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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The previous works of the author demonstrated the clinical heterogeneity of Gilles de la Tourette's syndrome (GTS). Based on statistical treatment of the efficacy of 138 courses of the treatment with benzodiazepine tranquilizers, neuroleptics, antidepressants, and anticonvulsants, methods of the individualized treatment of GTS were elaborated. It is recommended that low doses of neuroleptics (orap, haloperidol) be applied in patients with typical GTS. Schizophrenia associated with Tourette-like disorders requires the use of higher doses of neuroleptics and, in some cases, of the combined therapy. In encephalopathy accompanied by Tourette-like disorders, the treatment with anticonvulsants and benzodiazepine tranquilizers turned out most effective.
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PMID:[Differential therapy of Gilles de la Tourette's syndrome]. 166 19

Fifty-four children with Gilles de la Tourette's syndrome were examined from 1987 to 1989. In 11 of them, Gilles de la Tourette-like disorders occurred within the framework of schizophrenia and in 6, of encephalopathy. The characteristic features of hyperkinesis associated with those conditions and their differences from the routine syndrome are depicted. The typology of Gilles de la Tourette's syndrome reflecting its clinical pleomorphism is suggested.
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PMID:[Characteristics of the Tourette syndrome-like disorders in various mental disorders]. 170 97

Nicotine potentiates the catalepsy produced by haloperidol. Furthermore, nicotine as an adjunct to haloperidol produces a remarkable improvement in motor tics in Tourette's syndrome (TS) patients. The present experiments (1) compared the ability of nicotine to potentiate the catalepsy produced by haloperidol or the selective D1 dopamine receptor antagonist SCH 23390 and (2) examined the effects of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) on haloperidol-induced (0.1, 0.2, or 0.4 mg/kg) catalepsy and locomotor hypoactivity. In the first experiment, nicotine produced a five-fold increase in catalepsy following haloperidol but had no effect on the catalepsy produced by SCH 23390. In the second experiment, nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 but not the 0.1 mg/kg dose of haloperidol. Haloperidol (0.1 and 0.4 mg/kg) also produced a dose-related decrease in locomotion that was significantly potentiated by nicotine (0.1 mg/kg). Nicotine alone did not produce catalepsy or any significant changes in locomotion. These results indicated that nicotine's potentiation of haloperidol-induced catalepsy is likely related to striatal D2 receptor mechanisms. Nicotine potentiated the locomotor effects of doses of haloperidol that were previously found to be subcataleptic, indicating that catalepsy testing may actually underestimate the behavioral interaction between haloperidol and nicotine. Nicotine may prove useful for treating neuroleptic responsive disorders such as TS, schizophrenia, and Huntington's disease.
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PMID:Nicotine potentiates the behavioral effects of haloperidol. 177 13

Since the initial observation by Brown (1914) that electrical stimulation applied to the habenular efferent bundle in the chimpanzee evoked a pattern of respiration which closely resembled the act of laughter, the habenular complex has remained a mysterious structure. The anatomy of the habenular complex is well delineated (Jones, 1985) forming a major component of the dorsal diencephalic conduction system. Data derived mainly from animal experimentation over the past decade point to the fact that the habenular complex functions as an important link between the limbic forebrain and the midbrain-extrapyramidal motor system. The elucidation of the functions of the habenular complex may thus significantly increase the current insight into the understanding of the interaction between behavioral and motor functions. Clearly, such information would be of great relevance for further understanding of neuropsychiatric disorders such as schizophrenia, Parkinson's disease, Tardive dyskinesia, and Tourette's syndrome in which behavioral and motor impairments are interfaced. This review summarizes anatomical, functional, and pharmacological aspects of the habenular complex and discusses its potential contribution to the pathophysiology of selected neuropsychiatric and movement disorders.
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PMID:Relevance of the habenular complex to neuropsychiatry: a review and hypothesis. 182 82

Nicotine was found to potentiate the catalepsy and reduced locomotion following the administration of haloperidol. The ability of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) to potentiate the catalepsy produced by haloperidol (0.1, 0.2 or 0.4 mg/kg) was investigated. Nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 mg/kg doses of haloperidol, but had no effect following the lowest (0.1 mg/kg) dose of haloperidol. The nicotine potentiation of catalepsy produced by the highest dose of haloperidol was independent of the dose of nicotine used. Nicotine alone did not produce catalepsy. A second experiment evaluated the ability of nicotine to potentiate the decreases in spontaneous locomotor activity produced by haloperidol. Animals received nicotine (0.1 mg/kg) alone or in conjunction with haloperidol (0.1 or 0.4 mg/kg) and were tested in Digiscan Animal Monitors. Haloperidol produced a dose-related decrease in locomotion. Nicotine significantly potentiated the hypoactivity produced by both doses of haloperidol. These results indicated that: 1) nicotine produces a significant potentiation of both the catalepsy and locomotor decreases following haloperidol and 2) the Digiscam Animal Activity Monitors may provide a more sensitive assessment of the interaction between nicotine and haloperidol than the catalepsy bat test. These data suggest that adjunct treatment with nicotine may prove useful for treating neuroleptic responsive disorders such as Tourette Syndrome, schizophrenia and Huntington's disease.
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PMID:Nicotine potentiates haloperidol-induced catalepsy and locomotor hypoactivity. 187 Dec

