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

Some concepts and classifications of the epileptic psychoses are discussed with special regard to their capacity of being integrated into a multiconditionel view. In epileptics, too, the term of "psychosis" should no longer be connected to the axiom of the somatic origin of the psychic syndrome. The term of "twilight state" should be reserved to those among the epileptic psychoses which go along with troubles of consciousness. The socalled episodic morbid moods of the epileptics are no more merely to be understood as psychoses of somatic origin. They may as well develop as a psychic reaction. If one conceptualizes the psychic troubles of the epileptics as "transient syndrome" (Durchgangssyndrom), as functional psychosis, or as psychosyndrome originating from local or diffuse brain damage, their classification must be limited to the undoubtedly somatogenic psychoses. The term of "epileptic psychosis", however, includes the somatogenic, endogenic, as well as the psychogenic psychoses of the patients with epilepsy. The question of the psychogenesis of schizophrenia-like, maniac or depressive psychoses in epileptics until now cannot be answered because the psychosocial patterns which might condition them have not jet been investigated upon. Anyhow, the exclusive psychogenesis of a schizophrenialike epileptic psychosis leaves to be proved.
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PMID:[Concept determination and classification of the so-called epileptic psychoses]. 90 92

Evidence from multiple lines of study indicate that mood disorders, particularly depression, are a risk factor for developing tardive dyskinesia (TD). Important patient and treatment factors include: 1) frequent retrospective rediagnosis of affective disorders instead of schizophrenia when the long-term course of illness and response is evaluated, and 2) TD onset after relatively brief (few months to few years) exposure to low to moderate neuroleptic doses. Mechanisms underlying this increased sensitivity to TD are unknown. It has been hypothesized that the cyclic mono- and catecholamine activity during mood changes makes the brain more vulnerable to the direct neuroleptic effects or the compensatory processes initiated by these drugs. There may also be an interaction between neuroleptic drugs and antidepressant agents which produce greater vulnerability to TD. Additionally, neuroleptic drug use may be different in affective disorders, such as high doses for short time periods with mania. Treating TD in patients with mood disorders is often difficult. The psychiatric diagnosis should be the first priority in treatment regimens. Then, strategies for addressing TD should be considered. Occasionally lithium and/or antidepressants may be effective in treating both affective disorders and TD in some patients. Specific drug therapies for TD have not been consistently effective. Therefore, the passage of time may be the best treatment approach. Preventing TD should receive the highest priority. In the short term, neuroleptic drugs should be limited to managing acute psychotic symptoms in patients with mood disorders. In the long term, neuroleptics should be reserved for manic or depressive symptoms that do not respond to standard therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Affective disorders and tardive dyskinesia. 290 50

Interaction between schizophrenia and manic-depressive disease (MDI) has to be examined with respect to type, intensity and time points within the courses. Interactions are possible at the level of genetics, constitution, biological (e.g. biorhythmical) mechanisms, neurophysiological actions, biochemical complexes and psychopathological interferences including defense mechanisms of personality. The common denominator seems to be the energetic situation into the satellite-glia-neuron cooperation. Activity of G6PD and AK 2-1 could be a hint of a factor of bipolarity, existing independently from schizophrenia and MDI. Interactions of different psychoses should be designated as interference psychoses. Within this field, the term schizoaffective characterizes the interference between schizophrenia and MDI, mixed psychoses mean stages of rapidly alternating or stable combinations of symptoms within the MDI. 'Legierungspsychosen' should be reserved for interferences at the genetic level.
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PMID:Levels of interaction between schizophrenia and manic-depressive disease. 657 42

