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

Dermatoglyphic features of 52 male patients with borderline personality disorder (BPD) were compared with those of 200 male controls (control group-CG) and 195 males with schizophrenia (SCH). Quantitative analysis showed statistically significant differences between BPD-CG and between BPD-SCH, mainly regarding the palmar traits, but also the 5th, the 4th and the 1st finger of the right hand as well as the 5th and the 4th finger of the left hand between BPD and SCH patients. The canonical discriminant analysis permitted correct classification with 69.84% probability between the BPD and CG and with 76.11% probability between the BPD and the SCH group. Qualitative finger and palmar traits analysis showed differences between the BPD and SCH groups on the 3rd finger of the left hand, total frequency for all fingers and in the III interdigital space. Significant differences between the BPD and CG were found on the 3rd finger of the left hand. Our results show that the dermatoglyphic features of BPD differ from those of schizophrenia and from those of control subjects. The possible significance of these findings is discussed.
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PMID:Dermatoglyphic analysis in borderline personality disorder and schizophrenia--results of a Croatian study. 1009 30

The dimensions and limits of the concept of schizotypy are examined using an exploratory factor analysis of the 36 signs and symptoms in the Cluster A DSM-III-R personality disorders as well as those in Borderline Personality Disorder and Avoidant Personality Disorder in the 307 first-degree relatives and half-siblings of 123 probands with schizophrenia/schizoaffective disorder. The personality disorders examined were assessed using sections of the Structured Clinical Interview for DSM-III-R Personality Disorders (SCID-II) and hospital and clinic records. Interviewers were blind to the proband diagnosis. The resulting six-factor solution accounted for 40% of the variance. The results of the six-factor solution accounted for the greatest variance and gave the most easily interpretable simple structure of all the solutions examined. The six factors are labeled as (1) Borderline Symptoms, (2) Schizoid Symptoms, (3) Paranoid Symptoms, (4) Avoidant Symptoms, (5) Positive Schizotypy Symptoms, and (6) Disorganized Symptoms. The Schizotypal Personality items are spread across all but the 'Borderline Symptoms' factor. We conclude schizotypy is a multidimensional construct that is not adequately characterized by any one DSM-III-R personality disorder. It appears to consist of six distinct dimensions, which, interestingly, parallel current thinking on dimensions in schizophrenia.
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PMID:The factor structure of schizophrenia spectrum personality disorders: signs and symptoms in relatives of psychotic patients from the UCLA family members study 1057 47

In this study, the Rorschach scoring system for splitting developed by Lerner, Sugarman, and Gaughran (1981) was applied to the Holtzman Inkblot Technique (HIT). Normal individuals (n = 30), patients with neurotic disorders (n = 30), patients with borderline personality disorder (n = 30), patients with acute schizophrenia (n = 25), and patients with chronic schizophrenia (n = 25) were studied with respect to their use of splitting. Sufficient interrater reliability was demonstrated for the scoring of splitting in the HIT. Significant differences between borderline patients, acute schizophrenic patients, and chronic schizophrenic patients, on the one hand, and patients with neurotic disorders, on the other hand, were demonstrated. Furthermore, it was shown that the indicators of splitting were associated with measures of identity diffusion, primitive defense mechanisms, and other measures of psychopathology. The Lerner indicator of splitting proved to be multidimensional. Different forms of splitting seem to be characteristic of borderline patients and schizophrenic patients. The application of the Lerner criteria of primitive defenses to the HIT appears to be promising.
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PMID:Splitting: an empirical study. 1058 42

