46 However, others have reported decreased TST, significant disruption In sleep continuity, shortened REM latency, normal or Increased REM density with variable REM time, and normal or decreased SWS.13,45,47-50 After REM sleep deprivation, acute schizophrenics have no REM sleep rebound, while chronic schizophrenics with no active symptoms have more rebound than normal.51-53 With neuroleptic treatment and clinical Improvement over 3.5 weeks, Malxner et al demonstrated Improvements In sleep continuity

(sleep latency decreased, time spent asleep Increased, and sleep efficiency improved) and an Inhibitors,research,lifescience,medical Increase In REM latency and SWS during follow-up polysomnography.54 However, despite Improvement In these measures during neuroleptic treatment, these parameters remained abnormal when compared to normative data.54 In a longitudinal study of

schizophrenic subjects comparing baseline sleep data to results at 4 weeks and 1 year after starting treatment, Keshavan et al reported significant Improvement In sleep continuity measures Inhibitors,research,lifescience,medical and modest Increase in REM latency, with no other changes in sleep architecture at 4 weeks, while at 1 year, REM latency, REM duration, and average automated REM counts increased without significant changes in SWS parameters.55 These findings suggest that SWS parameters are relatively stable during follow-up, while REM parameters may vary In relation to the phase of Illness and treatment. Inhibitors,research,lifescience,medical In addition to the sleep disturbances noted above, a study of psychiatric hospital Inpatients referred for sleep Inhibitors,research,lifescience,medical evaluation reported higher rates of obstructive sleep apnea In schizophrenia patients.56 However, the schizophrenia patients had history of chronic neuroleptic usage and were heavier than patients with other disorders.56 Current theory on schizophrenia proposes an imbalance between dopaminergic and acetylchollnergic Influences on key central nervous system (CNS) structures, such that dopaminergic activity Is Increased during the psychotic phase, and a compensatory increase In Depsipeptide ic50 muscarinic acetylchollnergic activity results in Increased Inhibitors,research,lifescience,medical negative symptoms.22,57 Tandon et al reported decreased REM sleep latency and Increased REM density In association

with the negative symptoms of schizophrenia and attributed these to Increased CNS muscarinic 3-mercaptopyruvate sulfurtransferase activity.50 Treatment of schizophrenia and other psychoses may lead to use of new atypical antipsychotic medications. Some of these drugs have Important metabolic effects associated with Induction of Insulin resistance and leptin resistance. These abnormalities are seen mostly during the nocturnal period and are associated with development of significant weight gain and obesity. Due to these metabolic and body mass index (BMI) changes, patients may develop obstructive sleep apnea and associated sleep disruption. With use of some of these atypical antipsychotic drugs, the BMI increase Is rapid and treatment with nasal chronic positive airway pressure (CPAP) may be needed.