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)

Seventeen former inpatients with NPD were retrospectively compared to 19 patients with schizophrenia, 26 with MAD and 33 patients with BPD in terms of longitudinal course and outcome, exploring the validity of the NPD diagnosis. Two illustrative cases were presented. Results suggest that NPD is a valid diagnostic entity, more distinct from schizophrenia than MAD. NPD probably differs from BPD in terms of equal sex distribution in NPD; poor social functioning, especially in the low level of satisfaction with heterosexual relationships in NPD at follow-up; more rehospitalization in NPD; probably poorer global functioning in NPD at admission; and probably poorer overall follow-up functioning in NPD.
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PMID:Narcissistic personality disorder. A validity study and comparison to borderline personality disorder. 279 99

The external validity of 10 schizoid personality scales was assessed against dimensional measures of DSM-III borderline (BPD) and schizotypal (SPD) personality disorders in a sample of 37 top-security prisoners. Significant relationships with SPD or BPD emerged for schizophrenism, withdrawn-disturbed relationships, hallucinatory predisposition, schizoidia, disordered thinking and perceptual aberration (r = 0.30-0.66). The first four of these scales were significantly related to SPD (r = 0.29-0.51) after partialling out the effects of BPD, indicating an intrinsic link between these scales and SPD which may constitute the genetic affinity of SPD with schizophrenia. It is suggested that scales which assess the construct of schizophrenism or 'interpersonal aversiveness' may be the most central to Meehl's (1962) 'integrative neural defect' or genetic predisposition to schizotypy.
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PMID:Validation of schizoid personality scales using indices of schizotypal and borderline personality disorder in a criminal population. 342 52

Admission and mean 14-year follow-up Global Assessment Scale functioning were studied in 237 inpatients meeting DSM-III criteria for borderline (BPD) and schizotypal (SPD) personality disorders and compared to major affective disorder, schizophrenia and other diagnoses. BPD patients also meeting criteria for SPD functioned more poorly than other BPD or SPD patients at admission but improved their functioning at follow-up. Two BPD and SPD criteria which were associated with good follow-up functioning in BPD with SPD patients were found to predict poor admission functioning but good follow-up functioning in 18 of 237 former inpatients regardless of diagnosis.
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PMID:The significance of borderline and schizotypal overlap. 365 42

This study reports the first long-term follow-up of patients with schizotypal personality disorder (SPD) as defined by DSM-III. Patients with the pure syndrome (SPD, n = 10) were compared with patients with schizophrenia (S, n = 53) and borderline personality disorder (BPD, n = 81). Three "mixed" cohorts (S/SPD, n = 61; S/SPD/BPD, n = 30; SPD/BPD, n = 18) were added to investigate the effect of schizotypal disorder on the longitudinal course of comparison groups. Schizotypal personality disorder proved to be common in the Chestnut Lodge follow-up study patients, although it was rare as a pure syndrome. From the perspective of follow-up, SPD appeared related to S but not to BPD. The mixed axis II borderline syndrome (SPD/BPD) had a long-term profile closer to BPD than to SPD, and adding SPD to S appeared (unexpectedly) to enhance outcome.
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PMID:Schizotypal personality disorder. Chestnut Lodge follow-up study: VI. Long-term follow-up perspectives. 395 56

BPD is often associated with cognitive deficits that tend to be present regardless of mood state. Greater impairments tend to be seen in BPD patients who are older, have an early onset of the disease, and suffer a more severe course of illness. The literature also suggests that cognitive deficits are present early in patients with BPD and may be cumulative, showing an association with the number of affective (particularly depressed) episodes over time. Cognitive deficits in BPD may share some common characteristics with those seen in patients with schizophrenia, although the latter tend to show much greater and generalized cognitive impairment. For example, unlike patients with schizophrenia, patients with BPD typically do not score lower than normal persons on measures of global intellectual ability. There also is not overwhelming evidence of laterality or localization of cognitive deficits in BPD, although debate in the literature continues. More visuospatial deficits tend to be found in BPD and UPD than in schizophrenia, thereby raising the possibility of greater involvement of right hemisphere systems in mood disorders. In general, despite variability across investigations, deficits in executive functioning, episodic memory,sustained concentration, and, to a lesser extent, visuospatial skills seem to be the most consistent areas of impairment in BPD. Just as neuroimaging anomalies have been well documented in schizophrenia, structural brain abnormalities have been noted in BPD,most commonly involving the basal ganglia or white matter. Specific comparisons of cerebral atrophy and ventricular size between patients with schizophrenia and BPD have not been definitive, making it difficult to draw conclusions about structural brain abnormalities that might be specific to BPD. Nonetheless, there is enough evidence to suggest that white-matter abnormalities are reported with a greater frequency in BPD patients than in patients with UPD or schizophrenia. Functional neuro-imaging studies of mood disorders have indicated that the frontal cortex,basal ganglia, and temporal lobes are involved. The relationships between neuroimaging and neurocognitive abnormalities in BPD are worthy of additional investigation. Clearly, efforts directed toward phenotyping neuropsychiatric disorders using such measures, in addition to other clinical, neuroimaging, neurophysiologic, and genotypic information, may yield important insights into the development, nature, and course of illness. It is hoped that this understanding will lead to better identification of individuals who may be prone to greater cognitive impairment or decline and those who might be more responsive to specific treatments.
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PMID:Cognition in bipolar disorder. 1582 41

