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Ketamine, a NMDA antagonist, replicates both cognitive and psychotic features of schizophrenia when administered to healthy volunteers. In this study, we aimed to test whether the administration of IV ketamine would replicate with cognitive and electrophysiological patterns that was observed in schizophrenia patients and schizotypal individuals.
44 healthy volunteers were randomised to receive IV infusion of ketamine or placebo. A 64 channel EEG kit was used to obtain eventrelated potentials in response to a working memory (WM) task. The two groups were compared in respect to their performance task as well as the amplitude of the P1 and P300 ERPs.
The psychiatric scales scores (BPRS, CADSS) were significantly increased in the ketamine group when compared to saline. While there was no difference in terms of reaction times to the task, accuracy in the ketamine group worsened significantly with increase in working memory load than in controls. Ketamine significantly increased the P1 but lead to a decrease in P300.
In this study acute NMDA antagonism induced a WM deficit that was associated with visual processing and memory abnormalities. Specifically, ketamine increased the amplitude of the P1 potential and reduced the P300 amplitude. In addition P1 but not P300 predicted performance on the WM task. These effects could be mediated ketamine-induced acute glutamate release in the visual cortex, enhancing neuronal responses to visual stimuli and increasing the signal-to-noise ratio which in turn disrupted higher order cognitive function.
Sodium nitroprusside (SNP) has been reported to rapidly reduce psychotic symptoms in patients with schizophrenia. This has the potential to revolutionize treatment for schizophrenia. In this study, we tested the hypothesis that SNP leads to a reduction in psychotic symptoms and an improvement in spatial working memory (SWM) performance in patients with schizophrenia.
This was a single-centre, randomized, double-blind, placebo-controlled trial performed from 27 August 2014 to 10 February 2016 (clinicaltrials.gov identifier: NCT02176044). Twenty patients with schizophrenia aged 18–60 years with a diagnosis of schizophrenia or schizoaffective disorder were recruited from psychiatric outpatient clinics in the South London and Maudsley NHS Trust, London, UK. Baseline symptoms were measured using the Positive and Negative Syndrome Scale (PANSS) and the 18-item Brief Psychiatric Rating Scale (BPRS-18), and SWM was assessed using the CANTAB computerized test. Participants received either an infusion of SNP (0.5 μg/kg per min for 4 h) or placebo and were re-assessed for symptoms and SWM performance immediately after the infusion, and 4 weeks later.
SNP did not lead to any reduction in psychotic symptoms or improvement in SWM performance compared to placebo.
Although this study was negative, it is possible that the beneficial effects of SNP may occur in patients with a shorter history of illness, or with more acute exacerbation of symptoms.
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