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)

To investigate the possibility that anti-CNS antibodies may play a pathogenic role in a number of neurological and psychiatric disorders, a population study was undertaken. Serum samples were obtained from a total of 257 adults and were screened against sodium dodecyl sulphate polyacrylamide gel electrophoretic blots of various normal, necropsy-derived adult human brain regions. The incidence of IgG immunoreactive banding in the total sample was 30%. Within the diagnostic groups the incidence of banding was: controls 32%, schizophrenia 28%, mental retardation 27%, cerebellar ataxia 33%, Parkinson's disease 22%, myasthenia gravis 45% and epilepsy 31%. The differences are not statistically significant. There was no significant difference in the numbers and locations of bands between the various diagnostic groups and the controls. The overall incidence of immunoreactivity corresponding to the high molecular weight subunit of neurofilaments was only 6%, thus not confirming a previously reported incidence of 95%. The similarity between the diagnostic and the control sera suggests that caution should be exerted in interpreting the pathogenic significance of anti-CNS immunoreactive banding on Western blots.
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PMID:Anti-CNS antibodies in neurological and psychiatric disorders. 369 10

Of 2201 psychiatric patients in public facilities in a single metropolitan area evaluated for polydipsia, 34 (1.5%) were found to have a history of self-induced water intoxication. Among them, they had 101 episodes of water intoxication. Their mean age was 48.2 years, and they were predominantly white. Most had the primary diagnosis of schizophrenia. Compared with a matched control group, they had received more multiple courses of ECT but there were no significant differences in their use of psychotropic medications. Among nonpsychiatric medications, only phenytoin sodium and hydrochlorothiazide showed a trend toward significance.
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PMID:Self-induced water intoxication: a comparison of 34 cases with matched controls. 372 33

Ten patients (8 men, 2 women; mean age 38.7 +/- 8.1 years), 7 of whom had schizophrenic disorders and 3 of whom had bipolar disorder (manic-depressive illness), manifested psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome). The relationship between serum sodium and urinary water excretion among the 10 PIP patients is described in detail. The success of lithium in improving serum sodium levels and in decreasing urinary water excretion among the three PIP patients with bipolar disorder and the failure of changes in urinary water excretion to explain changes in serum sodium levels among the 10 PIP patients argue against "psychogenesis" as the explanation for the polydipsia and excessive water intake as the sole explanation for hyponatremia or complications ascribed to water intoxication.
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PMID:Psychogenic polydipsia and water intoxication--concepts that have failed. 406 21

Behaviour was augmented in rats by treatment with 10 mg/kgm d-amphetamine twice a day for 10 days. A greater activation of adenylate cyclase was found in dopamine rich areas of these rats brains than in normal controls when the enzyme was tested with sodium fluoride and quanylimidodiphosphate. These results parallel similar findings in the brains of schizophrenics obtained at post mortem and support the use of amphetamine sensitization in rats as a model for schizophrenia.
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PMID:Brain adenylate cyclase activity in the amphetamine sensitized rat. 408 98

Although there is a definite association between hyponatremia and schizophrenia, the true incidence and etiology have not been established. This report is a retrospective study of all admissions to the Baroness Erlanger Hospital over a three and one-half year period. There was a 5.8% incidence of hyponatremia in patients with schizophrenia as compared with a 0.36% incidence for all admission (P less than .01). Schizophrenic patients at risk for developing hyponatremia drank water excessively(P less than .01) and were most likely to be taking thioxanthene (P = .05(4)) antipsychotic and anticholinergic medications (P Less than .01). Most schizophrenic patients admitted with hyponatremia had dangerously low serum sodium levels (less than or equal to 120 mEq) and showed severe neurologic dysfunction. This retrospective study compares the clinical features of schizophrenic patients who develop hyponatremia and those who do not. The possible role of antidiuretic hormone is discussed
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PMID:Hyponatremia in patients with schizophrenia. 612 72

Studies on the treatments for neuroleptic-induced tardive dyskinesia published in the literature are reviewed. The great number of different treatments and the controversial results of most studies show that there is as yet no specific and safe treatment for tardive dyskinesia. Suggestions for well-designed treatment studies are given: Placebo-controlled double-blind design, larger patient populations, clear diagnostic and standard observing and rating conditions using different assessment methods and videotapes, withdrawal of neuroleptics and antiparkinsonian drugs to discover reversible tardive dyskinesia. If this procedure is not feasible, neuroleptics and other drugs should be maintained at a stable dose level. Longer term studies of some months are necessary to study the prolonged efficacy of different drugs. The effect of dopamine-antagonists such as neuroleptics and of dopamine-depleting agents such as reserpine and oxypertine is of limited duration. Dopamine-agonists such as L-Dopa, bromocriptine and amantadine help only few patients and may even aggravate the symptoms of tardive dyskinesia. In some double-blind studies cholinergic drugs such as lecithin and deanol have improved tardive dyskinesia, but further controlled studies are needed. Anticholinergic drugs such as antiparkinsonian agents should not be prescribed because they may aggravate tardive dyskinesia. Some patients respond to GABA-ergic agents such as baclofen, sodium valproate and the benzodiazepines, but further studies are needed before the value of GABA-ergic agents in the treatment of tardive dyskinesia can be properly assessed. After withdrawal of neuroleptics the average of remission rates within a year is 20%-30%. Elderly patients are more likely to have persistent dyskinesias. A progressive stepwise diminution of the neuroleptic dose and of the antiparkinsonian agents is recommended. When a patient's psychosis is exacerbated after withdrawal of the neuroleptics and tardive dyskinesia is also present, small doses of thioridazine, clozapine or tiapride can be administered. If this practice is not successful cholinergic or GABA-ergic agents may be useful. Because no currently available therapeutic agents satisfies the criteria of safety, marked effectiveness and prolonged efficacy in the treatment of tardive dyskinesia, prevention becomes more important. Prolonged use of a neuroleptic medication requires careful evaluation of indications and risks. The doses of neuroleptic drugs during the maintenance treatment of schizophrenia should be as small as possible.
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PMID:[Therapeutic measures in tardive dyskinesia]. 613 57

