Treatment Of Schizophrenic Symptoms Research Articles

Nardostachys jatamansi Targets BDNF-TrkB to Alleviate Ketamine-Induced Schizophrenia-Like Symptoms in Rats

Schizophrenia, a common neurological disorder appearing in the late teens or early adulthood, is characterized by disorganized thinking, behaviour, and perception of emotions. Aberrant N-methyl-D-aspartate (NMDA) receptor-mediated synaptic plasticity is a major pathological event here due to dysfunction of dopamine and glutamate transmission at NMDA receptors. De-regulated brain-derived neurotrophic factor (BDNF), i.e., its signalling through the tropomyosin receptor kinase B (TrkB) receptor, is a major feature of schizophrenia. With recent global awareness of traditional plant medicines in reducing side effects, the aim of our study was to evaluate the efficacy of the ethanolic root extract of a herb belonging to the Valerianacea family, Nardostachys jatamansi, against ketamine-induced schizophrenia-like model in rats. The effect of the N. jatamansi drug (oral dosage of 500 mg/kg body weight for 14 days) in ketamine-administered male Wistar albino rats (30 mg/kg body weight for 5 days) on modulating behaviour and the level of neurotransmitters like dopamine and glutamate was studied in whole-brain homogenates, and its influence on BDNF and TrkB levels in 2 relevant brain regions, the hippocampus and prefrontal cortex, was assessed. We observed that N. jatamansi treatment exhibited encouraging results in the modulation of ketamine-induced schizophrenia-like behaviours, principally the positive symptoms. Our drug both significantly upregulated the glutamate level and downregulated the dopamine level in whole-brain homogenates and retained the normal levels of BDNF (in the hippocampus but not in the prefrontal cortex) and TrkB (in both hippocampus and prefrontal cortex) induced by ketamine in rats. These findings suggest a neuroprotective effect of the ethanolic root extract of N. jatamansi against ketamine-induced schizophrenia-like symptoms in rats; possibly, regarding its effect on TrkB signalling. Further research is warranted in the treatment of schizophrenic symptoms.

P.3.a.035 Cognitive responce as a predictor of repetitive transcranial magnetic stimulation (rTMS) efficacy in schizophrenia

Schizophrenia is a disabling disease with a significant proportion of patients experiencing persistent symptoms. Repetitive transcranial magnetic stimulation (rTMS) is a promising new therapeutic tool that could benefit to schizophrenic patients. In this study we sought to assess the efficacy of active rTMS compared to sham stimulation in the treatment of patients with schizophrenia.Eighteen schizophrenic patients according to DSM-IV criteria were randomly allocated to receive active or sham rTMS for 10 days over the left temporoparietal cortex (80% of the motor threshold, 1 Hz, five trains of 1 min). Psychopathological dimensions were measured with the positive and negative syndrome scale and clinical global impression at baseline and after 10 session of rTMS.All patients were improved at the end of the trial but no significant group differences were found. Patients receiving sham stimulation showed the same pattern of improvement compared to active condition on all the subscales of the positive and negative syndrome scale and clinical global impression scores (p > 0.05).In our study, active rTMS failed to show superiority over sham stimulation in the treatment of schizophrenic symptoms. Although previous results have shown that rTMS reduces auditory hallucination, its efficacy on other positive schizophrenic symptoms is not yet established. Nevertheless, the results of our study, even though negative, provide further insights in the pathophysiology of schizophrenia.

Transcranial magnetic stimulation in the treatment of schizophrenic symptoms: A double blind sham controlled study

Background Schizophrenia is a disabling disease with a significant proportion of patients experiencing persistent symptoms. Repetitive transcranial magnetic stimulation (rTMS) is a promising new therapeutic tool that could benefit to schizophrenic patients. In this study we sought to assess the efficacy of active rTMS compared to sham stimulation in the treatment of patients with schizophrenia. Method Eighteen schizophrenic patients according to DSM-IV criteria were randomly allocated to receive active or sham rTMS for 10 days over the left temporoparietal cortex (80% of the motor threshold, 1 Hz, five trains of 1 min). Psychopathological dimensions were measured with the positive and negative syndrome scale and clinical global impression at baseline and after 10 session of rTMS. Results All patients were improved at the end of the trial but no significant group differences were found. Patients receiving sham stimulation showed the same pattern of improvement compared to active condition on all the subscales of the positive and negative syndrome scale and clinical global impression scores ( p > 0.05). Conclusion In our study, active rTMS failed to show superiority over sham stimulation in the treatment of schizophrenic symptoms. Although previous results have shown that rTMS reduces auditory hallucination, its efficacy on other positive schizophrenic symptoms is not yet established. Nevertheless, the results of our study, even though negative, provide further insights in the pathophysiology of schizophrenia.

