July 24, 2014
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Sleep deprivation led to symptoms of schizophrenia

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New study data suggest that 24 hours of sleep deprivation can lead to symptoms similar to schizophrenia among healthy people.

“It was clear to us that a sleepless night leads to impairment in the ability to concentrate,” Ulrich Ettinger, PhD, of the cognitive psychology unit at the University of Bonn in Germany, said in a press release. “But we were surprised at how pronounced and how wide the spectrum of schizophrenia-like symptoms was.”

Ulrich Ettinger

Ulrich Ettinger

Ettinger and colleagues evaluated 24 adults aged 18 to 40 years to determine the effects of sleep deprivation. At baseline, participants spent a normal night of sleep in a laboratory and then a week later were kept awake with movies, conversation, games and brief walks. Participants were then evaluated on their thoughts and feelings and also underwent prepulse inhibition.

“Prepulse inhibition is a standard test to measure the filtering function of the brain,” study researcher Nadine Petrovsky, PhD, also of the University of Boon, said in the release. “The prepulse inhibition demonstrates an important function of the brain: Filters separate from what is not important and prevent sensory overload.”

Prepulse inhibition tested a startle response in participants following a loud noise being heard through headphones. Researchers found that the ability to filter was significantly reduced after sleep deprivation.  

“There were pronounced attention deficits, such as what typically occurs in the case of schizophrenia,” Ettinger said. “The unselected flood of information led to chaos in the brain.

Participants also reported sensitivity to light, color or brightness. Specifically, perceptual distortions, cognitive disorganization and anhedonia occurred following sleep deprivation.

“In conclusion, we demonstrated that [sleep deprivation] induced sensorimotor gating deficits and elevated self-reported psychosis-like experiences in healthy humans,” the researchers wrote. “Extending previous rodent work, we conclude that [sleep deprivation], in combination with the [prepulse inhibition] biomarker, might be a promising translational surrogate model for psychosis as this method represents a possibility to partially and reversibly mimic the pathogenesis of psychotic states.”

Ulrich Ettinger, PhD, can be reached at University of Boon, Kaiser-Karl-Ring 9, 53111 Boon, Germany; email: Ulrich.ettinger@uni-bonn.de.

Disclosure: One researcher reports financial ties with the Biomedical Research Centre for Mental Health at the Institute of Psychiatry, King’s College London and the South London and Maudsley NHS Foundation Trust.