation of neurodevelopmental changes that are associated with schizophrenia in humans.
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PMID:Prenatal protein deprivation in rats induces changes in prepulse inhibition and NMDA receptor binding. 1469 97

The deficit syndrome is thought to be specific to and a subtype of schizophrenia; however, there are scarce or no data on the prevalence and characteristics of this syndrome in non-schizophrenic psychoses. The aim of this study was to explore the prevalence and correlates of different types of negative symptoms (NegS) in a mixed sample of psychotic disorders. Six-hundred and sixty psychotic inpatients were classified according to the presence and type of NegS into the following groups: no NegS, transitory NegS, persistent secondary NeS, persistent doubtful secondary NegS, and persistent primary NegS (i. e., deficit symptoms). Furthermore, the nosological status of this symptom classification such as its clinical and etiological correlates were examined. Depending on the diagnostic criteria used for diagnosing schizophrenia, the prevalence of the deficit syndrome in schizophrenia and in non-schizophrenic psychoses ranged from 14%-32% and 2%-22%, respectively. Deficit syndromes in both schizophrenic and non-schizophrenic patients shared most of the syndrome-related clinical features. Regarding the associated clinical pattern, the transitory NegS group was closer to the group without NegS than to the groups with enduring NegS. Patient groups with enduring primary and enduring secondary NegS did not show relevant clinical or etiological differences, thus, suggesting that the primary versus secondary issue may be less relevant than previously acknowledged. The deficit syndrome may be diagnosed irrespective of the specific categories of psychotic disorders.
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PMID:The deficit syndrome of the psychotic illness. A clinical and nosological study. 1520 70

Impaired premorbid functioning prior to the onset of acute psychosis has frequently been noted in schizophrenia. This study examined retrospectively the premorbid status of patients in their first episode of psychosis in order to determine relationships with baseline symptoms, treatment response, and medication side effects. One hundred eleven schizophrenic and schizoaffective patients participating in a large prospective study of first episode schizophrenia were evaluated with the Premorbid Adjustment Scale (PAS). Premorbid functioning in males became progressively worse over time. Deficit state patients exhibited worse premorbid functioning. A third of patients exhibited sustained poor premorbid functioning. At various developmental stages, lower "sociability and withdrawal" scores correlated with increased time to treatment response, more severe negative symptoms, increased drug-induced parkinsonism, and deterioration of premorbid functioning. Various mean PAS scores predicted susceptibility to tardive dyskinesia. Our findings suggest that prior to acute psychosis onset there are certain behavioral precursors reflected in premorbid functioning that may predict subsequent illness manifestations. Measures of premorbid functioning indicate that disease pathogenesis is manifest, albeit more subtly, prior to presentation of first psychotic symptoms.
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PMID:Premorbid functioning in schizophrenia: relation to baseline symptoms, treatment response, and medication side effects. 1527 45

Dissociative disorder is well-known in adulthood but in many cases it begins in childhood where it is usually not taken into consideration, rarely diagnosed, and often mistaken with borderline disorders. In childhood dissociation is well-defined: in a dimensional way by the presence of the dissociation symptoms over 2 SD and in a categorial view by the presence of primary symptoms. We made a psychiatric assessment on a child aged 11 years and 7 months, who said he heard "voices in his head". The assessment included: Children Dissociative Checklist (CDC), Adolescent Dissociative Experience Scale (A-DES), Children Depression Inventory (CDI), Wechsler Intelligence Scales for Children-Revised (WISC-R), Strength and Difficulties Questionnaire (SDQ), Children Behaviour Check-list (CBCL), (Scale Disturbi Attenzione Genitori, parent attention deficit scale, SDAG), Parent Conners Questionnaire, free conversation, a drawing, a neurological examination, an EEG-Holter and a semistructured psychiatric interview: K-SADS PL 1.0. SDQ, CDI and CBCL showed pathological scores in every area. K-SADS PL 1.0 excluded schizophrenia and showed: attention deficit, disthymic disorder, generalized anxiety disorder, oppositive-defiant disorder and conduct disorder with rage episodes, like borderline disorder. I.Q. was 76, SDAG (total 46) and Conners (mean points 1.81) showed a high score, simulating Attention Deficit with Hyperactivity disorder (ADHD). The presence of primary symptoms, like dissociative amnesia and very high scores in CDC (23, mean score for MPD) and in A-DES (85, mean 4.2) are useful for diagnoses. Dissociative disorder also exists in childhood, but it should be differentiated from ADHD and borderline disorder.
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PMID:Dissociative disorder in children. A case study. 1545 42


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