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

Some recent family studies have shown that the familial risk for schizophrenia is higher in female than in male schizophrenics. It is debated whether the risks for the other disorders, such as schizotypal personality disorder or affective disorders in families of schizophrenics are similarly influenced by the proband's gender. Also, the reason for the effect of proband's gender on the recurrence risk for schizophrenia has not been clarified. This family study (159 probands, 589 first degree relatives) confirms that schizophrenia, but also schizophrenia spectrum disorders were more frequent in families of female compared with male schizophrenics. Neither age at onset in probands nor the interaction between gender and age at onset in probands had a relevant impact on the risk figures in relatives. Affective disorders occurred in families independently of the probands' gender. Aetiological heterogeneity or ascertainment bias may account for the modifying effect of proband's gender in schizophrenia.
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PMID:The impact of gender and age at onset on the familial aggregation of schizophrenia. 849 97

Genetic analysis of schizophrenia and schizotypal personality disorder (SPD) was conducted on two pedigree samples. The results are interpreted in terms of a multifactorial threshold (MFT) model. A high rate of schizophrenia was found in relatives of both samples, but any excess of SPD was found only in relatives of the SPD sample. Based on these data, the hypotheses assuming a single liability with two thresholds (Reich's model) and different liability (Smith's model) for both disorders were rejected. The coefficient of genetic correlation is 0.61. Our data suggest that schizophrenia and SPD are separate nosological entities and that some of the factors which constitute liability to SPD influence the development of schizophrenia, but not vice versa.
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PMID:Relatedness of schizotypal personality to schizophrenic disorders: multifactorial threshold model. 851 86

We attempted to identify a locus for schizophrenia and related disorders in 24 nuclear families of schizophrenic probands using a predefined classification system for affected cases that included those disorders most clearly identified as sharing a genetic relationship with schizophrenia--schizoaffective disorder and schizotypal personality disorder. Initially, we evaluated 8 markers on chromosome 5 on the first 12 families with available genotyping and diagnostic assessments and, assuming autosomal dominant transmission, found a lod score of 2.67 for the D5S111 locus (5p14.1-13.1) in one large nuclear family (no. 17; sibship: n = 12; schizophrenia: n = 3; schizotypal personality disorder: n = 2); the other 11 families were much smaller, less complete, and provided little additional information. Other branches of no. 17 were then assessed and the 2-point lod score for family 17 rose to 3.72; using multipoint analysis the lod score in 17 was 4.37. When only schizophrenia was used to define affectedness, the positive evidence for linkage to D5S111 was greatly reduced. Sensitivity analysis indicated that the lod score is heavily dependent upon the predefined diagnostic criteria. Our studies of other families of schizophrenic probands eventually totalled 23, but linkage to D5S111 in these yielded a -2.41 lod score. The results provide evidence for genetic linkage of the D5S111 locus to schizophrenia and related disorders in one family. It may be of interest that over several generations, almost all the ancestors of family 17 could be traced back to a small, relatively isolated, hill region of Puerto Rico.
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PMID:Evidence of a locus for schizophrenia and related disorders on the short arm of chromosome 5 in a large pedigree. 872 43

