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

Many procedures with variable validity and reliability have been developed in research settings to evaluate adventitious movements and related phenomena in specific populations, e.g., people with schizophrenia treated with dopamine antagonists, but these only provide global assessments or rate specific movements. A battery for rating individuals with possible movements disorders in a comprehensive way in clinical settings is needed so a protocol to assess briefly and thoroughly potential movement disorders was videotaped for five prepubertal boys with autistic disorder and severe mental retardation in a clinical trial. Utilizing a Movement Assessment Battery, four raters independently scored videotapes of 10-16 movements assessments of each of the five subjects. Experienced raters attained agreement of 59% to 100% on ratings of tardive dyskinesia and 48% to 100% on tics. Hindrances to reliability included poor quality of some tapes, high activity of subjects, and fatigue of raters.
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PMID:Clinical assessment of adventitious movements. 992 47

Studies using in vivo imaging or microscopic analysis of autopsy specimens indicate abnormalities in the striatum of schizophrenics including lower striatal metabolism, a change which can be normalized by antipsychotic medication. To investigate the possibility that abnormalities in schizophrenia brain may be due, in part, to pathology in mitochondria, organelles which generate energy, postmortem brain tissue from schizophrenic and control cases was obtained from the Maryland Brain Collection. Mitochondria in electron micrographs of striatal neuropil were counted and digitized. The caudate and the putamen of the schizophrenic subjects contained significantly (P < 0.05) fewer (a decrease of approximately 20%) mitochondrial profiles throughout the neuropil than did normal controls. The numbers of mitochondrial profiles per axon terminal appeared lower in the subset of schizophrenics off-drug as compared to either the subset of schizophrenics on-drug or to controls, suggesting that neuroleptic treatment may normalize this measure. The structural integrity of mitochondrial profiles in the schizophrenic striata was not obviously different from that of controls. Fewer mitochondrial profiles suggest decreased energy demands or diminished capacity to respond to energy requirements in the structures that contain them. These data are consistent with other studies showing decreased metabolism in the striatum of schizophrenics and may identify, in part, the anatomical basis of this deficit.
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PMID:Mitochondrial pathology in human schizophrenic striatum: a postmortem ultrastructural study. 1002 85

Besides the well-known adverse effects of clozapine, such as granulocytopenia, tiredness and hypersalivation, acute pancreatitis is known to be a very rare complication of the drug. In the literature a total of five case reports have been published so far. We report a case of asymptomatic pancreatitis subsequent to clozapine treatment at therapeutic doses in a 38-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient was rehospitalized after an acute exacerbation of the psychosis subsequent to an attempt to change medication on an outpatient basis. Treatment with clozapine was initiated again. During phases of progressively increasing the clozapine dose, serum levels of amylase and lipase were increased; after maintaining daily doses of clozapine of 300 mg and/or 600 mg the pancreatic enzymes normalized quickly within a few days. The patient did not report any pancreas-related complaints, nor did specific diagnostic studies produce any indicative result, only a minor thickening of the head and body of the pancreas in the ultrasound. It is assumed that the phenomenon of subclinical, asymptomatic pancreatitis during increasing dosage of clozapine occurs more often than previously supposed. The monitoring of serum amylase levels during slow increase in clozapine is recommended; if leukocytosis or eosinophilia is present, the possibility of even a subclinical and asymptomatic pancreatitis should be considered.
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PMID:Asymptomatic pancreatitis associated with clozapine. 1033 68

The major purposes of this paper are to explore the phenomena of family structure, illness symptoms, family coping and adaptation for patients with schizophrenia or manic-depression psychosis. This paper tries to provide a good reference instrument for application by nurses in home care, in order to understand and evaluate family needs. Subjects are schizophrenic or manic-depression outpatients from 3 hospitals located in northern Taiwan. Data were collected through home interview with primary caregivers and observations. There were fifty subjects from each of the 3 hospitals, and 151 subjects in total. Descriptive statistics, t-test, one way ANOVA, Pearson correlation and multiple stepwise correlation were used to analyze data. Research indicates that most patients are aged between 31 to 40, with over 10 years elapsed since onset, and are not married. Most primary caregivers are parents over 60 years old. Most family development was at the stage with young adult offspring. The manic-depressive patients have more working opportunities than schizophrenic patients. For schizophrenic patients, paranoia was the most serious in active symptoms; lack of interpersonal interaction was the most serious in negative symptoms; the other major problem was sleep disturbance in emotion-behavior assessment. Patient's disposition was the most concerning issue for families and the worst coping efficiency occurred with lazy behavior and sleep disturbance. For manic-depressive patients, aggressive behavior was the most serious active symptom, lack of energy was the most serious in negative symptom, and sleep disturbance was the most concerning problem in emotion-behavior assessment. The patient's symptom was the most concerning issue for families and the worst coping efficiency was found in drug side effect. The result also indicates that active and negative symptoms are both related to coping efficiency.
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PMID:[The study of family structure, illness symptom, and stress adaptation of psychotic patients]. 1044 43

