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

Deficits on verbal memory tasks, as well as on spatial and auditory working memory tasks, have been observed in schizophrenia patients. A useful strategy in the determination of the premorbid indicator status of specific cognitive and memory deficits observed in patients is to examine those persons at increased biological risk for schizophrenia (e.g. first-degree relatives), schizotypal personality disorder patients, and/or psychometrically identified schizotypes for comparable deficits, though perhaps less profound than those seen in actual patients. We examined verbal memory and auditory working memory functioning in 31 schizotypic and 26 normal control subjects from a large randomly ascertained non-clinical university population. Schizotypy status was determined psychometrically using the well-known Perceptual Aberration Scale. Contrary to our theory-guided expectations, noteworthy deficits in verbal memory and auditory working memory were not observed in the schizotypic subjects and the two experimental groups did not differ significantly on any of the memory measures. These results were discussed in light of prior results obtained using the spatial delayed response task (i.e. spatial working memory) and Wisconsin Card Sorting Test performance on these same subjects. The theoretical implications of these findings are discussed in relation to the putative processes involved in the working memory system, as well as in relation to the schizotypy construct.
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PMID:Auditory working memory and verbal recall memory in schizotypy. 1074 48

Adolescents meeting diagnostic criteria for schizotypal personality disorder (SPD) are presumed to be at risk for developing schizophrenia in adulthood, making them an important group for exploring the developmental trajectory of the disease. Deficits in executive functioning have been documented in schizophrenia patients and adults with SPD. The present study examined executive functions in adolescents with SPD. It was predicted that the SPD group would score below comparison groups (normals and adolescents with other disorders) on measures of executive function, and that those with greater 'negative' signs of SPD would show more pronounced performance deficits. Analyses revealed that the performance of the SPD subjects was impaired relative to the other groups on the modified Wisconsin Card Sorting Test (MCST), but not on the Tower of London or the Controlled Oral Word Association Test. Consistent with prediction, regression analyses indicated that MCST deficits were associated with greater negative signs of SPD, but not positive signs.
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PMID:Executive functions in adolescents with schizotypal personality disorder. 1074 50

Evidence of long-standing social difficulties has been well documented in persons with schizophrenia. These deficits are often so rudimentary that a person with schizophrenia may never have developed the skills necessary to present as socially competent. Given the cognitive, biological, and neuroanatomical links between schizophrenia and schizotypal personality disorder (SPD), a study of social skills in persons with SPD may reveal a behavioral link. This study examined persons with SPD and their ability to label emotions in a recognition task, to display socially competent behaviors in a social role-play task, and to select appropriate behaviors from a multiple choice measure of social behavior. Results indicated that the performance of persons with SPD was similar to previously published findings in persons with schizophrenia. In terms of emotion recognition, the SPD group's ability to label positive emotions was significantly worse than their ability to label other emotions. Persons with SPD performed significantly worse than matched control participants on a social role-play task. However, the groups were equivalent in their ability to select socially appropriate behavior from a multiple choice measure. These results suggest that persons with SPD display social skills which mirror those previously reported in persons with schizophrenia.
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PMID:Social skills deficits in schizotypal personality disorder. 1076 Mar 82

The size and shape of the corpus callosum were assessed on sagittal section magnetic resonance images in 27 patients with schizophrenia, 13 patients with schizotypal personality disorder (SPD), and 30 healthy volunteers. High-resolution 1.2mm axial SPGR images were acquired and resectioned so that the sagittal plane passed through the anterior and posterior commissures and was parallel to the interhemispheric fissure. The corpus callosum and the whole brain were traced on midsagittal section slices of each brain, and the callosum was divided into 30 anteroposterior sectors. Pixel-by-pixel chi-square and thin-plate spline analyses were used to assess between-group shape differences. Size of the corpus callosum was smaller anteriorly in the genu of the corpus callosum and posteriorly in the splenium in schizophrenic patients than in normal controls. The genu of the corpus callosum was larger in SPD patients than in schizophrenic patients or normal controls. The posterior corpus callosum was largest in normal controls, smaller in SPD patients, and smallest in schizophrenic patients. Shape analysis was consistent with these size comparisons, and suggested a downward bowing of the corpus callosum in schizophrenic and SPD patients. SPD patients also had a region of the callosum just posterior to the genu that was narrower than in the other two groups. The decreases in corpus callosal size in schizophrenia varied directly with length of illness, perhaps indicative of a progressive process. The patient-control differences in callosal size and shape are consistent with a hypothesis of decreased connectivity between the left and the right hemispheres in schizophrenia and SPD.
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PMID:Shape and size of the corpus callosum in schizophrenia and schizotypal personality disorder. 1078 78

We hypothesized that male patients with schizophrenia spectrum disorders who have prodromal symptoms of obsessive-compulsive disorder (OCD) have ventricular enlargement compared with non-psychotic OCD patients, and that the difference in the ventricular size would offer a clue to the early detection of schizophrenia spectrum disorders. The ventricle-brain ratios (VBRs) in eight male patients with schizophrenia or schizotypal personality disorder (SPD) who had prodromal symptoms of OCD were compared with eight male patients with non-psychotic OCD and 14 normal male comparison subjects using three-dimensional magnetic resonance imaging (MRI). The VBR of the schizophrenia spectrum group was significantly larger than those of the OCD group or comparison subjects. Even the minimum VBR in the schizophrenia spectrum group was larger than the maximum VBR in the OCD group. These results may suggest the usefulness of three-dimensional MRI for early detection of patients with schizophrenia spectrum disorders who manifest OCD symptoms early in the course of the illness.
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PMID:Ventricular enlargement in schizophrenia spectrum patients with prodromal symptoms of obsessive-compulsive disorder. 1096 84