Larger CAG/CTG trinucleotide-repeat tracts in individuals affected with schizophrenia (SCZ) and bipolar affective disorder (BPAD) in comparison with control individuals have previously been reported, implying a possible etiological role for trinucleotide repeats in these diseases. Two unstable CAG/CTG repeats, SEF2-1B and ERDA1, have recently been cloned, and studies indicate that the majority of individuals with large repeats as detected by repeat-expansion detection (RED) have large repeat alleles at these loci. These repeats do not show association of large alleles with either BPAD or SCZ. Using RED, we have identified a BPAD individual with a very large CAG/CTG repeat that is not due to expansion at SEF2-1B or ERDA1. From this individual's DNA, we have cloned a highly polymorphic trinucleotide repeat consisting of (CTA)n (CTG)n, which is very long ( approximately 1,800 bp) in this patient. The repeat region localizes to chromosome 13q21, within 1.2 cM of fragile site FRA13C. Repeat alleles in our sample were unstable in 13 (5.6%) of 231 meioses. Large alleles (>100 repeats) were observed in 14 (1. 25%) of 1,120 patients with psychosis, borderline personality disorder, or juvenile-onset depression and in 5 (.7%) of 710 healthy controls. Very large alleles were also detected for Centre d'Etude Polymorphisme Humaine (CEPH) reference family 1334. This triplet expansion has recently been reported to be the cause of spinocerebellar ataxia type 8 (SCA8); however, none of our large alleles above the disease threshold occurred in individuals either affected by SCA or with known family history of SCA. The high frequency of large alleles at this locus is inconsistent with the much rarer occurrence of SCA8. Thus, it seems unlikely that expansion alone causes SCA8; other genetic mechanisms may be necessary to explain SCA8 etiology.
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PMID:An unstable trinucleotide-repeat region on chromosome 13 implicated in spinocerebellar ataxia: a common expansion locus. 1071 98

The present article comments on a classic study by Garfield (1947) then reviews research on the Rorschach and psychiatric diagnoses. Despite a few positive findings, the Rorschach has demonstrated little validity as a diagnostic tool. Deviant verbalizations and bad form on the Rorschach, and indices based on these variables, are related to Schizophrenia and perhaps to Bipolar Disorder and Schizotypal Personality Disorder. Patients with Borderline Personality Disorder also seem to give an above-average number of deviant verbalizations. Otherwise the Rorschach has not shown a well-demonstrated relationship to these disorders or to Major Depressive Disorder, Posttraumatic Stress Disorder (PTSD), anxiety disorders other than PTSD, Dissociative Identity Disorder, Dependent, Narcissistic, or Antisocial Personality Disorders, Conduct Disorder, or psychopathy.
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PMID:The Rorschach test in clinical diagnosis: a critical review, with a backward look at Garfield (1947). 1079 11

In a follow-up study the long-term changes of borderline symptomatic of 14 patients with the diagnosis borderline personality disorder (criteria by Kernberg and Rorschach test) are compared with 13 patients with diagnosis schizophrenia and 16 patients with diagnosis depression (each case according to ICD-9 criteria). The Diagnostic Interview for Borderline Patients (DIB) is evaluated to comprehend the structure and kinds of borderline symptoms before and 4 years after treatment. Borderline patients are treated in a setting of client-centred group psychotherapy (twice a week, approximately 100 sessions). The treatment of the patients joining the control group is based on clinical standard. As a result all patients reduced the borderline-like symptoms. However, the most significant changes can be seen in the borderline group. 2 out of 14 borderline patients still fulfill the DIB Criteria of borderline personality disorder. Nevertheless, there are differences in the reduction of specific categories of borderline symptoms. The greatest changes are in the categories "loss of impulse control" and "psychotic episodes", whereas there are only slight improvements in the category "interpersonal relationships".
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PMID:[Long-term changes in borderline symptoms of patients after client-centered group psychotherapy]. 1078 Jan 54