The introduction of the atypical neuroleptic, clozapine, has had widespread influence not only on the treatment of the seriously mentally ill patient, but also on new drug development and on hypotheses of the pathophysiology of schizophrenia. While clozapine differs from traditional neuroleptics in its lack of extrapyramidal side effects (EPS), it also is distinct in its profile of neurotransmitter receptor affinities. In our work examining the clinical and biological effects of clozapine in patients with schizophrenia, we have identified the presence of EPS during typical neuroleptic treatment as a consistent predictor of subsequent good response to clozapine. Further, our data suggest that clozapine should not be reserved for the most chronically ill patients, but rather be utilized in patients with less chronic courses of schizophrenia. Biological predictors of clozapine response are consistent with dopaminergic, serotonergic, and noradrenergic facets to its mechanism of action.
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PMID:Predictors of clozapine response in schizophrenia. 752 41

Currently, patients with schizophrenia are usually considered refractory to treatment if they continue to be floridly symptomatic despite receiving treatment with conventional antipsychotic agents. Attempts to improve their response by increasing the dosage, adding supplementary drugs, or switching to agents of another class have not been very successful, and may increase side-effects. Clozapine can be effective, but it is a difficult drug to administer and has therefore been reserved for patients who are doing poorly. With the recent introduction of newer, safer antipsychotic agents, however, even patients who have milder refractory symptoms that persist after treatment with conventional antipsychotics can now be treated.
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PMID:An approach to treatment resistance in schizophrenia. 1021 Nov 36

The introduction of atypical antipsychotics has triggered a reevaluation of treatment strategies in schizophrenia. Although research findings inform about the efficacy and safety of drugs, it is the decisions made daily in ordinary practice that affect the vast majority of patients. The aim of this paper was to examine the use of atypical antipsychotics in clinical care, by means of a survey of prescribing practices for clozapine, risperidone, olanzapine, sertindole and quetiapine for all patients treated for DSM-IV schizophrenia within a psychiatric service. Seventy-five (26%) of the 286 patients identified were on atypical antipsychotics. Patients on clozapine were mostly male, had more than 15 years of contact with psychiatric services and were poor responders. Patients prescribed other atypicals had responded to prior treatment with typical neuroleptics and had less than five years of contact with psychiatric services. Gender distribution was equal in this group. The use of research criteria for treatment resistance identified only one patient, as prolonged use of high-dose neuroleptics was uncommon. The new atypical antipsychotics appear to be replacing older neuroleptics as the first-line treatment of schizophrenia while clozapine is mostly reserved for poor responders. Clinicians' definition of treatment resistance was variable and below the threshold used in research.
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PMID:Atypical antipsychotics in ordinary clinical practice: a pharmaco-epidemiologic survey in a south London service. 1088 Dec 20

The reliability of expressed emotion (EE) ratings by the Camberwell Family Interview (CFI) and characteristics of EE were evaluated in families of patients with mood disorders in Japan. The subjects were 27 patients with mood disorders and 31 members of their families. The CFI was carried out with the family members. EE was rated by two raters independently, and the inter-rater reliability was evaluated according to Spearman's correlation coefficient by ranks and the kappa-value. The distribution of subscales of EE in these subjects was compared with that in families of patients with schizophrenia in Japan and families of patients with mood disorders abroad. Concerning critical comments (CC), hostility (H), and emotional over-involvement (EOI), which are important for EE rating, Spearman's correlation coefficient and the kappa-values were 0.4-0.8, and the reliability of EE ratings in mood disorders was not high. The proportion of positive agreement was particularly low in H and EOI. CCs were fewer in families of Japanese patients with mood disorders than in those with schizophrenia or families of American or European patients with mood disorders. Re-evaluation of the inter-rater reliability of EE ratings in mood disorders is needed. Expressed emotion was more suppressed in families of patients with mood disorders than in those of patients with schizophrenia. Expressed emotion was also more reserved in the Japanese subjects than in their Western counterparts.
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PMID:Evaluation of expressed emotion (EE) status in mood disorders in japan: inter-rater reliability and characteristics of EE. 1088 86

