Indian Journal of PsychiatryIndian Journal of Psychiatry
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ORIGINAL RESEARCH PAPERS
Year : 2005  |  Volume : 47  |  Issue : 3  |  Page : 133-138

REM sleep latency and neurocognitive dysfunction in schizophrenia


Department of Psychiatry and Drug De-addiction Centre, Lady Hardinge Medical College and Associated Hospitals, New Delhi 110001, India

Correspondence Address:
Mrinmay Das
Consultant Psychiatrist, Culverhay CMHC Paignton, TQ 45 BD, Devon, UK

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5545.55934

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Background: Cognitive deficits-the hallmark of schizophrenic deterioration-still remain elusive as far as their pathophysiology is concerned. Various neurotransmitter systems have been implicated to explain these deficits. Abnormalities in cholinergic neurotransmission in the brain are one of the postulations; acetylcholine has also been postulated to regulate rapid eye movement (REM) sleep, especially REM latency. Thus, REM latency in patients with schizophrenia might provide a non-invasive window to look into the cholinergic functions of the brain. Aim: To study REM sleep measures and neurocognitive function in schizophrenia, and the changes occurring in these parameters following pharmacological treatment. Methods: Thirty subjects (15 with schizophrenia and 15 normal non-relative controls) were evaluated in this study. Most patients with schizophrenia had prominent negative symptoms and deficits in the performance in neurocognitive tests battery. They were treated with antipsychotics for a variable period of time and post­-treatment evaluation was done using the same battery of neurocognitive tests and polysomnography. Patients were either drug-naive or kept drug-free for at least two weeks both at baseline as well as at the post-­treatment stage. Results: A positive correlation between the severity of negative symptoms and neurocognitive deficits (especially on the Wisconsin Card Sorting), and a negative correlation between these two parameters and REM latency was observed. Conclusion: It can be hypothesized that the acetylcholine deficit model of dementia cannot be applied to schizophrenic dementia, rather a hypercholinergic state results. This state warrants anticholinergic medication as a treatment option for negative symptoms of schizophrenia.



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