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)

The author notes that increased serum creatine phosphokinase (CPK) activity is found in the majority of hospitalized acutely disturbed schizophrenics and patients with affective psychoses. It is probable that some of these increases do not result from nonspecific factors such as activity, trauma, or stress, which do cause increases in some cases. Those patients who show increased CPK activity have more florid psychopathology and tend to have higher CPK levels in nonacute periods than those without increases. First-degree relatives of psychotic patients with elevated serum CPK have high-normal or slightly increased serum CPK. There is also evidence of other neuromuscular dysfunction in psychotic patients. The author concludes that the investigation of CPK may have considerable heuristic value for the study of schizophrenia and other psychoses.
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PMID:Serum creatine phosphokinase in schizophrenia. 125 26

The activity and content of the brain isoenzyme of creatine phosphokinase-BB (CPK-BB) were investigated in the peripheral tissues containing this isoenzyme (in the small intestine and heart) in health and schizophrenia. The decrease of CPK-BB activity and content in schizophrenic brain was shown before. The present work demonstrates the reduction of CPK-BB activity and concentration not only in the brain of mental patients but also in the intestine and heart tissues. A high correlation was discovered between the CPK-BB level in the brain and in the intestine of schizophrenic patients (r = 0.85).
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PMID:[Creatine phosphokinase isoenzymes (CK BB) of the brain in peripheral tissues in schizophrenia]. 166 49

Immunochemical and immunocytochemical studies were carried out to reveal the cerebral isozyme creatine phosphokinase (CPK BB) in autopsy brain of patients with different mental diseases. The studies covered schizophrenic patients (n-19), patients with senile dementia (n-9), with Alzheimer's disease (n-13) and controls without any mental pathology (n-17). It has been demonstrated that in mental pathology in the frontal cortex (field 10), there was an appreciable decrease in the content of immunoreactive CPK BB. That decrease was significantly more pronounced in Alzheimer's disease than in schizophrenia or senile dementia (p less than 0.01). Apparently, the decrease of the content of immunoreactive CPK BB determines to a considerable measure the early detected decrease of CPK BB activity in the patients' brain.
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PMID:[Decreased level of creatine phosphokinase BB in the brain of patients with mental disorders (complex immunochemical and immunocytochemical studies)]. 196 98

Patients with febrile attacks of schizophrenia showed clinical and laboratory correlations between the severity of the clinical picture on the one hand and parameters of the leukocyte index of intoxication, ESR, the NaK ratio and 17-CS secretion, on the other. The authors consider the possible causes of elevated levels of dopamine in the urine and of beta-lipoproteins and creatine phosphokinase in the cerebrospinal fluid. The study has revealed anti-brain antibodies and sensitization of leukocytes to neuroleptics. A possible role of neural viral infection in the etiology and pathogenesis of the studies conditions is discussed.
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PMID:[Clinico-pathogenetic patterns in the development of febrile attacks in schizophrenia]. 341 38

Regional localization of creatine phosphokinase BB was studied in postmortem human brain and its stability was shown. The content of CPK BB in different brain structures was unequal: from 0.5 mcg/mg of protein in the occipital lobe and tuber cinereum to 4.5 mcg/mg in the frontal lobe. In the regional localization of CPK BB in the postmortem brain of schizophrenia patients, some changes in isoenzyme content were found as compared to the control group. The reduction of CPK BB concentration at schizophrenia was found in the frontal lobe (45%, P less than 0.001) and s. nigra (70%, P less than 0.001); the concentration was higher in the thalamus and occipital lobe (15%, P less than 0.001), as well as in the parietal lobe, cingulate gyrus, tuber cinereum, cerebellum cortex, inferior olive--50-80%, P less than 0.001.
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PMID:[Creatine phosphokinase BB distribution in different structures of the human brain]. 344 34

The relationship between hypothalamic-pituitary-adrenal (HPA) function and the noradrenergic system was examined in patients with affective and with schizophrenic disorders. In response to the Dexamethasone Suppression Test (DST), serum cortisol, plasma catecholamine levels, and serum creatine kinase (CK) activity were measured. Among patients with major depression, those with higher post-DST cortisol levels had higher plasma catecholamine levels and lower serum CK activity. Among acute schizophrenic patients, those with higher serum CK activity had higher baseline and post-DST cortisol levels. These results indicate that in both major depression and in acute schizophrenia, there is a dysfunction of the HPA axis and the noradrenergic system, but the noradrenergic dysfunctions are different in the two disorders.
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PMID:Dexamethasone suppression test and noradrenergic function in affective and schizophrenic disorders. 370 36

The mean creatine phosphokinase level of 41 psychotic patients was significantly higher than that of 30 nonpsychotic psychiatric patients, as were their MMPI paranoia and schizophrenia scores. Their creatine phosphokinase level was negatively correlated with hysteria and psychopathic deviance.
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PMID:Creatine phosphokinase, the MMPI, and psychosis. 670 42

The study of biochemical processes in schizophrenia has continued to be influenced by new knowledge in neurobiology and clinical nosology. With increasing frequency, neurobiology is taking clinical factors into account. Areas updated in the current review from this perspective include the dopamine hypothesis, monoamine oxidase research, post-mortem studies, endorphins, endogenous hallucinogens and drug-induced psychoses, immunological and viral factors, and serum creatine phosphokinase.
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PMID:Biochemical processes in schizophrenia: an update. 699 79

In this study 18 patients with a research diagnostic criteria diagnosis of schizophrenia had a mean initial serum creatine phosphokinase level significantly higher than that of 36 control subjects with other RDC diagnoses. There were no corresponding elevations in the serum levels of nondrinking alcoholics or patients with primary or secondary affective disorders. The authors suggest that increased creatine phosphokinase levels in schizophrenic patients may be due to a sudden increase in the substance in the dopaminergic or limbic system due to increased muscle membrane permeability or to sympathetic nervous system or adrenergic dominance.
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PMID:Serum creatine phosphokinase levels in patients meeting the St. Louis research diagnostic criteria for schizophrenia. 706 96

Newly admitted psychotic patients often have elevations of serum creatine kinase (CK) enzymatic activity. Previous studies indicate that this increase consists of the muscle (MM) isozyme, and increases in the brain (BB) isozyme have not been observed. Using sensitive and specific radioimmunoassays that detect both active and inactive enzyme, we measured CK-MM and CK-BB in the serum and CSF of 100 patients with schizophrenia who were not newly admitted but whose conditions varied from acute to chronic to determine whether CK-MM or CK-BB appears in the CSF and whether CK-BB can be found in the serum of these patients. We found no unusual concentrations of either isozyme in CSF. We did observe a few elevations in serum CK-BB levels, but this test does not appear to be of diagnostic value for schizophrenic patients who are not newly admitted.
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PMID:Creatine kinase isozymes in the serum and CSF of schizophrenic patients. 729 65


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