Six clients with a diagnosis of schizophrenia were interviewed about their experiences of their lives in a home-like setting, their key care provider and the care received. Their narratives of lived experiences in care were interpreted as living a process of health in the midst of severe mental illness, involving: 'becoming more', 'being disabled', 'comforting/conforming relationship', 'discomforting/unconfirming relationship' and 'caring about the caring relationship'. Fatigue and lack of strength influenced the lives of most clients considerably, and the stories were about problems and conflicts. Nevertheless, the clients seemed really to struggle to make communal life work, and there were experiences of increased competence and better self-confidence in most of the stories. On the whole care was described as good, and the process of health seemed to be supported by experiences of comfort and being confirmed in the client-care provider relationship.
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PMID:Towards recovery: living in a home-like setting after the move from a hospital ward. 1082 12

"Cognitive inhibition" is a concept that has found a firm place in the interpretation of performance by normal subjects on tasks involving adherence to a plan and suppression of incorrect responses to distractors. The presence of "negative priming" is the classical indicator of cognitive inhibition. Negative priming occurs when, in a sequence of stimuli each of which is composed of a target and a distractor, the distractor of the first stimulus becomes the target of the second stimulus: reaction time to the second stimulus is slowed because of the inhibition applied to the distractor of the first stimulus. The concept has been extended to the interpretation of pathological behavior and symptoms. Pathological subjects have been found to show deficient negative priming. Thus, negative ideation in depression as well as intrusive paranoid associations in schizophrenia have been related to a deficit in the capacity to inhibit inappropriate representations. In this paper, we briefly review some of the experimental evidence from normal subjects that has contributed to the acceptance of cognitive inhibition as a key process in the control of normal cognition, as well as more recent evidence that has led to a revision of the concept. Negative priming in normal subjects has been found to be dependent upon characteristics of the experimental situation as perceived by the subject. In particular, priming is observed when the subject anticipates difficulty in determining the response and proceeds with caution. Thus, inhibition is not an automatic "brake" applied to irrelevant material, but rather the product of strategic considerations within the experimental situation. This revision of the cognitive inhibition hypothesis leads to a re-interpretation of the apparently deficient cognitive inhibition seen in depressed or schizophrenic subjects. According to this more recent interpretation, deficient cognitive inhibition in pathological subjects can be seen as a less adaptive strategic adjustment to the task. The pathology seems to touch higher-level executive functions rather than a deficient inhibitory "brake". In depressed subjects, abnormal performance in selective attention tasks could be related to the underlying pathology in two ways: some depressed subjects show a marked lack of energy and a psychomotor slowing: these subjects do not exhibit normal negative priming, probably because of a reduction of cognitive resources. Other depressed subjects show abnormal performance as reflected by negative priming greater than normal: this result could be related to an exaggerated tendency to verify a correct response. Schizophrenic subjects show a lack of negative priming that seems most plausibly to be related to an ineffectual integration of the experimental instructions concerning both speed and accuracy in the response. This re-interpretation of the cognitive deficiency in pathological patients provides a better fit with recent experimental results from normal subjects, and with cognitive deficits measured in pathological subjects.
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PMID:[Cognitive inhibition and psychopathology: toward a less simplistic conceptualization]. 1085 10

