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)

A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
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PMID:[A water intoxication patient who showed remarkable ST depression and suspected ischemic heart disease]. 152 80

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

The CPK levels of 79 patients with schizophrenia (36 males and 43 females and 88 normal control subjects (53 males and 35 females) were assessed. The result shows that the CPK level of the patients with acute schizophrenia (307.33 Iu/L) was significantly higher than that of the normal control subjects (160.51 Iu/L) (t = 3.534, N21, 88, P less than 0.01) and the CPK level of male schizophrerines rose more significantly. Meanwhile, some cases from the two groups were examined using the Type A behavior pattern inventory. No significant difference was shown between these two groups. It is considered that the change of some enzymes within the blood may affect the genetic vulnerability to schizophrenia.
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PMID:[A study on serum creatine phosphokinase and type A behavior in schizophrenia]. 259 Dec 74

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

This work is devoted to the study of CPK BB content in nuclear fraction of nervous cells in normal brain and in brains of mental (schizophrenia and Alzheimer disease) patients. With the help of the immunocytochemistry and immunoblotting was detected, that the nuclear membrane fraction of brain contains significant amount of CPK BB. On the contrary, in the nuclear membrane fractions of schizophrenic and Alzheimer disease brains the content of this isoenzyme decreased. Therefore in the brain of schizophrenic and Alzheimer disease patients the content of CPK BB decreased not only in cytosolic fractions, but also in the fractions of nuclear membranes. We demonstrated also, that cytosolic CPK BB associates not only with nuclear membranes, but with synaptosomal and microsomal fractions and mitochondrias of normal brain cells.
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PMID:[The detection of cytoplasmic creatinine phosphokinase BB in nerve cell nuclei under normal conditions, in schizophrenia, and in Alzheimer's disease patients]. 804 91

We report a 60-yr-old woman with schizophrenia, who manifested a neuroleptic malignant (NM)-like syndrome after acute organophosphate poisoning (OPP). She attempted suicide by ingesting 40% emulsions of DMTP (S-2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadizol-3-yl-methyl O,O-dimethyl phosphorodithioate) 100 ml. On admission, she was unconscious and demonstrated convulsions, depressed respiratory movements, miosis and profuse salivation. Plasma cholinesterase concentration (842 IU.L-1) was very low and OPP was diagnosed. She was treated with gastric lavage, atropine and pralidoxime (PAM). By the seventh day after admission, symptoms of OPP disappeared and serum ChE had recovered to a sub-normal level. On the 13th day, she demonstrated coma, high fever (41.0 degrees C) and lead-pipe rigidity. Serum CPK was increased (1631 IU.L-1). Dantrolene sodium iv was administered for three days. Body temperature began to decrease in 24 hr, and her consciousness, muscle rigidity and other neurological symptoms returned to normal by the 16th day after admission. She was discharged from the hospital without sequelae 55 days after admission. We conclude that OPP can predispose to an NM-like syndrome and that dantrolene may be effective in the management.
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PMID:Neuroleptic malignant-like syndrome: a complication of acute organophosphate poisoning. 859 Apr 92

