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

A case of episodic manifestation of semiparalysis agitans is described, accompanied by severe demential personality change and precursory hallucinatory symptoms, which is made the basis for the discussion of aspects of mental disorders, notably dementia and symptoms resembling schizophrenia, in Parkinsonian patients. By way of allusion to Glass, a diagnosis including a very extensive, complex, symptomatology is made of a Parkinsonian syndrome.
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PMID:[Episodic manifestation of hemiparkinson syndrome with severe dementia personality change and precursors of paranoid hallucination symptoms]. 258 67

A total of 44 patients suffering from slow-progressive schizophrenia with affective disorders prevalence were examined. A long latent stage was defined as Bonn's "masked mania", two variants of the development were singled out in the active period of the disease. The first variant was characterized by depressive disorders and "mixed states" type of a clinical picture. The patients were optimistic, demonstrating high self-estimation in spite of depressive complaints, flaccidity, suppression, weakness, apathy and pseudoneurotic disorders. Accelerated development of associations was retained and motor retardation was absent Personality changes were limited by emotional and psychopathic ones. The second variant represented affective paranoia, delusional disorders formed on the basis of chronic hypomania. Its expressivity correlated with the intensity of hypomanic effect. Personality changes included thought disturbances, autization, mild decrease of the energy potential.
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PMID:[Slowly progressive schizophrenia with signs of chronic hypomania during its course]. 682 56

Approaches to diagnosing schizophrenia are different. There is a distinct tendency either to narrow the limits of the disease or to expand it, which in some cases leads to a disagreement and even a tendency to disputes. The comprehensive studies conducted in the Mental Health Research Center, Russian Academy of Medical Sciences, have provided an overall notion of the disease in terms of its progression and outcome. The clinical picture of schizophrenia is characterized by obligatory specific disorders, such as autism, reduced energy potential, emotional thinking, and behavioral disorders. Personality changes may be seen as the smoothening of specific personality traits and the appearance of the features that are not inherent to the patients in the past. Schizophernia is also characterized by positive psychopathological syndromes: pseudoneurotic, affective, psychopathy-like, hallucinatory-paranoid and catatonic. A study of 7500 patients with schizophrenia demonstrated that there were clear-cut regularities in the development of the disease, which suggest that there are forms and types in its progression. The study identified 3 forms of development: continuous, recurrent, and attack-like progressive with varying degrees and rates of the process (severe, moderate, and mild). Genealogical and clinicogenetic studies demonstrated accumulation of psychoses and abnormal personalities in the families of probands, manifest and slowly progressive forms of schizophrenia and cases of schizoid psychopathy. Among the wide spectrum of pathogenetic concepts, priority should be given to the dopamine hypothesis, whose main point is accumulation of an excessive amount of dopamine in the brain tissue, especially in the nigrostriatal, mesocortical, and mesolimbic systems. This may lead to activation of dopaminergic brain structures with an increase of dopamine receptors. This hypothesis is confirmed by the neuropathological studies demonstrating a significant increase in the numerical density of the dendritic spines and dendritic trunks in the with layer of the prefrontal cortex. The highest index of the numerical density was observed in young patients with prevalent negative disorders. Inasmuch as there is no correlation of this index with the duration of the disease, it can be concluded that the abundance of synaptical connections is a result of disturbed brain development and a factor predisposing to severe progression of schizophrenia. Treatment modalities are determined by the form and rate of progression of and the pattern of the psychopathological syndrome. Of particular importance is the role of age, somatic state, and individual sensitivity to neuroleptic drugs. Another important factor in the treatment of schizophrenia is a simultaneous or consecutive impact on the psychopathological syndrome and the disease as a whole.
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PMID:[Current concept of schizophrenia: state of the art]. 1007 55

A case of Klinefelter's syndrome with schizophrenia-like symptoms is reported. He was given a diagnosis of schizophrenia at the age of 39. After being treated with medication for many years, he stopped taking them at the age of seventy-two and involuntary movements appeared in his limbs and the trunk. Upon admission to our hospital, he was experiencing delusion and psychosocial excitement. A physical examination showed him to be a thin man of 175.5 cm height, suffering from a mild degree of gynecomastia, testicular atrophy. Serum LH and FSH were both high 10.9 and 47.8 mU/ml respectively. Serum testosterone concentration was 0.2 ng/ml, much lower than the normal range (2.7-10.7 ng/ml). On the Wechsler adult intelligence scale (Revision), his total IQ was 103 (performance IQ 100, verbal IQ105). Karyotype analysis revealed an XXY pattern. Although slight auditory hallucinations remained, the delusional symptoms as well as the involuntary movements diminished after the administration of psychotrophics. Personality changes such as apathy and abulia was subsided. The psychological symptoms were very similar to these of cases in other reports of Klinefelter's syndrome associated with schizophrenia-like symptoms. Some reports about the relationships between sex hormones and schizophrenia including other psychotic disorders suggest that the X-chromosome plays an important part in the mechanism of psychosocial symptoms and in the prognosis in Klinefelter's syndrome.
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PMID:[A case of Klinefelter's syndrome with schizophrenia-like symptoms]. 1099 33