Pimozide, a diphenylbutylpiperidine neuroleptic which is FDA-approved as a backup treatment for Gilles de la Tourette's syndrome, has been used abroad for many years as a treatment of schizophrenia and has been recently reported to be particularly effective in treating monosymptomatic hypochondriacal psychosis and delusional jealousy. Pimozide may also have a role in the treatment of negative schizophrenic symptoms, pain syndromes, and obsessive compulsive disorder. After reviewing the relevant clinical literature supporting these indications, the authors review preclinical studies that provide points of departure regarding biochemical mechanisms underlying this unique therapeutic profile.
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PMID:The role of pimozide in clinical psychiatry: a review. 175 55

Evidence from experimental and clinical studies suggests the involvement of the endogenous opioid system in several neurologic and psychiatric disorders (Alzheimer's, Huntington's and Parkinson's diseases, drug-induced movement disorders, Gilles de la Tourette syndrome, stroke, ischemia, brain and spinal cord injury, epilepsy, schizophrenia and affective disorders). However, its involvement is rather a secondary one, perhaps being a severe consequence of a primary, nonopioid disturbance. Thus, treatment of an opioidergic manifestation of a disorder of nonopioidergic origin is necessarily symptomatic and targets only the restoration of the opioid system; such treatment may be beneficial in ameliorating the clinical symptoms of the disorder.
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PMID:The opioid system in neurologic and psychiatric disorders and in their experimental models. 218 70

Alterations in blink rate have been reported in several neuropsychiatric disorders presumed to result from abnormal central dopaminergic functions. Increased blink rate in schizophrenia, Tardive dyskinesia, Tourette's syndrome and Meige's disease are associated with enhanced dopaminergic functions. Parkinson's disease is associated with reduced dopaminergic functions and decreased blink rate. Thus, blink rate may reflect striatal and mesolimbic dopaminergic activity. Since acute light exposure suppresses melatonin production and darkness stimulates melatonin secretion, blinking may serve to regulate light-dark exposure to the pineal gland and thus to 'fine tune' melatonin production. As there is evidence to suggest that melatonin inhibits the release of dopamine in the striatum and limbic system, increased blink rate may serve to reduce light exposure, increase melatonin secretion and attenuate dopaminergic functions. Conversely, decreased blinking (as is observed in patients with Parkinson's disease) could reflect a compensatory mechanism to increase light exposure, reduce melatonin production and ultimately increase dopamine functions. This model is novel in that for the first time it suggests a functional link among blink rate, melatonin secretion and striatal dopaminergic functions in movement disorders.
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PMID:The significance of eye blink rate in parkinsonism: a hypothesis. 226 15

A review is presented of the diagnosis and drug treatment of the more common psychiatric and developmental disorders in the pediatric population. Where applicable, DSM III (Diagnostic and Statistical Manual of Psychiatric Disorders, III) criteria are utilized to describe the behavioral syndromes. The indications for usage and appropriate dosages of antipsychotics, antidepressants, anxiolytics, stimulants, and lithium are described. Those disorders discussed are attention deficit disorder, conduct disorders, anxiety disorders, sleep disorders, schizophrenia, autism, Tourette's syndrome, mental retardation, depressive illness, manic depressive illness, eating disorders, and enuresis.
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PMID:Pharmacologic treatment of psychiatric and neurodevelopmental disorders in children and adolescents (Part 1). 241 73

Childhood schizophrenia is an increasingly difficult disorder to identify. We review the DSM-III criteria for schizophrenia and raise the possibility that schizophreniform symptoms may be present in children with Tourette disorder to identify. We review the DSM-III criteria for seen in Tourette disorder that resemble the symptoms of schizophrenia are discussed and data from selected patients are presented. This data is presented to assist clinicians in making more appropriate diagnoses (that is, avoiding the incorrect diagnosis of schizophrenia) and in refining distinctions between the symptoms of schizophrenia seen in childhood and similar symptoms seen in other developmental disorders, especially Tourette disorder.
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PMID:Are schizophreniform symptoms present in attenuated form in children with Tourette disorder and other developmental disorders. 243 38


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