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)

Serum tryptophan and erythrocyte Na+/K+ ATPase were determined in 14 epileptics with and without psychosis. The nature of the psychosis in four patients was non-specific. The amino acid and the enzyme levels were also estimated in 11 patients with a diagnosis of functional affective psychosis, 14 patients with schizophrenia, and 9 normal subjects. Comparison of data among the patients and the normal subjects were done using analysis of variance. There were no significant differences in tryptophan profiles and Na+/K+ ATPase levels in epileptics with or without psychosis. In addition, the data obtained for these parameters for the schizophrenics were homogenous to those of epileptics. Significant differences were, however, obtained between the epileptics and patients with affective illness. The data thus suggested that the non-specific psychosis presented by the epileptics may be schizophrenia-like and lend support to a specific psychosis associated with epilepsy.
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PMID:Blood tryptophan and ATPase in psychosis of epilepsy. 182 59

A 39-year-old man developed disturbance of consciousness with hyponatremia during the treatment of schizophrenia in another hospital. He became alert after the correction of hyponatremia. But his consciousness deteriorated one day later in spite of normal serum sodium level, then he was referred to our hospital. The disturbance of consciousness, quadriparesis and rigidity were persisted even 4 months later. MRI (T2WI) showed well defined high intensity areas along the deep layer of the cerebral cortex and in the bilateral basal ganglia. But there were no lesions in the pons on MRI. Therefore, the diagnosis was made as extra-pontine myelinolysis (EPM) without apparent central pontine myelinolysis (CPM) according to the MRI findings. Recently, the EPM without CPM has been reported in 3 patients. Two cases were examined pathologically, findings of which were characterized by Morel's laminar necrosis at the deep layer of the cerebral cortex. But there is no report in the literature describing the detection of Morel's laminar necrosis on antemortem MRI. It seemed that the MRI findings of our case indicated Morel's laminar necrosis. Our case is suggestive in relation to the pathogenesis of EPM and CPM.
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PMID:[Morel's laminar necrosis like findings on MRI in a case of extra-pontine myelinolysis]. 189 77

We reported a case of acute water intoxication from compulsive water-drinking, who showed triphasic waves on EEG. The patient was a 50-year-old man who had been undergoing medical treatment in a mental hospital since he was suffering from schizophrenia diagnosed at the age of 35. He had sometimes had a tendency to drink a large amount of water since 45 years old. He began to drink water compulsively since three days ago. He vomited just after he drank excessive water with his mouth directly to the tap for several minutes, and soon fell into loss of consciousness. He was transmitted to our hospital because of acute consciousness disturbance on the next day. On neurological examination, he was profoundly comatose with miosis and conjugate deviation to the right side. His extremities showed decorticate posturing. On admission, serum sodium level was 101 mEq/l, and plasma osmolality was 208 mOsm/l. Serum enzymes derived from muscle and myoglobin were markedly elevated. But there was no laboratory evidence of the other metabolic disorders such as hepatic or renal disease. Computed tomography of the brain disclosed severely diffuse swelling with largely obliterated sulci and narrowed ventricles. EEG showed triphasic waves predominantly over centro-parieto-occipital portion, behind which there was slow wave activity with a loss of normal alpha wave activity. Immediately, treatment began by a combination of saline and glyceol infusion for the purpose of correcting severe hyponatremia, subsequently removing brain edema. As serum sodium level gradually returned to normal, the brain CT findings were getting better.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of acute water intoxication showing triphasic waves on EEG]. 193 65