Traumatic brain injury (TBI) can result in serious and disabling neuropsychiatric disorders, such as cognitive deficits and personality change, as well as severe and chronic psychosis. This review focuses on the relationship between TBI and schizophrenia-like psychosis (SLP) including its epidemiology, diagnostic criteria, clinical presentation, psychopathology, risk factors, and pathophysiology. The relationships between post-traumatic epilepsy and SLP, and brain trauma and schizophrenia, are also discussed. The risk of SLP does increase after TBI. The clinical presentation has considerable overlap with primary schizophrenic disorder, with a prominence of persecutory and other delusions and auditory hallucinations, as well as a lack of negative symptoms. The onset is often gradual, with a subacute or chronic course. More severe and diffuse brain injury, especially of the temporal and frontal lobes, is the most prominent risk factor. Genetic load may also play a role, but presence of epilepsy could be a protective factor. Further large and systematic longitudinal studies are needed.
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PMID:Psychotic disorder and traumatic brain injury. 1277 72

In the long term after traumatic brain injury, the most disabling problems are generally related to neuropsychiatric sequelae, including personality change and cognitive impairment, rather than neurophysical sequelae. Cognitive impairment after severe injury is likely to include impaired speed of information processing, poor memory and executive problems. Personality change may include poor motivation, and a tendency to be self-centred and less aware of the needs of others. Patients may be described as lazy and thoughtless. Some become disinhibited and rude. Agitation and aggression can be very difficult to manage. Anxiety and depression symptoms are quite frequent and play a role in the development of persistent post-concussion syndrome after milder injury. Depression may be associated with a deterioration in disability over time after injury. Psychosis is not unusual though it has been difficult to confirm that traumatic brain injury is a cause of schizophrenia. Head injury may, many years later, increase the risk of Alzheimer's disease. Good rehabilitation probably minimizes the risk of psychiatric sequelae, but specific psychological and pharmacological treatments may be needed.
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PMID:Long-term psychiatric disorders after traumatic brain injury. 1828 29

Depending on the criteria used to diagnose schizophrenia, the incidence, prevalence and morbidity risk figures vary. Schizophrenia is probably a group of diseases with separate etiology for which biological markers are still lacking. Genetics and environment both play a part in schizophrenia, but their roles have not been specified. The illness starts in early adult life and is precipitated in vulnerable people by biopsychosocial stress. Historical, demographic, and evolutionary considerations suggest the possibility of a viral pathogen. Birth trauma and family environment also play a role. Schizophrenia usually involves a marked personality change and there are many secondary effects of illness. Improvement generally occurs after many years.
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PMID:The epidemiology of schizophrenia. 2127 18

Mental manifestations are characteristic of the syndrome described by Steele, Richardson, and Olszewski as progressive supranuclear palsy (SRO). Discussions emphasize cognitive aspects, namely the "subcortical dementia" for which the disease is prototypical, but personality change has been mentioned beginning with the earliest accounts. Psychosis has been virtually absent from neuropsychiatric descriptions, perhaps curiously so in view of the association between subcortical disease and delusions. We report here a case of autopsy-proven SRO in which a schizophrenia-like psychosis was a central feature.
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PMID:Schizophrenia and atypical motor features in a case of progressive supranuclear palsy (the Steele-Richardson-Olszewski syndrome). 2448 43

Familial idiopathic basal ganglia calcification (Fahr`s disease) is a rare neurodegenerative disorder characterized by symmetrical and bilateral calcification of the basal ganglia. Calcifications may also occur in other brain regions such as dentate nucleus, thalamus, and cerebral cortex. Both familial and non-familial cases of Fahr`s disease have been reported, predominantly with autosomal-dominant fashion. The disease has a wide range of clinical presentations, predominantly with neuropsychiatric features and movement disorders. Psychiatric features reported in the literature include: cognitive impairment, depression, hallucinations, delusions, manic symptoms, anxiety, schizophrenia-like psychosis, and personality change. Other clinical features include: Parkinsonism, ataxia, headache, seizures, vertigo, stroke-like events, orthostatic hypotension, tremor, dysarthria, and paresis. Fahr`s disease should be considered in the differential diagnosis of psychiatric symptoms, particularly when associated with movement disorder. The disease should be differentiated from other conditions that can cause intracranial calcification. No specific treatment is currently available. Further research is needed to bridge the gap existing in our current knowledge of the prevalence, etiology, symptoms, and treatment of Fahr`s disease.
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PMID:Familial idiopathic basal ganglia calcification (Fahr`s disease). 2498 77