Large samples of multiplex pedigrees will probably be needed to detect susceptibility loci for schizophrenia by linkage analysis. Standardized ascertainment of such pedigrees from culturally and ethnically homogeneous populations may improve the probability of detection and replication of linkage. The Irish Study of High-Density Schizophrenia Families (ISHDSF) was formed from standardized ascertainment of multiplex schizophrenia families in 39 psychiatric facilities covering over 90% of the population in Ireland and Northern Ireland. We here describe a phenotypic sample and a subset thereof, the linkage sample. Individuals were included in the phenotypic sample if adequate diagnostic information, based on personal interview and/or hospital record, was available. Only individuals with available DNA were included in the linkage sample. Inclusion of a pedigree into the phenotypic sample required at least two first, second, or third degree relatives with non-affective psychosis (NAP), one whom had schizophrenia (S) or poor-outcome schizo-affective disorder (PO-SAD). Entry into the linkage sample required DNA samples on at least two individuals with NAP, of whom at least one had S or PO-SAD. Affection was defined by narrow, intermediate, and broad criteria. The phenotypic sample contained 277 pedigrees and 1,770 individuals and the linkage sample 265 pedigrees and 1,408 individuals. Using the intermediate definition of affection, the phenotypic sample contained 837 affected individuals and 526 affected sibling pairs. Parallel figures for the linkage sample were 700 and 420. Individuals with schizophrenia from these multiplex pedigrees resembled epidemiologically sampled cases with respect to age at onset, gender distribution, and most clinical symptoms, although they were more thought-disordered and had a poorer outcome. Power analyses based on the model of linkage heterogeneity indicated that the ISHDSF should be able to detect a major locus that influences susceptibility to schizophrenia in as few as 20% of families. Compared to first-degree relatives of epidemiologically sampled schizophrenic probands, first-degree relatives of schizophrenic members from the ISHDSF had a similar risk for schizotypal personality disorder, affective illness, alcoholism, and anxiety disorder. With sufficient resources, large-scale ascertainment of multiplex schizophrenia pedigrees is feasible, especially in countries with catchmented psychiatric care and stable populations. Although somewhat more severely ill, schizophrenic members of such pedigrees appear to clinically resemble typical schizophrenic patients. Our ascertainment process for multiplex schizophrenia families did not select for excess familial risk for affective illness or alcoholism. With its large sample ascertained in a standardized manner from a relatively homogeneous population, the ISHDSF provides considerable power to detect susceptibility loci for schizophrenia.
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PMID:Irish study on high-density schizophrenia families: field methods and power to detect linkage. 872 45

There is evidence that some schizophrenic patients have deficits on tests of cognitive function, particularly tests of executive function, including the Wisconsin Card Sorting Test (WCST) and the Trail-making Test, Part B. This study was conducted to determine the generalizability of these findings across the schizophrenia spectrum to schizotypal personality disorder (SPD). Forty DSM-III SPD patients, 56 nonschizophrenia-related other personality disorder (OPD) patients, and 32 normal volunteers from two medical centers performed tests of executive function such as the WCST, Trail-making Part B, Stroop Word-Color Test, and Verbal Fluency, as well as tests of more general intellectual functioning such as the Wechsler Intelligence Scale-Revised Vocabulary and Block Design subtests, and Trail-making Part A. SPD patients performed more poorly on the WCST and on Trail-making Part B than did OPD patients or normal subjects; the groups did not differ on tests of general intellectual functioning. SPD patients may share some of the cognitive deficits observed in schizophrenia.
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PMID:Cognitive function and biological correlates of cognitive performance in schizotypal personality disorder. 877 Dec 27

This study examined whether abnormalities in event-related potentials (ERPs), reported in schizophrenia, extend to patients with schizotypal personality disorder (SPD). Auditory ERPs in an oddball paradigm were obtained in 19 SPD patients, 17 schizophrenic patients, and 20 normal control subjects (NCs). Schizophrenic patients had lower P300 amplitude than NCs; the P300 amplitude of SPD patients was intermediate, showing a linear trend but not a significant group difference. P200 amplitudes showed a similar trend. SPD patients had N100 and N200 amplitudes intermediate to schizophrenic patients and NCs, without significant group differences. Results suggest diminished P300 amplitude may not be as prominent in SPD as in schizophrenia. Studies with larger sample sizes, multiple lead assessment strategies, and more demanding tasks may further characterize ERP deficits in schizophrenia-spectrum disorders such as SPD.
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PMID:Event-related potentials in schizotypal personality disorder. 884 99

There is some support for the hypothesis that the factor structure of schizophrenia symptoms is similar to the factor structure of schizotypal symptoms in nonschizophrenia populations. However, no studies to date have examined schizotypal symptoms in patients with personality disorders. In this study, confirmatory factor analyses were conducted to test the relative fit of several models of the factorial structure of schizotypal symptoms in patients diagnosed with personality disorders. The EQS: Structural Equations Program was used to analyze DSM-III symptoms of schizotypal personality disorder (SPD) based on structured clinical interviews with 213 patients meeting a diagnosis for at least one personality disorder. A subgroup of the total sample was also evaluated for DSM-III-R criteria (n = 143) to test competing models of the DSM-III-R symptoms of SPD. A three-factor model consisting of a cognitive-perceptual, interpersonal, and paranoid factor yielded the best fit to the data relative to the other models tested. These results suggest that the three-factor model of schizophrenia symptoms may not entirely correspond to the factors underlying milder schizotypal symptoms expressed in a clinical population. It is suggested that future research focus on both the similarities and the differences between SPD and schizophrenia.
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PMID:The factor structure of schizotypal symptoms in a clinical population. 887

