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Neurobiology of insomnia as measured with FMRI


Insomnia, the most common sleep disorder afflicting adults, is diagnostically characterized by a chronic complaint of difficulty sleeping at night and a report of consequent impairment in daytime functioning. Despite this diagnostic requirement and the relative prevalence of daytime distress in patients with insomnia, studies to date have shown only limited evidence of objective daytime impairment in this population. This investigation tested a neurobiological compensation model which attempted to explain how patients with insomnia overcome cognitive challenges resulting from chronic partial sleep loss (utilizing FMRI). The proposed model suggests that patients with insomnia might increase cortical activation during cognitive challenge (relative to good sleepers) to "compensate" for their sleep loss and that this compensation would lead to maintenance of performance. Furthermore, this study examined the relationship between brain activation and performance and brain activation and daytime complaint in patients with Primary Insomnia. 24 subjects, 13 with Primary Insomnia [PI] (7 female, 6 male) and 11 good sleeper controls [GS] (5 female, 6 male) were studied in this investigation. Patients and controls did not differ statistically in terms of age (PI: 39.8+/-8.0 yrs; GS: 37.1+/-7.7 yrs) or estimated IQ (PI: 116.3+/-8.0; GS: 115.8+/-8.5). Results from the study showed several statistically significant findings, including : a) Patients with insomnia have more disturbed sleep and greater complaints of impaired daytime functioning when compared to matched good sleeper controls b) Patients showed no evidence of cognitive impairment as a result of their sleep loss and despite their complaints of impaired daytime functioning c) Patients exhibit differential patterns of activation during the performance of cognitive tasks relative to controls d) Differences in activation between patients and controls depended to a large degree upon the type of task and level of task difficulty (patients had greater levels of activation on attention, working memory, and learning of easy words, but less activation on inhibition and learning of hard words) e) Within the insomnia sample, individuals who performed better had greater levels of activation (similar to controls) on each task f) Within the insomnia sample those individuals who had the greatest complaints of impaired daytime functioning showed less activation on each task. Overall, the results of this study provide some evidence for the effects of sleep loss on neurophysiologic activation in primary insomnia. However, these findings may suggest that the proposed "compensation" model may not adequately explain the complex interaction between sleep loss, daytime complaint, cognitive function, and activation for this population

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