WITHDRAWN: Transcranial magnetic stimulation in the treatment of schizophrenic symptoms: A double blind sham controlled study

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Potential role of dietary ω-3 essential fatty acids on some oxidant/antioxidant parameters in rats’ corpus striatum

Omega-3 ( ω-3) is an essential fatty acid (EFA) found in large amounts in fish oil. It contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. Evidences support the hypothesis that schizophrenia may be the result of increased reactive oxygen species mediated neuronal injury. Recent reports also suggest the protective effect of ω-3 EFA against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in antioxidant enzyme and oxidant parameters in the corpus striatum (CS) of rats fed with ω-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with ω-3 were decapitated under ether anesthesia, and CS was removed immediately. Thiobarbituric acid-reactive substances (TBARS) and nitric oxide (NO) levels as well as total superoxide dismutase (t-SOD) and xanthine oxidase (XO) enzyme activities in the CS were measured. Rats treated with ω-3 EFA had significantly lower values of TBARS ( P<0.001), NO ( P<0.002) and XO ( P<0.005) whereas higher values of t-SOD enzyme activity ( P<0.002) than the control rats. These results indicate that ω-3 EFA rich fish oil diet reduces some oxidant parameters in CS. This may be revealed by means of reduced CS TBARS levels as an end product of lipid peroxidation of membranes in treated rats. Additionally, reduced XO activity and NO levels may support this notion. On the other hand, although the mechanism is not clear, ω-3 EFA may indirectly enhance the activity of antioxidant enzyme t-SOD. Taken together, this preliminary animal study provides strong support for a therapeutic effect of ω-3 EFA supplemented to classical neuroleptic regimen in the treatment of schizophrenic symptoms and tardive dyskinesia.

Glutamatergic neurotransmission in schizophrenics

Glutamate is the most abundant amino acid in the brain, where it plays an important role as a well-established major excitatory neurotransmitter in the central nervous system. It has been suggested that reduced glutamate neurotransmission may be involved in the pathophysiology of schizophrenia. The glutamate hypothesis of schizophrenia postulates alterations in the glutamatergic system as an important neurobiochemical event in the pathophysiology of this group of psychotic disorders. An altered glutamate release from synaptosomes including a hypofunction of different glutamate receptors (i.e. NMDA receptors) from different brain areas have previously been reported. Furthermore, partial agonists at the glycine co-agonist site of the NMDA receptor might be a new approach in the treatment of schizophrenic symptoms but further studies are necessary to clarify the role and efficacy of these substances in schizophrenia. Changes in the glutamatergic cortico-striatal connections in schizophrenia could precipitate a potential perceptive overstimulation of the neocortex from thalamic input and an inhibiting influence of the striatum on the thalamus would modulate the information input of the cortex, thereby possibly counteracting the disturbed information processing which is relatively characteristic for schizophrenic psychoses.

Biobehavioral treatment and rehabilitation of schizophrenia.

The psychopathology and associated disabilities experienced by persons with schizophrenia have only partially responded to conventional pharmacological and psychosocial treatment approaches. Biobehavioral treatment and rehabilitation employs behavioral assessment, social learning principles, skills training, and a focus on the recovery process to amplify the effects of pharmacotherapy. Utilizing the Medline database, we review a selection of English-language studies published from 1970 to 1994 that support the effectiveness of each of the components of biobehavioral therapy, such as case management, psychopharmacology with behavioral assessment, psychoeducation, family involvement, and social skills training. An integrated biobehavioral therapy directed toward early detection and treatment of schizophrenic symptoms, collaboration between consumers and caregivers in managing treatment, family and social skills training, and teaching coping skills and self-help techniques has been documented to improve the course and outcome of schizophrenia, as measured by symptom recurrence, social functioning, and quality of life. A case vignette is presented to illustrate the successful integration of biobehavioral therapies into a treatment system that focuses on consumers' attempts to become increasingly responsible for recovering from illness.

Biobehavioral treatment and rehabilitation of schizophrenia

The psychopathology and associated disabilities experienced by persons with schizophrenia have only partially responded to conventional pharmacological and psychosocial treatment approaches. Biobehavioral therapy employs behavioral assessment, social learning principles, and skills training to amplify the effects of pharmacotherapy. An integrated biobehavioral therapy-aiming at early detection and treatment of schizophrenic symptoms, collaboration between patients and caregivers in managing treatment, family and social skills training, and teaching coping skills—has been documented to improve the course and outcome of schizophrenia as measured by symptom recurrence, social functioning, and quality of life. Biobehavioral therapies must be delivered in the context of continuous treatment teams, assertive case management, and a full range of medical, social, and community support services that together can optimize outcomes.