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 yin-yang hypothesis is presented linking noradrenergic activity, thromboxane, melatonin, left hemisphere functioning, and cyclic AMP on the one hand, and dopamine, beta-endorphin, calcium, right hemisphere functioning, and cyclic GMP on the other. It is further suggested that there is a yoking of NA, TXA2, serotonin and melatonin in the left hemisphere, and a similar yoking of DA, BE, calcium and cGMP in the right. Evidence is presented to support the hypothesis that each element (NA, TXA2, etc.) on one side can modulate or balance a corresponding element (DA, BE, etc.) on the other. It is suggested that thromboxane is the key element in noradrenergic overactivity and that not taking this into consideration has confounded much prior research. This theory takes into account information processing models as well as pharmacological data and neurochemical theory on coupling of adenylate cyclase to its hormone receptors. Inhibiting noradrenergic overactivity can be obtained by inhibiting thromboxane and concomitantly activating opiate receptors. This protocol may have clinical utility in treating a wide range of disorders such as: anxiety, depression, schizophrenia, sleeplessness, withdrawal states, enuresis, Gilles de la Tourette syndrome, Parkinsonism, Alzheimers, dementia, anorexia, infant ruminations, essential tremor, spasticity of spinal cord injury, diarrhoea, ulcerative colitis, extrapyramidal symptoms, akathisia, neuroleptic malignant syndrome, attention deficit disorder, hyperhidrosis, and possibly AIDS.
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PMID:Inhibiting noradrenergic overactivity by inhibition of thromboxane and concomitant activation of opiate receptors via dietary means. 254 22

The article briefly reviews the use of modern molecular genetic methods in research into the genetic bases of psychiatric diseases. It raises some basic methodological problems, and describes more recent technologies (RFLP/VNTR markers). Present knowledge about the molecular genetics of Alzheimer's disease, schizophrenia, manic depression, Tourette's syndrome and infantile autism is briefly reviewed in to order show the potential benefits of gene technological methods in this area of research.
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PMID:[Gene technology and mental disorders]. 257 4

The contribution of the environmental risk-factors has been studied in 25 children with Tourette's syndrome and 25 children with sluggish schizophrenia. It has been established that the levels of the severity of the toxicosis in pregnancy, the presence of the nephropathy, neuroinfections of the first year of life were significantly higher in the Tourette's syndrome, than in schizophrenia. Those data are not in line with the speculations about one major dominance gene transmission for the Tourette's syndrome, because genetic contributions in it and in the child schizophrenia are equal. The environmental risk-factors may morbogenic role in the development of Tourette's syndrome.
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PMID:[Comparative characteristics of somatic risk factors for the development of Tourette syndrome and slowly-progressing schizophrenia in childhood]. 272 34

Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement of concentration and attention span. Nicotine gum alone was without effect. While 80% of children showed improvement with nicotine gum, 70% completely discontinued the gum because of side-effects, primarily involving nausea and bitter taste. Nicotine may prove useful for treating other neuroleptic responsive disorders, such as schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome. 273 Sep 49

The role of neuroleptics in causing the tardive dyskinesia syndrome is controversial. To properly assess the contribution of drugs as the etiology of dyskinesias, the effects of aging, the natural history of psychosis, and characteristics of spontaneous dyskinesias must be considered. Though the buccolinguo-masticatory triad is seen more often in tardive than in spontaneous dyskinesias, these two disorders have many symptoms in common. Other dyskinesias, such as idiopathic and tardive dystonia or tardive Tourette's syndrome and dyskinesias in untreated schizophrenia, are poorly understood. Chronic neuroleptic treatment may only precipitate TD in those already predisposed to develop such movement disorders. Tardive dyskinesia is not a unique movement disorder, but rather spans several clinical and epidemiological phenomena which must be considered in a balanced evaluation of how much of the permanent dyskinesias should be attributed to neuroleptic drugs.
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PMID:Is tardive dyskinesia a unique disorder? 286 Jun 61

A 36 year-old female patient with schizophrenia and Tourette syndrome is described. Clinical course, present neurological and psychopathological state, results of psychological testing, computed tomography and MR tomography of the skull, EEG and evoked potentials are reported. Results of neurochemical analysis of CSF and plasma are presented. Possible relationships between Tourette syndrome and schizophrenia are discussed with particular reference to neurochemical findings.
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PMID:[Schizophrenic psychosis in a patient with Gilles de la Tourette syndrome]. 290 4

We report a patient in whom Tourette's syndrome (TS) and Type I schizophrenia coincided, and suggest, based on clinical features and pharmacological responses, that both conditions in this patient could have a common pathophysiological basis.
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PMID:Gilles de la Tourette's syndrome associated with chronic schizophrenia. 316 70

In North Dakota children, the prevalence rate for DSM-III schizophrenia is 0.19 per 10,000 for both sexes; for males 0.35 per 10,000 and 0 per 10,000 for females. In this report we utilize case studies to convey the symptomatic courses of the 2 child patients with DSM-III-R defined schizophrenia. Both patients first developed Tourette Disorder (TD) and later developed schizophrenia by DSM-III and by DSM-III-R criteria. Among North Dakota children with TD the prevalence rate of schizophrenia is 8.7% for boys. The ramifications of concordance for the two disorders are explored.
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PMID:Tourette disorder and schizophrenia in children. 322 53

The unmistakable symptoms of Gilles de la Tourette Syndrome are classically of muscular spasms or tics, often accompanied by uncontrolled verbal outbursts or shouting of obscenities. Anecdotal as well as clinical reports suggest that these patients also suffer some psychological distress. This study used traditional MMPI scales to evaluate the psychopathological features that may underlie or accompany this disorder. In addition, we analyzed individual items of the MMPI to learn more of the phenomenology of this disorder. Data were collected from 29 Tourette patients and 29 normal controls matched for age and sex. A multivariate analysis of the clinical MMPI scales revealed group differences in score profiles. Univariate analyses indicated that Tourette subjects scored higher on the following scales: Schizophrenia, Depression, Psychopathic Deviate, Psychasthenia and Hypochondriasis. The results indicate that Tourette patients are in considerable psychological distress.
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PMID:Psychological aspects of Gilles de la Tourette syndrome. 345 22

A Gilles de la Tourette's syndrome (TS) patient is described who experienced a schizophrenic episode 11 years after TS onset. Analogies and differences between the two syndromes are reviewed, leading to the conclusion that TS is a definite entity independent from schizophrenia, but that they share some common features of symptomatology and pathophysiology and have closely related anatomical lesions.
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PMID:Gilles de la Tourette's syndrome and schizophrenia. 345 99


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