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Insomnia and sleep deprivation both describe experiences marked by too little sleep, but the two no-rest afflictions differ in meaningful ways. Insomnia refers to the inability to sleep despite having the opportunity to do so. Sleep deprivation is the state of being under-slept, and may happen for a number of reasons, including as a result of insomnia.

When scientists use neuro-imaging tools to peer into the sleep-starved brain, they’re typically assessing the impact of sleep deprivation on the oh-so-plastic human noggin. The basic question here is: How do our cognitive, emotional and sensory-related brain processes fare when we haven’t gotten adequate sleep for the amount of time we’ve been awake? 

Both male and female insomniacs (but especially female) exhibited over-activity in the brain’s arousal networks.

But, using fMRI (functional Magnetic Resonance Imaging) to look at the insomniac brain typically concerns a slightly different, expanded goal: understanding how brain activity and structure differ between a diagnosed insomniac and a “normal sleeper,” meaning someone who can fall and stay asleep well and long enough to elude clinical labeling. When researchers do observe differences, they ask some central questions, such as:

  • Which of the observed brain differences contributed to the development of insomnia and which came about as a result of not sleeping, or another related condition, such as depression or schizophrenia?
  • Which changes are reversible with sleep?
  • Is the cause-and-effect relationship between the brain and the disorder more complicated, i.e., the insomniac brain is both fundamentally distinct from the "normal brain," but also changes as a result of sleep loss, which further exacerbates the neural other-ness? (Ding, ding, most likely.)
  • Do other essential biological characteristics — sex, for example — affect brain development in a way that sets the stage for insomnia to develop?
  • Once insomnia sets in, how does the disorder affect the brains of men and women differently?

At this point, we have no answers for these questions because scientific efforts to pin down the neurobiological substrates of insomnia, in men and women, haven't been too fruitful — but they're trying. 

A recent study, published this month in the Journal of Clinical Sleep Medicine, highlights some of the progress and impediments involved in the project of mapping insomnia in the brain. A neuroscience research team from China scanned the brains of male and female insomniacs as well as demographically comparable “good sleepers."

They were interested in comparing the subjects' brains in four ways:

  • Insomniacs (without respect to sex) vs. good-sleepers
  • Female insomniacs vs. female good-sleepers
  • Male insomniacs vs. male good-sleepers
  • Female vs. male insomniacs

First, to confirm physiological differences between the quantity and quality of sleep between the insomniacs and normals, researchers used activity trackers (fit bits) to measure their sleep patterns.

Check. Insomniacs exhibited the sort of fragmented, reduced sleep expected of them. Then, researchers warmed up the brain-scanner.

This observation, they believe, supports the theory of insomnia as a disease of hyperarousal, meaning insomniacs can’t sleep because their brains won’t stop reacting to and processing the outside world.

A number of other research teams, including the current one, have performed similar studies. In this case, study authors wrote in the paper, they used a technique for assessing brain activity, called ALFF, that no one else has used in neuro-insomnia research specifically, and which they believe was well-suited for the task at hand. 

Taken together, previous research in the same vein offers anything but a cohesive portrait of the insomniac brain. Research groups have observed plenty of neural wonkiness, with little consistency across studies. Here are a few: reduced gray-matter volume in various areas of the cortex, cerebellum and hippocampus, as well as altered activity in and between regions including the amygdala (the brain’s emotional watchdog), various frontal regions involved in cognition and several sensory-processing areas.

In the current study, researchers observed enough changes to draw some, admittedly limited conclusions. Both male and female insomniacs (but especially female) exhibited over-activity in the brain’s arousal networks. This observation, they believe, supports the theory of insomnia as a disease of hyperarousal, meaning insomniacs can’t sleep because their brains won’t stop reacting to and processing the outside world.

They also saw disturbed connectivity between regions (including frontal lobe areas) involved in memory. There’s plenty of evidence that sleep loss impairs memory, so they interpreted these connectivity differences as evidence of the negative cognitive impact of sleep loss. They also saw significant differences in abnormal regional activity between male and female insomniacs.

So what does this mean? Well, they're working on it. Researchers see these differences as meaningful and deserving of further exploration. Not the most shocking conclusion. It does mean that this research has moved the needle ever so slightly.