Recently, with the increase in elderly population, we have had more opportunities to administer neuroleptics to elderly patients for hallucinatory delusional state, delirium, psychomotor excitement, wandering etc. However, little is known about the characteristics of the neuroleptic malignant syndrome (NMS) in elderly patients, which is the most serious side effect of neuroleptics. In this paper, we present the clinical course of five NMS patients in the presenium and senium. Case 1 was 72-year-old male who was diagnosed as having dementia of Alzheimer's type (with late onset). He showed nocturnal wandering, insomnia, and irritability. Tiapride 60 mg per day had been administered previously. Just after the addition of oxypertine 10 mg per day, NMS occurred, and he died of pneumonia a week later. Case 2 was 75-year-old male who was diagnosed as having vascular dementia. He showed insomnia, hyperactivity and wandering. He had been given levomepromazine (LPZ) 10 mg per day over a long period of time. At first, he had daily episodic fever, however, serum CPK levels did not increase at that time. A month later, all the symptoms of NMS appeared and then the patient's condition suddenly deteriorated and he died three days later. Case 3 was a 64-year-old male who was diagnosed as having dementia of Alzheimer's type (with early onset). He showed insomnia, irritability and violence. Tiapride 50-125 mg per day was administered along with oxypertine 50-115 mg per day. Almost two months later, NMS occurred. He had daily episodic fever at first, extrapyramidal symptoms and autonomic instabilities gradually increased. Soon after symptoms of NMS were completed. In this case, NMS seemed to be induced by bacterial pneumonia after long term administration of LPZ 5 mg per day. Case 4 was a 75-year-old female who was diagnosed as having dementia of Alzheimer's type (with late onset). She showed hallucinatory delusional state. Although she had autonomic instabilities just after adminstration of haloperidol 1-2 mg per day, NMS itself occurred after discontinuing the neuroleptic. Case 5 was a 61-year-old female who was diagnosed as having schizophrenia at the age of forty. She was given various neuroleptics over a period of time. The neuroimaging in SPECT showed her cerebral cortex was generally hypoactive. She had a tendency to have autonomic instabilities after the administration of relatively high potential neuroleptics. Risperidone 3-6 mg per day was administered, and almost a month later, autonomic instabilities increased and she was diagnosed as having NMS. All the patients would be able to have brain dysfunction, which suggested that such patients may be liable to NMS. In our patients, NMS occurred after the additional administration of oxypertine 10 mg per day or after long time administration of LPZ 5 mg per day. It was suggested that NMS could occur after the administration of low dose and relatively low potential neuroleptics in elderly patients. Our 3 of 5 patients showed the delayed type of NMS, which might be relatively more frequent in senior and presenior patients than in younger patients. In case 3, NMS was induced by the somatic disease (bacterial pneumonia), however in other cases, NMS was not always induced by somatic disease. Our 4 of 5 patients experienced some of the symptoms of NMS--episodic fever, extrapyramidal symptoms and autonomic instabilities--before the onset of NMS. Such symptoms may be "pre-steps" to NMS. Once NMS occurred, the patient's systemic condition tended to deteriorate acutely. Due to the fact that our 2 of 5 patients died, it was suggested that the prognosis of the NMS patients in presenium and senium tends to be much worse. It is important to find the "pre-steps" to NMS and treat them as soon as possible for better prognosis.
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PMID:[A study of neuroleptic malignant syndrome in the presenium and senium]. 974 53

The discovery of lithium's efficacy as a mood-stabilizing agent revolutionized the treatment of patients with bipolar disorder and after 5 decades this drug continues to be the mainstay of treatment of this disorder. Valproate, which is dissimilar structurally to lithium, shares most of the effects of lithium at the level of protein kinase C (PKC). Both drugs reduce the activity of PKC, though via different mechanisms. In comparison to patients with major depressive disorder, schizophrenia, or healthy controls, PKC activity is significantly elevated in manic patients, suggesting that changes of PKC activity may be a central pathological trait of the illness. The precise physiological role of PKC activity in the regulation of mood is unclear. The enzyme modulates cellular responses via phosphorylation of numerous substrate proteins. Such substrates of PKC include cytoskeletal proteins, neurotransmitter and hormone receptors, G proteins, GAP-43, MARCKS etc. Further studies are required to clarify any causal role of CPK changes in bipolar-disorder.
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PMID:[On the relevance of protein kinase C to lithium therapy in bipolar disorder]. 1552 99

A 62-year-old woman was treated for schizophrenia for 40 years. When the symptoms had deteriorated and new medications had to be added, CPK rose and she malignant syndrome was suspected. The electroconvulsive therapy (ECT) was proposed because of no improvement of the symptoms. We employed rocuronium bromide instead of suxamethonium considering malignant syndrome. The maintenance of anesthesia was necessary, because the duration of rocuronium bromide is longer than that of suxamethonium chloride. Anesthesia was induced and maintained using target controlled infusion (TCI) of propofol. After ECT was performed, sugammadex sodium 4 mg . kg-1 was administered at 2 post-tetanic counts (PTC) and the patient could come out the operating room safely and speedy. ECT using rocuronium bromide and sugammadex sodium can be performed safely and speedily, when suxamethonium chloride cannot be used.
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PMID:[Anesthetic management for electroconvulsive therapy using rocuronium bromide and sugammadex sodium in a patient with suspected malignant syndrome]. 2225 79


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