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

The severity and profile of cognitive dysfunction in first episode schizophrenia and psychotic affective disorders were compared before and after antipsychotic treatment. Parallel recruitment of consecutively admitted study-eligible first-episode psychotic patients (30 schizophrenia, 22 bipolar with psychosis, and 21 psychotic depression) reduced confounds of acute and chronic disease/medication effects as well as differential treatment and course. Patient groups completed a neuropsychological battery and were demographically similar to healthy controls (n=41) studied in parallel. Prior to treatment, schizophrenia patients displayed significant deficits in all cognitive domains. The two psychotic affective groups were also impaired overall, generally performing intermediate between the schizophrenia and healthy comparison groups. No profile differences in neuropsychological deficits were observed across patient groups. Following 6 weeks of treatment, no patient group improved more than practice effects seen in healthy individuals, and level of performance improvement was similar for affective psychosis and schizophrenia groups. Although less severe in psychotic affective disorders, similar profiles of generalized neuropsychological deficits were observed across patient groups. Recovery of cognitive function after clinical stabilization was similar in mood disorders and schizophrenia. To the extent that these findings are generalizable, neuropsychological deficits in psychotic affective disorders, like schizophrenia, may be trait-like deficits with persistent functional implications.
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PMID:A comparison of neuropsychological dysfunction in first-episode psychosis patients with unipolar depression, bipolar disorder, and schizophrenia. 1945 Sep 52

The aetiological role of parasitic infection has been well established, through epidemiological studies, for many chronic diseases prevalent in the tropics. Examples include Schistosoma mansoni infection leading to portal hypertension, Schistosoma haematobium infection leading to obstructive uropathy and squamous cell carcinoma of the bladder, Clonorchis sinensis leading to cholangiocarcinoma, and Taenia solium infection leading to epilepsy. Our understanding of the pathogenesis of these associations, however, continues to evolve, with new insights from many fertile avenues in chronic disease research. There are also tenuous associations such as schizophrenia with toxoplasmosis, and the findings from observational studies that link malignancy and epilepsy with a range of helminthic infections. Imprecise case definitions, and the lack of good animal models, are limitations to the evidence for a causal role of parasitic infection in these diseases.
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PMID:Parasites as aetiological agents in chronic diseases. Epidemiological associations and potential mechanisms of pathogenesis. 1982 4

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

Diabetes mellitus is a chronic disease affecting approximately 6% of the general population. Depression and schizophrenia are often comorbid with diabetes. There are two main ways to explain this phenomenon. Firstly, patients with diabetes mellitus have higher incidence of psychiatric disorders and secondly, antidepressants and antipsychotics may cause metabolic abnormalities. Antidepressants with noradrenergic activity have the highest potential to cause metabolic abnormalities. In schizophrenia, the risk is highest with clozapine and olanzapine pose the highest risk, moderate for risperidone and quetiapine, while ziprasidone and sertindole have not been associated with diabetes. American Diabetes Association and American Psychiatric Association suggested that optimal management of patients with schizophrenia should include baseline assessment on their weight, waist circumference, blood pressure, blood glucose level and lipidogram and family history on obesity, diabetes, dyslipidemia, hypertension and cardiovascular illness. During the first three months, weight gain should be monitored on monthly basis, while biochemical analysis should be performed after the first three months, and then once a year. In patients with significant weight gain, increase of blood glucose level or dyslipidemia, the first intervention should be switch to another antipsychotic. If necessary, a patient should be referred to an endocrinologist and advised on changing their life style.
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PMID:The comorbidity of diabetes mellitus and psychiatric disorders. 1993 98

Schizophrenia is a chronic disorder that is usually characterized by relapses alternating with periods of full or partial remission. We examined whether combined therapy with a psychosocial intervention for relapse prevention (PIRP) and risperidone administered by long-acting injection (RLAI) would be more effective in reducing relapses than RLAI with treatment-as-usual (TAU) among outpatients with schizophrenia. We conducted a prospective, controlled study over 2 years in 46 patients with schizophrenia receiving RLAI, of which 21 and 25 patients were assigned to the PIRP and TAU control groups, respectively. The 1- and 2-year relapse rates were lower and medication compliance was higher in the PIRP group than in the TAU group. Cox proportional analysis revealed that time from baseline to relapse was associated with RLAI discontinuation. These results indicate that PIRP can be effective in maintaining medication compliance, and that discontinuation of long-acting atypical antipsychotics might be predictive of the next relapse. However, these results need to be replicated in studies with larger samples.
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PMID:Effectiveness of a psychosocial intervention for relapse prevention in patients with schizophrenia receiving risperidone via long-acting injection. 2002 20

