Brain scans identify working memory deficits associated with insomnia
Abnormal neural function identified in patients with primary insomnia may help explain why those with the sleep disorder have difficulty performing daytime tasks, according to functional magnetic resonance imaging results.
"We found that insomnia subjects did not properly turn on brain regions critical to a working memory task and did not turn off 'mind-wandering' brain regions irrelevant to the task," Sean P.A. Drummond, PhD, associate professor in the department of psychiatry at the University of California, San Diego, said in a press release. "Based on these results, it is not surprising that someone with insomnia would feel like they are working harder to do the same job as a healthy sleeper."
Sean P.A. Drummond
In the study, 25 patients with primary insomnia (mean age, 32.3 years) and 25 healthy sleepers (mean age, 32.4 years) underwent functional MRI while performing the N-back working memory task. Sleep was measured using self-reports and actigraphy, and patients underwent polysomnography for 2 consecutive nights.
Results, published in the journal Sleep, indicated that patients with insomnia did not differ significantly from healthy sleepers in objective cognitive performance. However, as the working memory task increased in difficulty, patients with insomnia showed reduced activation of task-related working memory regions, particularly in the right dorsolateral prefrontal cortex. Additionally, patients with insomnia exhibited increased activation of default mode regions, which are typically active when the mind is "wandering."
“I think the results set the groundwork for a better understanding of the discrepancy between self reports of cognitive difficulties and the objective findings of intact performance in those with insomnia," Drummond said in an interview. "However, that does not yet change how we treat patients.”
Disclosure: The study was supported by a grant from Actelion Pharmaceuticals. Drummond and Matthew Walker, PhD, report financial relationships with Actelion.