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)

Early results for an uncontrolled study of 555 patients with florid schizophrenia suggest that propranolol can be used safely in high dosage, and in a proportion of cases it appears to control schizophrenic symptoms. This method of treatment is now being submitted to controlled trial. Evdence from this uncontrolled study suggests that there was a therapeutic dose range in which symptoms steadily improved as a low dose was ineffective and a high dose, particularly if reached too rapidly, caused toxic effects. Rapid increases (400-800 mg) in the daily total intake when given in divided doses (4 to 10/day) produced gross toxic effects that included ataxia with unprotected falls, drop attacks, visual hallucinations, and confusional states. Severe toxic effects were uncommon when the dose was raised by regular, gradual increments (e.g. by 40-80 mg/day), when propranolol was given twice daily, when the dose was held steady as the patient started to improve, and when the daily total dose was reduced if the fall in pulse rate or blood pressure was excessive, or if there was evidence of toxicity. The observation of gradual, progressive improvement was the most valuable positive guide to the dose of propranolol. All schizophrenic symptoms remitted, at least temporarily, in 26 of 55 patients (in 15 of 17 patients who had been ill for less than one year and in 11 of 38 patients who had been ill for longer than a year). Patients who then stopped propranolol usually relapsed within hours or days.
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PMID:Safeguards in the treatment of schizophrenia with propranolol. 96 74

Phencyclidine (PCP), a drug inducing schizophrenia-like symptoms in humans, is reported to be a non-competitive antagonist at the N-methyl-D-aspartate (NMDA) subtype of excitatory amino acid receptors. In rats, PCP produces three dose-dependent stages of EEG patterns: 1) increase of cortical desynchronization duration; 2) increase of the amplitude of the high-frequency (20-30 Hz) low-voltage (30-50 microV) cortical background activity; 3) appearance of cortical slow (2-3 Hz) wave-sharp wave complexes. These EEG changes are accompanied by stimulatory-depressive effects such as stereotypy (circling, head weaving) and ataxia. In the present study, the EEG and behavioural effects induced by systemic administration of the NMDA antagonists dizocilpine (MK 801), dextromethorphan (DM), [(+)-alpha-(4-chlorophenyl)-4- [(phenyl)methyl-1-piperidine ethanol] (SL 82.0715), (+)3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) have been compared to those of PCP in rats. The rank of potency for inducing PCP-like EEG stages 1-3 was as follows: MK 801 > PCP > CGS 19755 > CPP. These drugs also induced PCP-like behavioural effects. On the contrary, DM and SL 82.0715, administered up to the dose of 100 mg/kg IP, failed to induce PCP-like behavioural effects and elicited only the stage 1 of PCP-like EEG. These results strongly suggest the involvement of NMDA neurotransmission in the behavioral and EEG effects of PCP.
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PMID:Different capability of N-methyl-D-aspartate antagonists to elicit EEG and behavioural phencyclidine-like effects in rats. 136 27

The clinical and biochemical characteristics of metachromatic leukodystrophy (MLD), true adult forms and late juvenile forms which are still living at adulthood, are reviewed as they both are observed in adult Neurology and Psychiatry departments. Mental deterioration is often the first symptom, evolving progressively; and dementia finally occurs. The latency before the appearance of neurological objective symptoms may be long and extend for several years. In many cases, the behavioral abnormalities are the first symptoms. Some of these forms have been diagnosed as schizophrenia. Very seldom, neurological symptoms, especially ataxia, occur without cognitive or psychiatric disturbances. Most of these cases have pyramidal and cerebellar symptoms, at diverse degrees. Seizures can also occur which is some cases can be early symptoms associated to mental deterioration. The association of central and peripheral neurological symptoms is very characteristic of MLD. The peripheral neuropathy is not generally clinically evidenced, but is rarely missing electrophysiologically. Arylsulfatase A determination should be performed for diagnosis as a first step, and confirmed by the accumulation of sulfatide, either by quantitative determinations in urine or by the sulfatide loading test. It is as yet not clear why certain forms have a rather rapid evolution in 5 years, and others have a very protracted course during decades.
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PMID:Adult forms of metachromatic leukodystrophy: clinical and biochemical approach. 168 76

The benzodiazepine clonazepam was approved for the treatment of epilepsy in 1976. To study its use in acute mania, the author compared clonazepam with lithium in a crossover trial. Clonazepam proved more effective than lithium in controlling the symptoms of mania and caused fewer manifestations of parkinsonism. Associated side effects included ataxia, drowsiness, and behavioral changes. No treatment-emergent depression was observed. Neither clonazepam nor any other benzodiazepine is recommended in schizoaffective or schizophrenic disorders because of the high risk of dependence in those patients, in contrast to manic-depressives. For the maintenance treatment of bipolar disorder, lithium is recommended as the initial agent, with L-tryptophan added if concomitant medication is needed. Clonazepam can then be added as the anticonvulsant, if necessary. In the treatment of acute mania, clonazepam is recommended for the first week of treatment, and lithium is added in the beginning of the second week, thus avoiding the use of neuroleptics.
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PMID:The use of benzodiazepines in the treatment of manic-depressive illness. 290 43