Schizophrenia is a common and chronic disease with acute exacerbations. The chronic form of the disease results in a long-standing thought disorder and psychosocial impairment. The fluctuating nature of the disease results in a variety of presentations, for which the physician must choose the appropriate biological, psychological and social therapies. The stages of schizophrenia are described in terms of the patient's reaction to his symptoms and disabilities: anxiety, denial, ambivalence, depression and acceptance. The treatment plan must be modified according to these stages and the patient's circumstances.
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PMID:The stages of schizophrenia and their management. 2128 47

Schizophrenia is a chronic disease of body and mind that affects 1% of the population. The existence of the person with schizophrenia should be understood, at least, from two perspectives: one considering the integration of the individual into the social community, another understanding that there is a patient with a medical problem treatable with medications and psychotherapies. There is a large group of patients with 'treatment-resistant schizophrenia," that is, cases in which a minimum degree of remission with conventional treatments is not obtained. These cases have pointed to the fact that even today we still lack an integrative treatment model obtained through the assembling of specific interventions with verifiable effectiveness. The concept of treatment-resistant schizophrenia should have evolved in accordance with the advancing of the currently available knowledge and therapeutic resources. Why hasn't this happened? This article reviews the history of the concept of "resistance" to account for such failure and proposes a methodological approach to overcome this stagnation.
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PMID:The evolving concept of Treatment- Resistant Schizophrenia. 2176 47

Sex and gender differences in disease prevalence, pathogenesis and modulation have been frequently reported. The menstrual cycle represents the opportunity to study the physiological effect of hormonal fluctuations in vivo on the immune function and chronic disease modulation. Reports on the effect of the cycle on immune cell numbers and activity fluctuations are scarce, but recent publications demonstrate an increasing interest in the subject. The menstrual cycle might affect immune cell numbers and modulate their activity throughout the 4-week cycle, as demonstrated in the case of regulatory T cells. The implications of these fluctuations are particularly relevant in the field of chronic diseases affecting women of reproductive age. In fact, baseline inflammation and immune cell activation in association with other mechanisms, such as regulation of receptor expression, modulation of muscular contraction and behavioral aspects might explain the menstrual-associated fluctuations described in chronic and acute diseases. In the following review the current knowledge about the modulatory effects of the menstrual cycle on both immune cells and systemic diseases, such as autoimmune diseases, asthma, diabetes, cardiac arrhythmia and schizophrenia, is reported. Most of these diseases display worsening of symptoms premenstrually or during menses due to physiologic effects on the target tissue mediated by progesterone and estrogen fluctuations and, thus, display paradigmatic changes potentially relevant to numerous other conditions.
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PMID:Immunology and the menstrual cycle. 2215

The FISE (Federazione Italiana Sport Equestri) Pindar is a multicentre research project aimed at testing the potential effects of therapeutic riding on schizophrenic patients. Twenty-four subjects with a diagnosis of schizophrenia were enrolled for a 1 year-treatment involving therapeutic riding sessions. All subjects were tested at the beginning and at the end of treatment with a series of validated test batteries (BPRS and 8 items-PANSS). The results discussed in this paper point out an improvement in negative symptoms, a constant disease remission in both early onset and chronic disease subjects, as well as a reduced rate of hospitalization.
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PMID:Non conventional psychiatric rehabilitation in schizophrenia using therapeutic riding: the FISE multicentre Pindar project. 2219 76

Goal-directed human behavior is enabled by hierarchically-organized neural systems that process executive commands associated with higher brain areas in response to sensory and motor signals from lower brain areas. Psychiatric diseases and psychotic conditions are postulated to involve disturbances in these hierarchical network interactions, but the mechanism for how aberrant disease signals are generated in networks, and a systems-level framework linking disease signals to specific psychiatric symptoms remains undetermined. In this study, we show that neural networks containing schizophrenia-like deficits can spontaneously generate uncompensated error signals with properties that explain psychiatric disease symptoms, including fictive perception, altered sense of self, and unpredictable behavior. To distinguish dysfunction at the behavioral versus network level, we monitored the interactive behavior of a humanoid robot driven by the network. Mild perturbations in network connectivity resulted in the spontaneous appearance of uncompensated prediction errors and altered interactions within the network without external changes in behavior, correlating to the fictive sensations and agency experienced by episodic disease patients. In contrast, more severe deficits resulted in unstable network dynamics resulting in overt changes in behavior similar to those observed in chronic disease patients. These findings demonstrate that prediction error disequilibrium may represent an intrinsic property of schizophrenic brain networks reporting the severity and variability of disease symptoms. Moreover, these results support a systems-level model for psychiatric disease that features the spontaneous generation of maladaptive signals in hierarchical neural networks.
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PMID:Spontaneous prediction error generation in schizophrenia. 2266 98


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