The present study was carried out to investigate the routine use of second-generation antipsychotic drugs in the Italian psychiatric care system. Seven outpatient psychiatric services enrolled a consecutive case series of patients who were being treated, or had started treatment, with clozapine, olanzapine, risperidone, or quetiapine. Information on sociodemographic and clinical variables, current psychotropic drug use, side-effects and past use of typical drugs was collected. In addition, patient symptoms and functional status were evaluated by the Health of the Nation Outcome Scale. Patients receiving off-label prescribing of second-generation antipsychotics were identified. A total of 209 patients were collected. In comparison with patients receiving other second-generation antipsychotics, living in residential facilities, unemployment, long psychiatric histories, and problems with activities of daily living and living conditions were more common in clozapine-treated patients. Nearly 80 % of patients receiving clozapine had schizophrenia compared to less than 50 % of those receiving other second-generation antipsychotics. Overall, 109 patients (52 %) received off-label prescriptions of second-generation antipsychotic drugs. This survey indicates that clozapine was mostly reserved for severe cases and poor responders; the high rate of off-label prescriptions highlights the gap existing between recommendations derived from randomised clinical trials and the current use of drugs.
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PMID:Prescribing second-generation antipsychotics and the evolving standard of care in Italy. 1251 73

Until the early 1990s, first-line drug therapy for patients with acute schizophrenia was usually a traditional antipsychotic, such as haloperidol. As recently as 1997, we recommended that newer, so-called 'atypical' antipsychotic drugs, such as olanzapine and risperidone, should be reserved for patients unable to tolerate traditional drugs. Now, atypical antipsychotics are widely regarded as better than traditional drugs, being generally less likely to cause troublesome extrapyramidal effects or hyperprolactinaemia. Current atypical antipsychotics differ from one another in important respects. Here we consider how important differences in their unwanted-effect profiles may influence the choice between these drugs for patients with schizophrenia.
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PMID:Which atypical antipsychotic for schizophrenia? 1531 Jan 54

This paper is a review of the principal, currently proposed, biological models of schizophrenia. The convergence of recent neurobiological studies indicates that schizophrenia may be a neurodevelopmental and progressive disorder with multiple biochemical abnormalities involving dopamine, serotonin, glutamate and gamma-aminobutyric acidergic systems. In post-mortem tissue, structural abnormalities and alterations in synaptic connectivity have been observed in the intracortical circuitry of the prefrontal dorsal cortex. These morphological modifications could be sequelae of earlier environmental insults and genetic processes. There are probably multiple susceptibility genes, each of small effect, which act in conjunction with environmental factors: obstetric abnormalities, intra-uterine infection and abnormal nutrition. Candidate identified genes could influence neurodevelopment, synaptic plasticity and neurotransmission. If schizophrenia is clearly related to an abnormality of early brain development, the clinical expression of the illness itself is delayed typically for about two decades after birth. A similar delayed onset is also observed in the secondary psychosis associated with metachromatic leukodystrophy, a genetic disease affecting myelin. Schizophrenia is a term reserved for idiopathic cases of chronic psychosis. Strictly speaking, schizophrenia is a syndrome. There are no established laboratory tests, neuro-imaging studies, electrophysiological paradigms or neuropsychological testing batteries that can explicitly confirm this behavioural disorder to the exclusion of symptomatology: what physicians diagnose as schizophrenia today may prove to be a cluster of different illnesses, with similar and overlapping symptoms. The diagnosis criteria of the various DSM reflect the American psychiatrists' concern for establishing a consensus classification preserving a wider definition of schizophrenia or more precisely of the schizophrenic disorder. One can presume that research work established from too numerous and insufficiently specific variables doesn't permit the definition of one or several aetiologies. We hope that one day all schizophrenia will be correlated to one precise causal factor permitting the optimal targeting of interesting therapeutic approaches. The multiplicity of concepts and models reflects our questioning.
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PMID:[Biological models of schizophrenia: an update]. 1709 55


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