The neuronal dopamine transporter/uptake site can be covalently labeled with the photoaffinity probe 1-(2-[bis-(4-fluorophenyl) methoxy]ethyl)-4-[2-(4-azido-3-[125I]iodophenyl)ethyl]piperazine [( 125I]FAPP) and visualized following sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography. Upon photolysis, [125I]FAPP specifically incorporated into a polypeptide of apparent Mr = 62,000 in membranes from both the putamen and the caudate nucleus of control, Alzheimer's, schizophrenia, and Huntington's diseased brain, and following complete deglycosylation, migrated as an Mr approximately 48,000 polypeptide. In parkinsonian postmortem putamen, however, there was no detectable photoincorporation of [125I]FAPP into the ligand binding subunit of the dopamine transporter. [125I]FAPP did specifically label the Mr 62,000 polypeptide of parkinsonian caudate, although with efficiencies of 20-50% of control. The asymmetrical loss of the dopamine transporter in Parkinson's diseased striatum was confirmed in reversible receptor binding experiments using [3H]GBR-12935 (3H-labeled 1-[2-(diphenylmethoxy) ethyl]-4-(3-phenylpropyl)piperazine). In parkinsonian putamen, mazindol competitively inhibited the binding of [3H]GBR-12935 with an estimated affinity (Ki approximately 2,000 nM) 10 times lower than in controls (Ki approximately 30 nM), while the affinity of maxindol for [3H]GBR-12935 binding in the caudate was equal to that seen with controls (Ki approximately 50 nM). The proportion of [3H]GBR-12935 binding sites recognized by mazindol with high affinity in Parkinson's diseased caudate was, however, reduced by 50-80%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The dopamine transporter is absent in parkinsonian putamen and reduced in the caudate nucleus. 198 18

Three mechanisms of lithium transport across erythrocyte membrane [lithium-sodium countertransport (LSC), lithium-potassium cotransport (LPC), and passive lithium diffusion (PLD)] were estimated in 27 acutely schizophrenic patients, 27 acutely depressed affective patients and in 18 control subjects. The activities of all mechanisms studied were significantly lower in both schizophrenic and depressed patients compared with controls. Analysis by gender showed that in control subjects, mean values of erythrocyte LSC and LPC were significantly higher in males compared with females. The decrease of LSC and LPC in depression and LSC in schizophrenia compared with control subjects was observed only in male patients but not in female ones. The results obtained suggest that lithium transport abnormalities during acute psychotic episodes are not specific to affective patients where lithium exerts its therapeutic action, but are also observed in schizophrenia. These abnormalities are more evident in male patients.
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PMID:Abnormalities of lithium transport across the erythrocyte membrane in depression and schizophrenia. 203 77

The present review deals with the molecular mechanisms and elementary phenomena underlying the activation of the voltage- and chemo-sensitive membrane macromolecules: sodium- and potassium-ion channels and nicotinic ACh receptors and their associated ion channel. To achieve an understanding of their various kinetics and conformational states, a number of novel alkaloids, BTX, HTXs, gephyrotoxins, and certain psychotomimetic drugs such as phencyclidine, and many other pharmacologically active agents have been used. Biochemical assays and various electrophysiological techniques have been used in a number of biological preparations--e.g., Torpedo membranes, brain synaptosomes, amphibian and mammalian neuromuscular preparations--to describe the action of such agents. The availability of BTX and scorpion toxins together with aconitine and veratridine as activators and TTX and STX as antagonists of the voltage-sensitive sodium channels, made possible the identification and the physiological and pharmacological characterization of these channels. These studies provided the basis for understanding the mechanisms underlying electrical excitability and culminated, more recently, in the purification and reconstitution of sodium channels from rat brain and in the successful cloning of these channels with the elucidation of their primary structure. We now know that the sodium channel has a molecular mass of 316,000 daltons, consists of five subunits, and has multiple sites for various ligands. In contrast to sodium channels, various classes of potassium channels (inward and outward rectifier potassium channels and Ca(2+)-activated potassium channels) have been described. Unlike the sodium channels, there are no known specific activators for potassium channels. However, a number of potassium channel blockers such as 4-aminopyridine, HTX, histamine, and norepinephrine have been identified which complement the varying types of potassium channels in different neurons. One class of potassium channel blockers with profound medical and social implications comprises PCP and its analogues. The blockade of the potassium-induced 86Rb+ efflux from brain cells, the resulting prolongation of muscle and nerve action potentials, and the increase in transmitter release observed with PCP and some analogues are all highly suggestive of a role for the potassium channel in the behavioral effects of these drugs and its potential involvement in schizophrenia. A number of toxic principles of both plant and animal origin played a significant role in the development of our knowledge about the nAChR.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Macromolecular sites for specific neurotoxins and drugs on chemosensitive synapses and electrical excitation in biological membranes. 248 4

