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)

This review assesses the usefulness of beta-blockers in the treatment of aggression and describes the parameters for their clinical use. A Medline search using the terms "beta-blockers," "aggression," "propranolol," and "brain injury" identified relevant journal articles published in English between 1977 and 1993. Open, prospective and double-blind, placebo-controlled studies, as well as case reports, were included. Beta-blockers appear to be effective in decreasing the frequency and intensity of aggressive outbursts associated with a wide variety of conditions, such as dementias, attention-deficit disorder, personality disorders, Korsakoff's psychosis, posttraumatic stress disorder, schizophrenia, profound mental retardation, autism, and brain injury. A general discussion attempts to resolve some of the issues surrounding the possible mechanisms of beta-blocker effects, reviews the anatomic and neurochemical bases of aggression, and explores implications of the clinical use of beta-blockers.
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PMID:Beta-blockers and the treatment of aggression. 938 11

Risperidone has proven efficacy with reduced likelihood of causing extrapyramidal symptoms in the treatment of schizophrenia. Initial work suggests its utility in the management of aggression and self injury in patients with mental retardation. The use of risperidone in eight adult patients with moderate to profound mental retardation is described. Risperidone in these individuals was associated with significant reduction in aggression and self injurious behavior. Side effects were primarily those of sedation and restlessness. These cases illustrate the possible utility of risperidone in the treatment of aggression and self injury in adult patients with moderate to profound mental retardation.
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PMID:Risperidone for aggression and self-injurious behavior in adults with mental retardation. 965 34

The symptoms of schizophrenia were examined in a residential sample of adults with severe or profound mental retardation. Three groups were compared: those with a significant elevation on the schizophrenia subscale of the Diagnostic Assessment for the Severely Handicapped (DASH-II) and a psychiatric diagnosis of schizophrenia; those with a significant elevation on the same subscale but no formal diagnosis of schizophrenia; and those with no elevation on any of the DASH-II subscales. A one-way analysis of variance showed statistically significant differences between the groups. Symptoms of schizophrenia among those in the first group were found to fall mainly into the categories of reality distortion and disorganization, with less evidence of negative symptoms.
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PMID:Characteristics of schizophrenia among persons with severe or profound mental retardation. 1087 59

Adults with predominantly severe and profound mental retardation (N = 180) who lived in a developmental center were assessed with the Behavior Problems Inventory and the Diagnostic Assessment for the Severely Handicapped-II. Individuals with self-injurious, stereotyped, or aggressive/destructive behavior had generally higher psychopathology scores than individuals without, and the presence of behavior problems increased the likelihood of almost all psychiatric conditions up to three-fold. Factor analysis revealed that behavior problems tended to be associated with psychiatric conditions conventionally linked with behavior problems. A Self-Injury and Aggression/Destruction factor was related to impulse control and conduct problems, and a Stereotyped Behavior factor was linked to pervasive developmental disabilities and somewhat less so to schizophrenia. Stereotyped Behavior factor was independent of the Self-Injury/Aggression/Destruction factor.
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PMID:Relationships between psychiatric conditions and behavior problems among adults with mental retardation. 1465 52