Five vervet monkeys were administered increasing doses (4--12 mg/kg/day) of d-amphetamine over a period of 35 days. Three phases od behavioural change were discerned: phase 1 during which animals exhibited repetitive stereotyped action sequences with rapid head movements, occasional abnormal grooming, picking at the cage, hand-staring and snatching; phase 2 in which behaviour became progressively more restricted and animals became markedly unresponsive to auditory, visual and tactile stimuli; phase 3 was characterised by the abrupt development of gross over-responsiveness to environmental stimuli, ataxia and tremor. At post-mortem, by comparison with controls, amphetamine-treated monkeys showed marked depletions of the monoamines dopamine (DA), noradrenaline (NA) and serotonin (5-HT) in corpus striatum and cerebral cortex and reductions in the activities of tyrosine hydroxylase and dopa decarboxylase in striatum. Turnover of these monoamines, assessed by high-performance liquid chromatography determinations of their respective metabolites, was also reduced. These findings are interpreted as evidence of monoamine neurone destruction, most severely in the case of DA neurones. Though there was a non-significant reduction in 3H-spiperone binding (reaching almost 50% in nucleus accumbens), numbers of receptors for the monoamines nA and 5-HT were not significantly changed, and the activities of the enzymes choline acetyltransferase and glutamine decarboxylase were similar in experimental and control animals. The contrast of these findings with those seen in post-mortem brains in schizophrenia is discussed.
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PMID:Behavioural and biochemical effects of chronic amphetamine treatment in the vervet monkey. 613 May 56

There is still another type of convulsive movement, involving the muscles of the eye and speech, which is both characteristic and of frequent occurrence in dementia praecox. Some of these movements correspond exactly to the movements of expression; wrinkling of the eyebrow, distortion of the mouth, rolling the eyes, and those other facial movements which are characterized as grimacing. These movements remind one of choreic movements and are quite independent of the ideas and feelings. They may be associated with the smacking of the lips, clucking the tongue, sudden grunting, sniffing, and coughing. Furthermore, in the lips we observe very rapid rhythmical movements. More often there exists a peculiar choreiform movement of the mouth which may be described as an athetoid ataxia.
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PMID:Pathophysiology of schizophrenia. 634 68

Argininosuccinic aciduria (ASA-uria) is a rare inborn error of the urea cycle, in which there is massive excretion of argininosuccinic acid (ASA) in the urine together with elevated concentrations of ASA in the plasma and the CSF. The characteristic symptoms are either those of overwhelming metabolic disease in the newborn period, or variable psychomotor retardation. The present patient, the first Finnish one to be reported, was a 49-year-old woman. She was hospitalized at the age of 26 with a diagnosis schizophrenia and mental retardation. Her clinical symptoms consisted of ataxia, disturbance of coordination, clumsiness, intention treMor and a positive Romberg's sign. The laboratory findings were consistent with the mild, late-onset type of ASA-uria.
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PMID:Argininosuccinic aciduria in a Finnish woman presenting with psychosis and mental retardation. 713 86

Recently, it has been demonstrated that unstable trinucleotide repeats are the etiologic factor in myotonic dystrophy, fragile-X syndrome, Kennedy's disease, Huntington's disease, spinocerebellar ataxia type 1, and dentatorubral-pallidoluysian atrophy. All available evidence suggests that these expanded trinucleotide repeats, or unstable DNA, are the biological basis of the clinical phenomenon of genetic anticipation. Two components of anticipation, increased severity and earlier age of onset in subsequent generations, have been widely observed in schizophrenia. We review the evidence for and against genetic anticipation in schizophrenia. Although the major criticisms of the anticipation hypothesis can be questioned, so can the evidence in favor of it. We conclude that molecular genetic approaches might be the most useful means of resolving ambiguity in clinical arguments about the origin of the anticipation-like phenomenon in schizophrenia.
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PMID:Genetic anticipation in schizophrenia: pro and con. 758 22

Phencyclidine (PCP), in a dose of 15 mg/kg, produced delayed cognitive dysfunction (at 24 h) in rats subjected to water maze tasks. At 24 h after PCP administration, ataxia, hyperlocomotion and stereotyped behavior were not induced. NE-100, N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-enthylamine monohydrochloride, a selective and potent sigma receptor ligand, was administered orally 10 min after PCP administration or 15 min before the first trial (24 h after PCP administration). In both cases, NE-100 dose-dependently attenuated the delayed cognitive dysfunction induced by PCP. As these findings show that ingestion of PCP led to delayed cognitive dysfunction similar to the cognitive signs of psychosis seen in humans, NE-100 is being further studied for possible treatment of subjects with schizophrenia.
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PMID:Effect of NE-100, a novel sigma receptor ligand, on phencyclidine- induced delayed cognitive dysfunction in rats. 760 28

Niemann-Pick disease type C (NPC) is a neurometabolic genetic disorder that is distinguished from Niemann-Pick disease by its later onset, more insidious progression, variable visceromegaly, and abnormalities of intracellular cholesterol metabolism. We describe a patient who presented with an 8-year history of psychosis requiring chronic neuroleptic therapy for a presumed diagnosis of schizophrenia. He was subsequently diagnosed with NPC as the emerging features of dementia, ataxia, dysarthria, and vertical supranuclear ophthalmoplegia were recognized. The characteristic features of adult-onset NPC and the obstacles to early diagnosis are reviewed.
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PMID:Psychosis as the initial manifestation of adult-onset Niemann-Pick disease type C. 864 5


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