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)

There are correlations between schizophrenia and the limbic seizure system on the one hand and the manic-depressive or bipolar syndromes and the generalized seizure system on the other hand, which are theoretically related to the different (although overlapping) neural substrates underlying the two major syndromes of psychosis. Evidence is reviewed that indicates that in ECT-responsive depression (with both bilateral and unilateral nondominant ECT) the modus operandi hinges on right-hemispheric neural events. At the same time the relevance of the complex interactions existing between limbic and generalized seizures, REM suppression, right limbic epilepsy and REM activation is discussed as well as the role of carbamazepine in these interactions.
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PMID:[Cerebral mechanisms of the efficacy of electroshock therapy]. 345 May 4

The neurophysiological systems subtending generalized seizures (activated by ECT) and temporal-limbic seizures are described as well as the interactions existing between the two seizure systems. There are correlations between schizophrenia and the limbic seizure system on the one hand and the manic-depressive or bipolar syndromes and the generalized seizure system on the other which are theoretically related to the different (although overlapping) neural substrates underlying the two major syndromes of psychosis. Evidence is reviewed that indicates that in ECT-responsive depression (with both bilateral and unilateral nondominant ECT) the modus operandi hinges on right-hemispheric neural events. Neurophysiological, neurological, and acoustic threshold evidence is discussed: all of which emphasizes the importance of the nondominant hemisphere in the genesis of endogenous depressions and in their treatment with convulsive therapies. In addition, studies showing that psychotropic agents with specific antidepressant effects produce asymmetric activation of the right hemisphere (EEG) are related to the above issues.
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PMID:Electroconvulsive therapy and lateralized affective systems. 351 73

This study examines differential attention deficits in 19 temporal lobe epilepsy (TLE) patients, 15 generalized seizure patients (GSP), and 19 schizophrenic patients, compared to 20 normal controls. All participants were tested on a variable foreperiod reaction time (RT) task and continuous performance test (CPT). Temporal lobe epilepsy patients and schizophrenic patients show crossover deficits on the RT task requiring a conscious, effortful, preparatory motor set; while GSP show impairments on the CPT requiring vigilant, self-directed attention to external stimuli. The results suggest separate cortical and subcortical brain systems in the respective attentional deficits and in the etiologies of TLE, GSP, and schizophrenic disorders.
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PMID:Assessment of differential attention mechanisms in seizure disorders and schizophrenia. 911 Mar 37

Neuropeptides: corticotropin releasing factor (CRF), neuropeptide Y (NPY) and somatostatin (STS) have been associated with depression and anxiety, while neurotensin (NT), calcitonin gene-related peptide (CGRP) and tachykinins [neurokinin A (NKA) and substance P (SP)] are presumed to also play a role in the function of the dopaminergic system. Moreover, investigations in the past decade have shown that psychotomimetics and antipsychotic drugs as well as lithium affect brain synthesis, tissue concentrations, and release of some neuropeptides. In view of the above, experiments were carried out to explore whether changes in neuropeptides constitute one of the mechanisms of action of electroconvulsive treatment (ECT). Human cerebrospinal fluid (CSF) was studied before and after ECT, and brains from healthy and models of depression rats were investigated in electroconvulsive stimuli (ECS)-treated and sham-treated animals. The major findings were that a series of ECTs, in parallel to clinical recovery, increased CSF concentrations of NPY-like immunoreactivity (-LI), STS-LI, and CRF-LI, and in one study endothelin-LI. A series of ECS, but not a single treatment, reproducibly elevated concentrations of NPY-LI, NKA-LI, and STS-LI--but not NT-LI, SP-LI, galanin-LI, or CGRP-LI--in hippocampus, frontal cortex, and occipital cortex. No changes were measured in other regions, e.g., striatum. NPY and STS mRNAs were also increased indicating that ECS affects peptide synthesis. Generalized seizures induced by, e.g., kainic acid or pentylenetetrazole, had similar effects on neuropeptides. The changes persisted for at least 1 week after the last treatment. Pretreatment with compounds reducing seizures, such as benzodiazepines and MK-801; had no effect on magnitude of neuropeptide changes although the seizure duration was decreased by > 50%. On the basis of these findings, it is suggested that neuropeptides are involved in ECT's mechanisms of action. Since ECT is therapeutically efficient in both schizophrenia and depression and, taking into account that antipsychotic drugs and psychotomimetics as well as lithium selectively affect some neuropeptides, it is hypothesized that distinct combinations of neuropeptide and monoamine changes in selected neuronal populations constitute the underpinnings of ECT's effects on specific disease symptoms, conceivably independent of diagnosis.
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PMID:Neuropeptides and electroconvulsive treatment. 1018 19

We report on a case of rhabdomyolysis induced by the correction of hyponatremia after psychogenic polydipsia and clozapine use, where the switch to a high dose of olanzapine resulted in the non-recurrence of rhabdomyolysis. The 46-year-old patient with the diagnosis of schizophrenia paranoid type, who had been on clozapine treatment for the previous 4 years, was admitted with the symptoms of generalized seizure and vomiting, and as severe hyponatremia was proved, its correction with the parallel use of clozapine treatment was done. CK concentrations increased to 48 120 U/L without any symptom of neuroleptic malignant syndrome. To prevent acute renal insufficiency, high-volume alkaline diuresis was initiated and clozapine was tapered and stopped. On the day 12 of treatment, olanzapine was started and was elevated to 30 mg/day. CK concentration began to fall returning to the normal concentration on day 20. Six months after the switch to olanzapine no recurrence of rhabdomyolysis was detected; clinical and laboratory findings were normal. We suggest that after a benzodiazepine-type antipychotic-induced rhabdomyolysis, a switch to another atypical antipsychotic can be a cautious clinical strategy.
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PMID:Successful switch to olanzapine after rhabdomyolysis caused by water intoxication and clozapine use. 1687 73

We report a case of a patient with schizophrenia treated with high-dose risperidone, who developed syndrome of inappropriate antidiuretic hormone secretion (SIADH) with the only early symptom of tonic-clonic seizures. A 40-year-old woman with schizophrenia was treated with risperidone 2 mg/d. After the dosage was titrated to 6 mg/d, she experienced generalized seizure attacks. Laboratory screening revealed that the serum sodium level was 106 mmol/L, the urine sodium concentration was 41.2 mmol/L, and the urine osmolality was 371 mOsm/kg H2O. A diagnosis of SIADH was made, and risperidone was stopped. After infusion of hypertonic saline, the serum sodium returned to normal levels, and seizures did not recur. In this patient, SIADH advanced in a latent manner because the first and only symptom of SIADH was seizure attack. High-dose risperidone treatment is the most probable cause, and the mechanisms may be related to risperidone's high affinity for the 5-hydroxytryptamine 2A and dopamine 2 receptors. Patients with schizophrenia can display atypical features of medical illnesses. Routine physical and laboratory examinations may prevent silent disease progression.
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PMID:High-Dose Risperidone Induced Latent Syndrome of Inappropriate Antidiuretic Hormone Secretion With Seizure Presentation. 2616 41