From the data provided by our investigations we may conclude that in all pathologic processes of the cortex which end in dementia and death, the fatty degeneration of the elements of the cortex plays a not unimportant part. The characteristic change for most of the psychoses is found in a great increase in amount of fatty deposits when compared to normal individuals of the same age. In some processes such as senile dementia and dementia praecox the fatty substance appears to fill completely the cell body, and these cells have apparently lost all their functioning power. It is not common to find the fatty deposits in the processes of the ganglion cells except in dementia praecox, and to a limited extent in senile dementia. In other cases the pathological variety of the fatty deposits in the ganglion cells is seen to be diffused over the whole ganglion cell. We were able especially to observe this in infectious psychoses, in general paralysis, and in epilepsy. The so called central neuritis assumes a peculiar attitude in that it plainly leads swiftly to an acute fatty degeneration of the ganglion cells, in which there exists an inclination of the fatty granules to flow together into large masses. Frequently the fatty degeneration of the ganglion cells appears to be connected with the sclerosis of the cells, especially when it is a matter of slowly progressing alterations of degeneration. The behavior of the glia is not wholly uniform in the various disease processes. In chronic disease processes we often find that the extent of the fatty accumulations in the ganglion cells does not correspond to an equal increase in the glia cells, while the otherwise acutely degenerative alteration in the nuclei of the glia is noticeable. In acute processes we see regularly an equal accumulation of the fat in both species of cell. The conditions of the cells in the vascular wall are wholly similar to those of the glia cells. We must therefore assume that in chronic diseases the fatty substance has been carried out of the glia and the vascular walls while it has been retained longer in the ganglion cells. Among all the disease processes amaurotic idiocy assumes a peculiar position. We have observed that in addition to the fatty materials of the scarlet fat stain, still other fatty materials, lipoid in character, have made their appearance. While the study of the fatty deposit in the cerebral cortex offers some points for a differential diagnosis, yet it is not adopted in all cases, since the distinction in individual disease processes is not always characteristic. From the preceding examination, however, in many cases there result important findings which briefly we summarize as follows: 1. In all degenerative alterations in the cerebral cortex the mass of the lipoid materials in the ganglion cells in comparison with that in healthy individuals of equal age is found to be considerably augmented. In the alteration of the lipoid materials in the ganglion cells two types in general may be distinguished: (a) An augmentation of the lipoid materials in the ganglion cells, in places where normally a small amount of fat is found, (b) An augmentation of the lipoid materials over the entire cell. 2. The first type we find also characteristic in senile dementia. The second type occurs in acute infectious psychoses, general paralysis, and well advanced epilepsy. 3. While the advanced lipoid degeneration of the ganglion cells in senile dementia has already been described in many ways, it has appeared from our investigations that also in the young chronic cases of dementia praecox far-reaching fatty degeneration of the ganglion cells, especially in the second and third cortical strata, likewise occurs. These findings should constitute an important contribution to the pathological anatomy of dementia praecox. 4. The so called central neuritis represents a peculiar disease process according to the appearance of the fatty degeneration, since this fatty degeneration reaches a very advanced degree, and also in so far as it deviates from other disease processes in that here there comes out very distinctly in the picture an inclination of the fatty granules to flow together. 5. Amaurotic idiocy also represents a particular disease process in respect to the lipoid degeneration, since here in addition to otherwise distributed scarlet stain lipoid materials, still other specific lipoid materials make their appearance.
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PMID:FATTY DEGENERATION OF THE CEREBRAL CORTEX IN THE PSYCHOSES, WITH SPECIAL REFERENCE TO DEMENTIA PRAECOX. 1986 33

Since the discovery of early infantile autism (1943), the etiology of the disease has for long been a matter of dispute-from a form of innate schizophrenia, maltreatment by 'refrigerator mother', to dysfunction of speech development. After the re-discovery of Asperger syndrome by Wing (1981), the concept of this diverse syndrome complex has merged to pervasive developmental disorders (PDD) or autism spectrum disorders (ASD). People suffering from Asperger syndrome do not show impairments in speech development, in fact, they have good linguistic abilities. They can explain their own psychopathology, which helps in the understanding of classical autism with profound mental retardation. Currently, ASD is prevalent in 1 of 150 births with strong genetic inheritance. ASD is therefore thought a psychiatric common disease. Asperger syndrome has frequently been the subject of neuroimaging studies,since social communication is an important characteristic of human behavior. This review encompasses a historical and clinical overview of ASD and puts force the current perspectives on the researches in animal models,genetic studies of animal and human samples,and neuroimaging studies. Our current focus is the possible role of oxytocin,which was recently found to have an effect on empathy,in the etiology of ASD.
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PMID:[Autism spectrum disorders--recent advances in the research on the impairment in social communication]. 2084 8