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Low frequency rTMS of the prefrontal cortex have been shown to have a statistically and clinically significant antidepressant effect. The present pilot study was carried out to investigate if right prefrontal low frequency rTMS as an add-on to ECT accelerates the antidepressant effect and reduces cognitive side effects.
In this randomized, controlled, double blind study thirty-five patients with major depression were allocated to ECT+placebo or ECT+ low frequency right prefrontal rTMS. The severity of depression was evaluated during the course using the Hamilton scale for depression (the 17-item as well as the 6-item scale) and the Major Depression Inventory. Furthermore, neuropsychological assessment of cognitive function was carried out.
The study revealed no significant difference between the two groups for any of the outcomes, but with a visible trend to lower scores for MDI after treatment in the placebo group. The negative impact of ECT on neurocognitive functions was short lived and scores on logical memory were significantly improved compared to baseline 4 weeks after last treatment. The ECT-rTMS group revealed generally less impairment of cognitive functions than the ECT-placebo group.
The addition of low frequency rTMS as an add-on to ECT treatment did not result in an accelerated response. On the contrary, the results suggest that low frequency rTMS could inhibit the antidepressant effect of ECT.
evaluated the involvement of NLRP3 inflammasome in schizophrenia-like behavior in young animals exposed to MIA.
To this aim, on the 15th gestational day, the females received an injection of lipopolysaccharides. When the animals completed 7, 14 and 45 postnatal days, they were killed and the whole brain was dissected for biochemical analysis. Animals with 45 postnatal days were submitted to behavioral tests of locomotor activity, social interaction and stereotyped movements.
It was observed that the animals presented schizophrenia-like behavior at 45 postnatal days associated to the increased of NLRP3 inflammasome expression and IL-1β levels on 7, 14 and 45 postnatal days.
This study show that MIA may be associated with a schizophrenia-like behavior. This behavior can be induced to a neuroinflamatory profile in brain. These evidences may base future studies on the relationship between neuroinflammation and psychiatric disorders.
We evaluated processing-speed and shift-cost measures in adults with depression or ADHD and monitored the effects of treatment. We hypothesized that cognitive-speed and shift-cost measures might differentiate diagnostic groups.
Colour, form, and colour-form stimuli were used to measured naming times. The shift cost (s) were calculated as colour-form naming time minus the sum of colour and form naming times. Measurements were done at baseline and endpoint for 42 adults with depression and 42 with ADHD without depression. Patients with depression were treated with Transcranial Pulsed Electromagnetic Fields and patients with ADHD with methylphenidate IR.
During depression treatment, reductions in naming times were recorded weekly. One-way ANOVA indicated statistical between-group differences with effect sizes in the medium range for form and colour-form. In both groups, naming times were longer before than after treatment. For the ADHD group, shift costs exceeded the average-normal range at baseline but were in the average-normal range after stabilization with stimulant medication. For the depression group, shift costs were in the average-normal range at baseline and after treatment. Baseline colour-form naming times predicted reductions in naming times for both groups with the largest effect size and index of forecasting efficiency for the ADHD group.
The cognitive-processing speed (colour-form) and shift-cost measures before treatment proved most sensitive in differentiating patients with depression and ADHD. Reductions in naming times for the depression group were suggested to reflect improved psycho-motor skills rather than improved cognitive control.
It has been hypothesized that neuropsychiatric symptoms, including psychosis, can be the result of a milder brain bioenergetic defect produced by mitochondrial dysfunction; however, mitochondrial dysfunction can be present in other organs or systems. The aim of the study was to investigate whether clinical conditions associated with mitochondrial disorders (CAMDs) were frequently present in schizophrenia.
A previously used questionnaire regarding the CAMDs was administered to patients and controls in a direct interview with a trained psychiatrist. The frequencies of CAMDs in 164 patients with schizophrenia were compared to those in 156 age- and sex-matched controls.
Severe fatigue, seizures, constipation and diabetes were significantly more frequent in patients with schizophrenia than in control subjects and apparently not related to pharmacological treatment.
The results of the present study suggest that multi-systemic mitochondrial dysfunction may be an underlying mechanism involved in schizophrenia.