Abstract
Introduction
The combination of artificial light and lack of exposure to natural light can delay the circadian clock, dysregulate the circadian cycle, and decrease alertness upon waking. This effect has been especially significant during the COVID-19 pandemic, where overexposure to artificial light at improper hours has contributed to increased rates of clinical insomnia. Artificial light may also contribute to concomitant neurological conditions such as primary headache, but the mechanisms by which light triggers sleep deprivation-induced headache are not well-understood.
Methods
To measure pain sensitivity, we habituated 13 wild-type male mice to von Frey filaments applied to the periorbital area until there was no response to 0.6g stimulus. We then applied 5 lux of continuous dim light to mice during their usual 12-hour dark cycle. The 12-hour light cycle remained unchanged with 200 lux continuous light. Three groups of mice experienced the dim light stimulus for one, three, or five consecutive days. Ambulation and rest activity were measured using SOF-812 Activity Monitor machines. After the experiment concluded, we waited 24 hours and measured mechanical threshold using von Frey filaments at 1, 3, 5, 8, and every 3 days subsequently until mice no longer responded to 0.6g stimulus.
Results
Artificial light triggered changes in circadian behavior including increased number of rest periods during 12-hour dark (dim light) cycle and shortened sleep duration during 12-hour light cycle. Following the artificial light stimulus, there was a significant decrease in mechanical threshold (P<0.05), representing allodynia. The one-day group displayed one day of significant allodynia. The three-day group displayed three days of significant allodynia. The five-day group displayed five days of significant allodynia.
Conclusion
Artificial light may trigger circadian dysregulation, and the duration of artificial light exposure seemed to be directly correlated to the duration of allodynia up to one week after the stimulus was removed. We will repeat these experiments and analyze CNS and PNS tissue samples to understand the underlying physiological and biochemical bases of how artificial light triggers sleep deprivation-induced headache. This knowledge could increase our understanding of the pathophysiology and comorbidity of sleep deprivation and headache.
Support (if any)
Funding was received from the National Institute of Health (NS104200).
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