Desynchronization of circadian rhythmicity resulting from rapid travel through at least 4 time zones leads to symptoms of jet lag syndrome. The most commonly experienced symptoms in normal individuals are sleep disorders, difficulties with concentrating, irritability, mild depression, fatigue, and gastrointestinal disturbances. There is strong evidence relating affective disorders to circadian rhythm abnormalities, such as occur in jet lag. Less convincing suggestions relate jet lag to psychosis. We presume, relying on the literature and our accumulated experience, that in predisposed individuals jet lag may play a role in triggering exacerbation of, or de novo affective disorders, as well as, though less convincing, schizophreniform psychosis or even schizophrenia. An illustrative case vignette exemplifies the possible relationship between jet lag following eastbound flight and psychotic manifestations.
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PMID:[Jet lag causing or exacerbating psychiatric disorders]. 1088 40

Jet lag is a travel-induced circadian rhythm phenomenon that afflicts healthy individuals following long- distance flights through several time zones. The typical jet-lag manifestations - insomnia during local sleep time, day fatigue, reduced concentration, irritability, and exhaustion with mild depression - are attributed to transient desynchronization in the circadian rhythm until the internal biological clock is rephased to the new environmental conditions. There is strong evidence relating affective disorders with circadian rhythm abnormalities. Less convincing suggestions relate jet lag to psychosis. It can be hypothesized that in predisposed individuals jet lag may play a role in triggering exacerbation or even de novo affective disorders. Furthermore, we propose the possibility that psychosis and even schizophrenia can be elicited by jet lag. This outlook gains its support from case studies and some common underlying phase-advanced biological denominators involved in both jet lag sufferers and psychotic patients.
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PMID:Psychiatric aspects of jet lag: review and hypothesis. 1113 50

This report examines clinical features of 'pure' dysthymic disorder (DD, without superimposed major depressive disorder, MDD) in a sample of children and adolescents. Profiles of symptomatology and comorbidity as a function of age and gender are described. The sample consisted of 48 subjects (22 males, 26 females, age range 7-18 years, mean age 12.1 years) screened from consecutively referred children and adolescents. All subjects were comprehensively diagnosed with structured diagnostic interviews (Schedule for Affective Disorders and Schizophrenia for School Age, Diagnostic Interview for Children and Adolescents-Revised), according to DSM-IV criteria. Depressed mood, irritability, loss of energy and fatigue, guilt and low self-esteem were present in more than 70% of the subjects. Differences in symptomatic profile between males and females were not significant. Children showed less symptoms than adolescents, but the symptomatic profile was comparable (only anhedonia was significantly more frequent in adolescents). Anxiety disorders were more commonly comorbid with DD, especially separation anxiety disorder in children (33%) and generalised anxiety disorder in adolescents (67%). Externalising disorders were less frequently represented in our sample (14%). An early diagnosis of 'pure' DD before the first episode of MDD is crucial for a timely intervention.
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PMID:Depressive symptoms in children and adolescents with dysthymic disorder. 1115 Sep 28

Chronic fatigue syndrome (CFS) is characterized by unexplained, disabling fatigue and is associated with high rates of comorbid depression. While the aetiology is unknown, findings from recent twin surveys suggest that genetic factors may be relevant to prolonged fatigue states (> 1 month). To date, however, there has been no exploration of the role of familial/genetic factors in operationally defined CFS. The aims of the present study were: (i) to examine whether CFS is familial by comparing the rates of CFS in the first-degree relatives of CFS cases and medical control subjects; and (ii) to determine whether the high rate of comorbid depression in CFS is reflected in a greater familial loading for affective disorder. Twenty-five CFS cases and 36 medical control subjects were assessed for fatigue symptoms based on the Centre for Disease Control (CDC) criteria for CFS, and for lifetime psychiatric symptoms using the Schedule for Schizophrenia and Affective Disorders-Lifetime Version. Informant family history was obtained regarding first-degree relatives using the CDC criteria and the Family History Research Diagnostic Criteria. In addition, informant history was supplemented by sending a questionnaire to first-degree relatives. There were significantly higher rates of CFS in the relatives of CFS cases compared with the relatives of control subjects. The rate of depression in the CFS cases was similar to previous studies but did not appear to reflect a greater familial loading for depression when compared with control subjects. However, these analyses were complicated by higher than expected rates of depression in the control group. These findings suggest that familial factors are important in the aetiology of chronic fatigue syndrome.
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PMID:A family history study of chronic fatigue syndrome. 1170 53


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