As most diet therapy texts provide little information about psychiatric illnesses and their treatment, this article is intended as a brief introduction for dietitians. Several psychiatric illnesses, including schizophrenia, mood disorders, eating disorders, and substance abuse, may adversely affect food intake and nutritional status. The drugs used to treat those disorders similarly have effects on appetite and gastrointestinal function and interact with food and nutrients. Antipsychotics, antidepressants, and monoamine oxidase inhibitors (MAOIs) cause dry mouth, constipation, and weight gain. Lithium may cause nausea, vomiting, diarrhea, polydipsia, and weight gain. MAOIs have well-known interactions with foods containing tyramine. Lithium interacts with dietary sodium and caffeine; decreasing dietary intakes of those substances may produce lithium toxicity. Despite claims to the contrary, major psychiatric illnesses cannot be cured by nutritional therapies alone. Dietitians can, however, play an important role as part of a multidisciplinary team in the treatment of patients with psychiatric illness. Such a role includes nutrition assessment and monitoring, nutrition interventions, patient and staff education, and some forms of psychotherapy, including supportive and behavioral therapies for patients with eating disorders.
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PMID:Nutritional aspects of psychiatric disorders. 267 98

The psychoneuroendocrinology of schizophrenia derives from the presumption that neurotransmitter or receptor abnormalities in the limbic regions might extend to or influence the hypothalamus, which plays a role in the regulation of prolactin (PRL) secretion from the anterior pituitary gland. Since a GABA disturbance has been recently proposed in the pathogenesis of certain schizophrenic symptoms, and since a tuberoinfundibular-GABA (TI-GABA) system has been shown to modulate PRL secretion in humans, we tested the activity of this system both in controls and in chronic schizophrenic women. For this purpose the GABAergic drug sodium valproate (800 mg) was administered orally to 20 healthy women and 18 chronic schizophrenic women. Plasma PRL levels were measured before and after the drug administration. Sodium valproate decreased PRL concentrations only in the healthy women. Although the hypothesis of a GABA disturbance in schizophrenia at present is only speculative, these results might suggest a defect of the TI-GABA system in chronic schizophrenia.
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PMID:Failure of the GABAergic drug, sodium valproate, to reduce basal plasma prolactin secretion in chronic schizophrenia. 300 77

The hypothesis of a gamma-aminobutyric acid (GABA) involvement in the pathophysiology of schizophrenia has been recently proposed but not confirmed. As GABA has been shown to affect basal growth hormone (GH) secretion in humans, the assessment of plasma GH response to a GABAergic drug, such as sodium valproate (SV), in schizophrenic subjects might be a tool with which to investigate central GABA activity in this illness. For this purpose, we administered orally 800 mg of SV or placebo to 13 chronic schizophrenics and to 10 normal controls, and measured plasma GH levels before and after the drug administration. SV enhanced basal GH secretion in healthy male volunteers, but not in chronic schizophrenics. These results suggest a defect of the endogenous GABA system in chronic schizophrenia. Whether the reduced responsiveness observed represents a primary defect or a secondary alteration of the GABA system in schizophrenia is as yet unknown.
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PMID:Growth hormone response to sodium valproate in chronic schizophrenia. 308 38

The effect of zinc nutriture and metabolism on brain function has been reviewed. Zinc nutriture and its effect on the concentration and metabolism of essential elements (e.g. zinc, copper, manganese, magnesium, sodium, potassium and calcium) and on the concentration and metabolism of toxic elements (e.g. aluminum and lead) are discussed in relationship to brain function. In addition, possible interrelationships between zinc nutriture and metabolism and its effect on a number of diseases including acrodermatitis enteropathica, Pick's disease, Alzheimer's disease, schizophrenia, fifth day fits, and epilepsy are discussed. Descriptions and comparisons of methods to measure brain zinc are presented. Behavioral changes and the altered brain morphology which have been associated with zinc deficiency are reviewed. Some possible mechanisms for the association of anorexia with zinc deficiency are outlined. Perinatal brain damage produced by early zinc deficiency followed by rehabilitation with adequate zinc appears to be long term, maybe permanent. Interrelationships between zinc nutriture and aspects of neurochemistry are outlined. Some of the neurochemistries discussed include nucleic acid and protein synthesis, cytoskeletal proteins, neurotransmitters (e.g. catecholamines, indoleamines, glutamate, gamma-aminobutyric acid, and neuropeptides), neurotransmitter receptors, 7S nerve growth factor and zinc-binding proteins. Recent evidence linking zinc and neurotransmission is discussed.
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PMID:Zinc and the central nervous system. 330 3


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