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The neurodevelopmental hypothesis defends the existance of factors that would cause an early impairment on the normal brain development. The neurodegenerative hypothesis proposes the existance of later and progressive pathological phenomena, responsible of the appearance of clinical manifestations and changes on neuroimaging. Both hypotheses would be complementary. Neurodevelopment is completed during adolescence. Within this period, these deficts on executive functions would become apparent, reflecting a neurodevelopmental impairment. Glutamate is the main excitatory neurotransmitter, present throughout the normal postnatal brain development and maduration. In schizophrenic patients and unaffected relatives, a glutamatergic hypofunction has been found and so, an alteration of the dopaminergic mesocortical limbic and nigrostriatal pathways.
Usage of molecules that are capable of reversing the glutamatergic hypofunction would be potentially benefitial for either positive or negative symptomathology in schizophrenia.
We have performed a review of several clinical trials (on humans and animals) using glutamatergic drugs alone and combined with neuroleptics to diminish behavioural disturbances related to NMDA blockage.
Usage of glycine binding site agonists (glycine, D- cicloserine, D-serine) has been proposed. D-serine is effective both as monotherapy and combined with neuroleptics. D-cicloserine is not effective on negative symptoms. Usage of high doses of oral glycine (30–60 mg a day) on its own has not shown any clinical change but there is an improvement on negative and positive symptoms if combined with neuroleptics.
Nowadays, there is no glutamatergic agonist used in schizophrenia treatment. Out of the three previously mentioned drugs, only D-serine has shown some efficacy.
Induced delusional disorder (also known as shared paranoid disorder or folie à deux) is an uncommon disturbance characterized by the presence of similar psychotic symptoms in two or more individuals. Most commonly a primary case can be distinguished from other one or more cases, in whom the symptoms are induced. the patients implied in the shared delusional symptoms are frequently linked by close relationship bonds, mostly family ties. Its epidemiology remains unclear, because very few data is available. There are some requirements concerning the persons involved for the development of this disorder:
1. Close coexistence and intimate emotional links between the two people are observed;
2. The delusional content is plausible and can be based on past events or expectations;
3. Typically, the induced individual has an easily influenciable personality.
We describe and comment one case of shared paranoid disorder between a 29 year old schizophrenic patient and her 43 years old sister. both share a persecution and prejudice delusion involving the Chinese community of their hometown. after a few days of inward treatment at separated psychiatric wards, the delusional symptoms in the older sister started to improve.
Our intention is making a review on a diagnosis that remains controversial nowadays. Treatment should begin with the separation of the induced and the inducer. Anyhow, a psychopharmacological treatment is required in both individuals. It seems clear, however, that the prognosis of the induced and the inducer is different, according to a variety of factors.
N-acetil-aspartate (NAA) is located inside the soma and dendrites. Its believed to be an indirect indicator of the metabolic activity of these cells. Phosphomonoesters (PME) are involved in synthesis of neuronal membranes and phosphodiesters (PDE) in its degradation. Glutamine, an aminoacid produced by glial cells, is transported into the neurone for its transformation into glutamate and gamma aminobutyric acid.
Review clinical trials performed on schizophrenic patients with SF-MRI, with 31P y 1H, to measure concentration of NAA, PME, PDE and glutamine.
Detecting chemichal alterations that could be used as indicators in schizophrenia.
NAA concentration in temporal and frontal cortex of schizophrenic patients, are significantly lower than in healthy controls. In other trials, differences in NAA concentration (measured in prefrontal cortex) have not been found, comparing patients during their first psychotic episode and healthy controls. Lowered concentrations of PME and increased ones of PDE in prefrontal cortex of schizophrenic patients have been found. Glutamine levels are increased in schizophrenic patients, being directely correlated with the duration of the process. These levels are reduced when antipsychotic drugs are used.
The decrease on NAA levels at schizophrenia onset and on healthy relatives remark its value as an endophenotypical indicator, but not as an illness indicator. Changes on PME and PDE concentrations cannot be used as illness indicators. The increase on glutamine synthesis could be due to glutamatergic hypofunction in schizophrenic patients, but there are other factors that may cause it, so it cannot be used as an indicator.
The coexistence of comorbidity in schizophrenia (somatic, dual pathology, personality…) can conditionate evolution and prognosis in this severe mental illness, those aspects should be taken in account to planify treatments and follow up issues.
We are interested in this work in evaluate previous and developed comorbidity in schizophrenic patients; we also analyzed comorbidity consequences in clinical, therapeutical management, treatment adherence, relapses and hospitalizations.
Material and method:
In 50 Schizophrenic patients (DSM-IV TR Diagnostic criteria) with at least one previous psychotic episode we have studied longitudinal and transversally sociodemographic, clinical and therapeutical variables, related comorbidity (somatic, drugs related and dual pathology) and evolution, prognosis, clinical, treatment adherence and tolerance variables were also studied. We also evaluate psychopathologic and medical status (EEG, EKG, Chest RX, BMI, body weight, general analysis) secondary effects were registered. Uxue and CGI were the scales used.
Between 20% and 25% had other medical conditions, and 25-30% had some kind of drug abuse, those were who had worse prognosis, more secondary effects and usually were treated with classic antipsychotics.
The results are discussed, and we propose integrative treatments for schizophrenia and the co morbidities, focusing on affectivity and tolerance.
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