Prepulse Inhibition (PPI) of the startle response and the P50 auditory-evoked potential suppression are used to assess impairments in the regulation of the neural substrates and to determine the clinical significance of inhibitory deficits in schizophrenia. The study of gating deficits in schizophrenia and in related animal model studies have already advanced our understanding of the neural substrates of information processing abnormalities in patients with schizophrenia. Individuals with schizotypal personality disorder as well as clinically unaffected family members of patients with schizophrenia show PPI and P50 suppression deficits. These "schizophrenic spectrum" populations are not grossly psychotic, nor are they receiving antipsychotic medications. Therefore, the gating deficits are presumed to reflect core (eg, intermediate phenotypic) schizophrenia-linked information processing abnormalities. Several studies have reported that gating deficits are associated with clinical ratings of psychiatric symptoms, thought disorder, and neuropsychologic deficits in patients with schizophrenia. In addition, recent human pharmacologic studies have indicated that gating deficits can be reversed by rationally-selected compounds. Animal model studies have generally shown convergence with the human studies and may lead to improved identification of efficacious new antipsychotic medications for patients with schizophrenia.
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PMID:Human and animal studies of schizophrenia-related gating deficits. 1112 3

Schizotypal personality disorder is the prototype of the schizophrenia-related personality disorders and has been demonstrated to have phenomenologic, biologic, treatment, and outcome characteristics similar to those of schizophrenic patients. These studies suggest that patients with schizotypal personality disorder, like schizophrenic patients, show cognitive impairment, but the impairment is more focal and involves primarily working memory, verbal learning, and sustained attention rather than generalized intellectual deficits. Schizotypal patients, like schizophrenic patients show reductions in temporal lobe volume, but seem to be spared the frontal volume reductions found in some studies of schizophrenic patients and in our laboratory. Better frontal "buffering" may prevent the more severe cognitive and social deterioration associated with schizophrenia. Furthermore, schizotypal patients appear to show less susceptibility to psychotic symptoms, in part perhaps because of better buffered subcortical dopaminergic activity as suggested by recent data from a SPECT/amphetamine paradigm, glucose metabolic study, and structural studies of basal ganglia. These findings are discussed in terms of a model of schizotypal personality disorder where schizotypal patients have better capacity for compensatory buffering in lateral and subcortical brain regions, protecting them from the more severe symptoms of chronic schizophrenia.
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PMID:New perspectives on schizotypal personality disorder. 1112 34

We sought to show that (1) schizotaxia (Meehl's term for the predisposition to schizophrenia) is a clinically consequential condition, and (2) distinguishing it from schizotypal personality disorder may be useful from both clinical and scientific perspectives. We review the features of schizotaxia that may be relevant in clinical settings and discuss their implications for the diagnosis, psychosocial functioning, family intervention and treatment of people in schizophrenia families. Our review indicates that prior work finds some of the nonpsychotic and nonschizotypal relatives of schizophrenia patients to have a psychiatric syndrome characterized by negative symptoms, neuropsychological impairment, and psychosocial dysfunction. Following Meehl, we call this constellation of clinical and neurobiological features schizotaxia. The studies we review suggest it may be worthwhile to consider schizotaxia as a separate diagnostic class. Doing so would alert clinicians to a neurobehavioral syndrome not adequately covered by current diagnostic criteria and would motivate researchers to develop diagnostic and therapeutic approaches aimed at helping schizotaxic individuals and, perhaps, preventing the onset of schizophrenia.
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PMID:"Schizotaxia": clinical implications and new directions for research. 1121 39

A preliminary but growing body of evidence supports the existence of biological substrates in personality disorders. Based on a review of the literature, the article deals with the major biological markers: genetic, cognitive, biochemical, electrophysiological and organic markers, of schizotypal and borderline personality disorders. In addition, the article compares these findings in these two types of pathological personality. In the field of genetics, we notice several indices in favour of a relationship between schizotypal personality disorder (SPD) and chronic schizophrenia. In contrast, in borderline personality disorder (BPD), indices were lacking for such a relationship between this disorder and one of the axis I diagnosis, or a clear genetic transmission. In the field of cognitive tests, we can note in both SPD and BPD, that the abnormalities which would be at the level of temporal and frontal lobes, may be implicated in the observable cognitive troubles in these two disorders. In the field of neurobiochemistry, the dopaminergic and serotonergic systems seem to be implicated in the etiology of SPD while several data point out the fact that several neurotransmitter systems (dopaminergic, serotonergic, noradrenergic and cholinergic) seem to be involved in the etiology of BPD. Finally, in the field of electrophysiology, we notice that some of these tests observed in SPD (smooth pursuit eye movements, evoked potentials, modification of the electrodermic response) seem reinforcing the relationship between SPD and schizophrenia while those observed in BPD seem reinforcing either a relationship between BPD and depression (sleep studies), or a relationship between BPD and schizophrenia (evoked potentials, smooth pursuit eye movements).
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PMID:[Biological markers in schizotypal and borderline personality disorders]. 1121 38

There is evidence that reduced cholinergic activity may play a role in the pathophysiology of cognitive impairment in the schizophrenia spectrum. We tested the effects of physostigmine, an anticholinesterase inhibitor, on visuospatial working memory as evaluated by the Dot test, and on verbal learning and recall as measured by a serial learning task in patients with schizotypal personality disorder. Physostigmine tended to improve the Dot test, but not serial verbal learning performance in these patients.
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PMID:Physostigmine and cognition in schizotypal personality disorder. 1127 49


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