In recent years, Asperger disorder became a key issue in Japan. Serious crimes which have been caused by high-functioning PDD adolescents have become a social problem. Total population study of PDD showed the increase of these children, and the most recent study reported the prevalence to be 2%, in Nagoya City. Now, we have at least one PDD in every school class. It poses a serious problem for Japanese school education. On the other hand, it had gradually become apparent that there are many PDD adult who had been misdiagnosed with other psychiatric disorders; schizophrenia, BPD and so on. The author discusses the relevant issue of Asperger disorder and high-functioning PDD from a clinical perspective.
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PMID:[Asperger syndrome; the issue and the truth]. 1735 49

While it is premature to provide a simple model for the vulnerability to the development of either borderline (BPD) or schizotypal (SPD) personality disorder, it is clear that these heritable disorders lend themselves to fruitful neurobiological exploration. The most promising findings in BPD suggest that a diminished top-down control of affective responses, which is likely to relate to deceased responsiveness of specific midline regions of prefrontal cortex, may underlie the affective hyperresponsiveness in this disorder. In addition, genetic and neuroendocrine and molecular neuroimaging findings point to a role for serotonin in this affective disinhibition. Clearly SPD falls within the schizophrenia spectrum, but precisely the nature of what predicts full-blown schizophrenia as opposed to the milder symptoms of SPD is not yet clear.
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PMID:Recent advances in the biological study of personality disorders. 1863 45

The SCZ (schizophrenia)-associated GABA(A) receptor (gamma-aminobutyric acid type A receptor) beta(2) subunit gene GABRB2 was recently associated with BPD (bipolar disorder). Although weaker than its association with SCZ, significant association of GABRB2 with BPD was found in both German and Chinese, especially for the haplotypes rs1816071-rs187269 and rs1816072-rs187269 for which the M-M variants showed higher frequency in disease than the control. Significant genotype-dependent reduction in GABRB2 expression was shown for BPD, but to a lesser extent than that for SCZ. Temporal effects on GABRB2 expression were observed. Moreover, for the homozygous major genotypes of rs1816071, rs1816072 and rs187269, expression increased with time in CON but decreased in SCZ and BPD. The genotypes of these three SNPs (single nucleotide polymorphisms) were further correlated with antipsychotics dosage in SCZ cohorts. The findings highlight the importance of GABRB2 in neuropsychiatric disease aetiology, with respect to haplotype association, as well as reduction of and temporal effects on gene expression in both SCZ and BPD, but to a lesser extent in the latter, supporting the suggestion that functional psychosis can be conceptualized as a continuous spectrum of clinical phenotypes rather than as distinct categories.
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PMID:GABRB2 in schizophrenia and bipolar disorder: disease association, gene expression and clinical correlations. 1990 88

Recent research studies have been confirming the evidence that patients with personality borderline disorder (BPD) suffer significant neuropsychological disorders. Neurocognitive dysfunction of BPD seems to mainly affect the functions characteristic of the prefrontal areas that participate in information processing and management and in the regulation of complex behavioral responses. Neuropsychological disorders not only are seen in the specific tests but are also reflected and could play an important role in the clinical manifestations of borderline disorder, such as emotional dysregulation and impulsive behaviors. Neurocognitive rehabilitation therapy has been used successfully in psychiatric disorders such as schizophrenia, also characterized by the presence of neuropsychological dysfunctions. Thus, it can be expected that rehabilitation of the neurocognitive functions affected in BPD contributes to the patient's functional improvement. The present work describes a series of five patients with BPD who presented important neuropsychological dysfunctions and who were treated successfully with a specific program of neurocognitive rehabilitation. The results observed justify the performance of controlled clinical studies on the efficacy of this technique in the treatment of BPD.
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PMID:[Neuropsychological rehabilitation in patients with borderline personality disorder: a case series]. 1992 37

Structural brain abnormalities are central to schizophrenia (SZ), but it remains unknown whether they are linked to dysmaturational processes crossing diagnostic boundaries, aggravating across disease stages, and driving the neurodiagnostic signature of the illness. Therefore, we investigated whether patients with SZ (N = 141), major depression (MD; N = 104), borderline personality disorder (BPD; N = 57), and individuals in at-risk mental states for psychosis (ARMS; N = 89) deviated from the trajectory of normal brain maturation. This deviation was measured as difference between chronological and the neuroanatomical age (brain age gap estimation [BrainAGE]). Neuroanatomical age was determined by a machine learning system trained to individually estimate age from the structural magnetic resonance imagings of 800 healthy controls. Group-level analyses showed that BrainAGE was highest in SZ (+5.5 y) group, followed by MD (+4.0), BPD (+3.1), and the ARMS (+1.7) groups. Earlier disease onset in MD and BPD groups correlated with more pronounced BrainAGE, reaching effect sizes of the SZ group. Second, BrainAGE increased across at-risk, recent onset, and recurrent states of SZ. Finally, BrainAGE predicted both patient status as well as negative and disorganized symptoms. These findings suggest that an individually quantifiable "accelerated aging" effect may particularly impact on the neuroanatomical signature of SZ but may extend also to other mental disorders.
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PMID:Accelerated brain aging in schizophrenia and beyond: a neuroanatomical marker of psychiatric disorders. 2412 15


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