Summary of “Establishing the Objective Sleep Phenotype in Hypersomnolence Disorder [IH] with and without Comorbid Major Depression”

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David Plante, MD, PhD, HF MAB member

It can be challenging for doctors to distinguish between idiopathic hypersomnia and depression. It is also possible for one patient to have both conditions. Researchers are looking for better ways to tell the difference between the two so doctors may more accurately diagnose which one (or both) is the cause of symptoms. Dr. David Plante, an esteemed member of our MAB, has provided HF with a summary of research findings showing that high-density EEG sleep studies can be a useful tool in accurate diagnosis.

(Note: This research refers to hypersomnolence disorder, which has very similar diagnostic criteria to IH. Also, the term “comorbid” refers to two different medical conditions, which may or may not be related, occurring at the same time.)

A research team from the University of Wisconsin-Madison recently used high-density EEG sleep studies to examine brain activity in persons with depression and/or hypersomnolence. The team examined differences in standard sleep architecture between 22 individuals with major depression and comorbid hypersomnolence disorder, 22 persons with major depression but without comorbid hypersomnolence, 17 persons with hypersomnolence disorder but without depression, and 22 healthy comparison participants.

The main findings were that persons with hypersomnolence disorder, regardless of the presence or absence of depression, had very similar sleep at night, and slept significantly longer than healthy persons when allowed to sleep without a predetermined wake-up time while in the sleep lab. Particularly interesting was that persons with hypersomnolence disorder, both with and without depression, demonstrated similar local reductions in slow wave activity during sleep, that were different from persons with depression but without hypersomnolence.

Slow waves play a key role in the restorative aspects of sleep. These changes in slow wave activity in persons with hypersomnolence were localized to specific parts of the brain — the supramarginal gyrus, somatosensory cortex, and transverse temporal cortex. These findings suggest there may be a shared brain abnormality in persons with hypersomnolence disorder, regardless of the presence or absence of depression. This finding may lead to future therapies that target this specific abnormality.

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