While structured psychiatric interviews have generally succeeded in identifying higher rates of schizotypal personality disorder in relatives of schizophrenia versus control probands, self-report questionnaires designed to assess schizotypy have been less successful at distinguishing these groups of relatives. In the Roscommon Family Study, an epidemiologically based, case-controlled study conducted in the west of Ireland, relatives were administered a short form of Eysenck's Psychoticism scale and shortened and modified versions of the scales for magical ideation and social anhedonia developed by Chapman and colleagues. We compared, with relatives of matched controls, relatives of four proband groups: schizophrenia, other nonaffective psychoses (ONAP), psychotic affective illness (PAI), and nonpsychotic affective illness (NPAI). Only social anhedonia scores successfully differentiated, at modest levels of significance, relatives of schizophrenia versus control probands. Levels of magical ideation did not distinguish relatives of schizophrenia, ONAP, PAI, or NPAI probands from relatives of controls. Compared to controls, ONAP probands had significantly elevated psychoticism scores, but no such increase was seen in relatives of schizophrenia, PAI, or NPAI probands. Dimensions of schizotypy assessed at personal interview were significantly better at differentiating relatives of schizophrenia and control probands than our measures of social anhedonia, magical ideation, or psychoticism. Although psychiatric interviews in this sample have shown that clinically assessed schizotypal personality disorder and traits strongly aggregate in relatives of schizophrenia patients, of the three self-report instruments designed to assess schizotypy, only one even modestly identifies relatives of schizophrenia versus control probands. These results suggest that, compared with psychiatric interviews, self-report questionnaires are less successful at assessing underlying familial vulnerability to schizophrenia.
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PMID:Self-report measures of schizotypy as indices of familial vulnerability to schizophrenia. 887 1

Schizophrenic patients have consistently been reported to show deficits in preattentive information processing as demonstrated by impairments in visual backward masking and texton detection tasks. Texton detection refers to Julesz's texton theory, which defines a certain limited number of texton elements (e.g., one 'L' among many '+') that can be detected readily and simultaneously without attentional effort irrespective of the size of the rest of the visual field. The present study investigated whether deficits of preattentive information processing are more prevalent in a group of adolescents of high genetic risk for schizophrenia compared to matched control subjects. Although differences in the performance in visual backward masking tasks could not be detected with our experimental approach, preattentive texton detection was to a certain extent disturbed in subjects at risk. Moreover, subjects at risk did not show the advantage of the right hemisphere in processing texton elements which was found in the control group. This may point to a subtle dysfunction of the right hemisphere in the risk group. It is concluded from the present study that deficits in preattentive texton detection may represent an indicator for a schizophrenic disposition. However, further studies including other high risk groups, schizophrenics in remission and individuals with a schizotypal personality disorder are needed to confirm this hypothesis.
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PMID:Preattentive information processing as measured by backward masking and texton detection tasks in adolescents at high genetic risk for schizophrenia. 888 45

Individuals with schizotypal personality disorder (SPD) are thought to be phenotypically related to individuals with schizophrenia. This assumption is partially supported by the fact that SPD patients have deficits on biological markers similar to those found in schizophrenia. Visual backward masking (VBM) performance and critical stimulus duration (CSD), measures of information processing found to be abnormal in schizophrenia patients, were assessed in 14 SPD and 21 comparison subjects. There was no significant difference between groups in VBM performance; however; there were significant correlations between VBM deficits and the number of SPD symptoms, as well as elevated scores on the Ego. Impairment Index (EII). Additionally, there was a trend (p = 056) toward elevations in CSD in the SPD versus the comparison group and CSD inflation appears to be most prominent in individuals with a greater number of social deficit symptoms and elevated physical anhedonia scores. These findings suggest an important relationship between symptoms of SPD and neurophysiologic deficits.
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PMID:The relationship of information-processing deficits and clinical symptoms in schizotypal personality disorder. 889 71


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