Now, a new study from the University of California, Berkeley, published in The Journal of Neuroscience explains why.
It confirms that sleep deprivation has a direct effect on how our brains process pain, leading to more intense pain the following day.
The study sheds light on the perpetuating relationship between chronic pain and poor sleep — a vicious cycle.
“In a sense, it’s scary to see. People can be so drastically changed by losing sleep,” said lead author and UC Berkeley PhD student Adam Krause.
To research how sleep deprivation can affect pain, Krause and his team recruited 25 individuals from the undergraduate student body to undergo a pain stimulus test — once with a full night of sleep and then a week later after staying up all night.
Using a heated electrode applied to the left leg, researchers were able to gather information about pain based on the temperature applied to the skin.
In both cases the students were observed for the full overnight period, ensuring compliance in either a healthy period of sleep, or none whatsoever.
During the experiment when the subjects were sleep deprived, they reported a lower threshold for pain, meaning that patients reported feeling pain at lower temperatures than they did when well-rested.
“What was surprising to me personally was how large that effect was. Nearly 80 percent of our participants reported an increase in pain if they didn’t sleep the night before. That’s a very reliable effect,” Krause told Healthline.
Researchers also used MRI scans of the subjects’ brains to measure brain activity related to pain. What they found was surprising.
Areas of the brain associated with feelings of pain, such as the somatosensory cortex, showed increased activity after sleep deprivation. This was expected.
However, they also found that other areas — the striatum and insular cortex — that have the more complex function of classifying pain stimuli were functioning less.
“We can see that the brain, after sleep deprivation, is basically letting in more pain, but then the regions that would normally regulate or evaluate that incoming pain signal are disrupted or inhibited by sleep deprivation,” said Krause.
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