Neuroleptic drugs are believed to control schizophrenia by blocking brain dopamine receptors, although most act also on a number of other neuronal systems in brain. Substituted benzamide drugs in general, are more specific for the dopamine system. Brain dopamine receptors, however, are not a single entity. They can be divided on the basis of their linkage to adenylate cyclase. Substituted benzamide drugs are selective antagonists of the adenylate cyclase independent dopamine receptor population. They may be selective antagonists of one sub-population of these adenylate cyclase independent receptors, for unlike typical neuroleptics the receptor interaction of substituted benzamide drugs with brain dopamine receptors depends upon the presence of sodium ions. The specificity of substituted benzamide drugs for brain dopamine receptors is reflected in their behavioural profile. Typical substituted benzamide drugs do not cause catalepsy and, in general, only weakly inhibit motor phenomena. This inability to act in vivo cannot be entirely explained by the poor penetration of these drugs into brain. The unique properties of the substituted benzamide drugs might explain their clinical value in the treatment of schizophrenia and in the treatment of dyskinesias.
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PMID:Multiple dopamine receptors in brain and the pharmacological action of substituted benzamide drugs. 614 87

Two patients who developed the neuroleptic malignant syndrome (NMS) are described, and pertinent literature is reviewed. A 30-year-old man developed NMS, apparently as a result of haloperidol treatment of chronic undifferentiated schizophrenia. Treatment with cooling blankets, acetaminophen, dantrolene sodium, and bromocriptine mesylate decreased abnormal vital signs, but catatonia continued. After 30 treatments with electroconvulsive therapy over a one-month period, the patient's catatonia was resolved, and he was discharged on no medication with the schizophrenia in remission. The second patient was a 22-year-old woman who developed NMS after five weeks of therapy with haloperidol and thiothixene for an acute episode of abnormal behavior. She did not respond to therapy with cooling blankets, acetaminophen, antibiotics, and amobarbital sodium. Dantrolene sodium therapy produced no improvement except for some relief of muscular rigidity. Electroconvulsive therapy (22 treatments over one month) successfully decreased the patient's elevated liver enzymes and leukocyte count, but periodic temperature elevations and catatonia continued. Prompt diagnosis and treatment of NMS are essential, as the mortality rate is 20%. Acute lethal catatonia and malignant hyperthermia are considered in differential diagnosis. Both central and peripheral pathophysiologic mechanisms are probably involved in NMS, and most cases are seen in patients with psychiatric illness. Onset of NMS does not seem related to duration of neuroleptic therapy and, in susceptible persons, additional factors may be required to trigger onset of NMS. Symptoms, including diffuse muscular rigidity, akinesia, and fever, develop within 24-72 hours. Neurologic symptoms may develop or worsen, and leukocytosis and elevated levels of liver enzymes occur. Death can result from respiratory or cardiovascular failure, and rhabdomyolysis can lead to acute renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection and management of the neuroleptic malignant syndrome. 614 37

The time courses of changes in amplitudes of muscle action potentials (MAPs) obtained from gastrocnemius and soleus muscles by 5 Hz prolonged tibial nerve stimulation were studied. Subjects included muscular dystrophy (MD), spinal muscular atrophy, Issacs syndrome, idiopathic muscle spasms, psychiatric disorders such as autism and schizophrenia, and normal controls. In normal subjects, MAPs obtained at 5 minutes from gastrocnemius muscles was 87-102% of those at initiation of the stimulation. In soleus muscles, MAPs at 5 minutes was 95-105% of those at the beginning. In gastrocnemius muscles, MAPs increased in disorders such as Duchenne MD, Fukuyama type congenital MD, facioscapulohumeral MD, myotonic dystrophy, dermatomyositis, Kugelberg-Welander syndrome, viral myelitis, malignant hyperpyrexia, autism and schizophrenia. In soleus muscles, the increase of MAPs was demonstrated in Duchenne MD, Fukuyama type congenital MD, myotonic dystrophy and autism. MAPs remained within normal range in infants with Werdnig-Hoffman disease, Issacs syndrome and idiopathic muscle spasms. In two cases with Duchenne MD, MAPs obtained from gastrocnemius muscles reduced in amplitudes by the administration of dantrolen sodium. While the pathogenesis of the increased MAPs is not clear, several possible factors are discussed. It is considered that this 5 Hz examination may provide an important information for detecting the effect of dantrolen sodium on Duchenne MD, and it is also suggested that the examination will be a useful test for finding latent malignant hyperpyrexia.
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PMID:Increased muscle action potentials by 5 Hz prolonged nerve stimulation in neurological and neuromuscular disorders--clinical usefulness for detecting underlying pathophysiology. 648 78

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32


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