The P300 wave is one of the cognitive components of the event-related potential (ERP) that is used to investigate the cognitive processes, and which can be used to study patient populations with a variety of psychiatric disorders. Its clinical utility has been increased by the identification of factors that contribute to the variability in its amplitude and latency. However, its value as a diagnostic index has not been entirely established. It can provide a useful recording of patients' information processing, and indicate the severity of the clinical state and its possible evolution. It can also assist in determining what therapeutic approach to adopt. In the present review, the findings in the literature concerning interindividual variation in the P300 wave are first described; several variables significantly influence the amplitude and latency of this wave, such as age, gender, intelligence and personality. Following this, the relevance of the data in the literature on the clinical applications of P300 in psychopathology is examined, including the studies undertaken to obtain an objective diagnostic index for mental disorders and also those carried out to assess the problems concerning the interpretation of information connected with the mental pathologies examined. P300-associated findings on dementia, schizophrenia, depression, alcoholism, drug addiction, anxiety disorders (panic disorder, obsessive-compulsive disorder, and post-traumatic stress syndrome) and on personality disorders (schizoid, antisocial or borderline personality disorder) have been examined in detail.
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PMID:[The p300 cognitive event-related potential. II. Individual variability and clinical application in psychopathology]. 1101 95

Neurological and psychiatric illnesses are among the most common and most serious health problems in developed societies. The most promising advances in neurological and psychiatric diseases will require advances in neuroscience for their elucidation, prevention, and treatment. Technical advances have improved methods for identifying brain regions involved during various types of cognitive activity, for tracing connections between parts of the brain, for visualizing individual neurons in living brain preparations, for recording the activities of neurons, and for studying the activity of single-ion channels and the receptors for various neurotransmitters. The most significant advances in the past 20 years have come from the application to the nervous system of molecular genetics and molecular cell biology. Discovery of the monogenic disorder responsible for Huntington disease and understanding its pathogenesis can serve as a paradigm for unraveling the much more complex, polygenic disorders responsible for such psychiatric diseases as schizophrenia, manic depressive illness, and borderline personality disorder. Thus, a new degree of cooperation between neurology and psychiatry is likely to result, especially for the treatment of patients with illnesses such as autism, mental retardation, cognitive disorders associated with Alzheimer and Parkinson disease that overlap between the 2 disciplines.
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PMID:Prospects for neurology and psychiatry. 1117 65

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

The history of antipsychotic medications begins in the 1950s with chlorpromazine, developed originally as an antihistamine but found to be an aid in the reduction of symptoms of delusions and hallucinations. This phenothiazine derivative was followed by numerous others in the same class (e.g., thioridazine) and then by antipsychotics in other classes (e.g., the popular haloperidol of the butyrophenone class). This group of medications is associated with a number of unpleasant side effects and complications. These included extrapyramidal symptoms (EPS), orthostatic hypotension, hyperprolactinemia and last, but certainly not least, tardive dyskinesia (TD). As a consequence, other alternative antipsychotics were developed in which D(2) blockade effect generally associated with EPS and TD was offset by 5-HT(2) antagonism. The first of this class was clozapine; however, it is associated with agranulocytopenia of sudden onset as well as seizure induction. However, olanzapine, a close structural relative, was soon synthesised for treatment of psychosis and particularly schizophrenia (Zyprexatrade mark, Eli Lilly). It was released in the US in November 1996 with FDA approval for that indication. However, antipsychotics have always been used for other psychiatric disorders, aside from schizophrenia. This includes, in particular, mania, where chlorpromazine use predated lithium as an effective treatment. Other uses for antipsychotics have included other mood disorders, dementia, childhood disorders and personality problems. Here, information on the application of olanzapine to non-schizophrenic disorders is reviewed. Despite the fact that the research post-dates FDA approval in 1996, there was already sufficient evidence for olanzapine's effectiveness in acute mania to obtain approval from the US FDA in March 2000. Other research supports its use as adjunctive therapy in depressive disorders. Phase IV studies and case reports have found limited support for olanzapine's use in a variety of other psychiatric disorders, behavioural disorders of dementia (including Alzheimer's disease), pervasive developmental disorder of childhood, obsessive-compulsive disorder and borderline personality disorder. In each of these latter diagnoses, double-blind studies are either underway or are planned to establish efficacy.
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PMID:Use of olanzapine in non-psychotic psychiatric disorders. 1133 15


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