Sleep apnea is one of the underdiagnosed sleep disturbances that has a direct relationship with pain, and therefore treating it will help treat the pain.
Two main mechanisms link obstructive sleep apnea (OSA) to increased pain:
- Sleep fragmentation and deprivation: Repeated arousals prevent restorative deep and REM sleep. Poor sleep quality lowers pain thresholds, heightens pain sensitivity, and amplifies existing pain.
- Intermittent hypoxia (low oxygen levels): Repeated drops in oxygen trigger inflammation and release of cytokines that “prime” pain-sensing nerves (nociceptors), making them more sensitive and prolonging pain responses. Recent experimental work shows this can create a lasting state of heightened pain sensitivity.
As a result, patients with both conditions often experience higher pain intensity, greater interference with daily function, more daytime sleepiness, worse insomnia symptoms, and lower quality of life. On the other hand, treating OSA, particularly with positive airway pressure (CPAP or similar PAP therapy), frequently improves pain outcomes:
- Systematic reviews and clinical studies show that effective PAP therapy can reduce headache pain substantially, especially morning headaches.
- It often increases pain tolerance and threshold (patients become less sensitive to experimental pain stimuli).
- Improvements have also been seen in temporomandibular disorder pain and, in some studies, overall pain intensity.
- Benefits are clearest when patients use the therapy consistently for adequate hours each night. Gains can appear within weeks and are often maintained with ongoing adherence.
- Evidence for non-headache chronic pain is promising but still less consistent than for headaches; larger high-quality trials are still needed.
Because the link is strong and treatment can meaningfully help both sleep and pain, screening for sleep apnea should be a routine part of evaluating patients with chronic pain. Key clinical clues include loud snoring, witnessed breathing pauses, excessive daytime sleepiness or fatigue, morning headaches, unrefreshing sleep, and, importantly, frequent nighttime urination (nocturia). Nocturia can result from reduced nocturnal production of antidiuretic hormone (ADH). In obstructive sleep apnea, repeated arousals and intermittent hypoxia disrupt the normal nighttime surge of ADH that usually concentrates urine and reduces urine output during sleep. The resulting increased urine production wakes the patient multiple times, further fragmenting sleep and amplifying the cycle of poor rest and heightened pain sensitivity.
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Once OSA is diagnosed (typically by home sleep apnea testing or in-laboratory polysomnography), the link to pain tolerance becomes clinically useful. Untreated OSA is associated with lower pain thresholds and reduced pain tolerance, while patients feel experimental and clinical pain more intensely. Effective treatment, especially consistent CPAP therapy, often raises pain thresholds and improves tolerance, making other pain interventions more effective. Successful treatment of OSA becomes another useful “tool in the toolbox” and the one that addresses a modifiable amplifier of pain rather than just the pain itself.
This connection is especially relevant in fibromyalgia. Fibromyalgia involves widespread pain, fatigue, sleep disturbance, and central sensitization. A substantial proportion of patients with fibromyalgia have undiagnosed or undertreated obstructive sleep apnea (prevalence estimates often range from approximately 20 percent to over 38 percent in studied cohorts). The sleep fragmentation and intermittent hypoxia of OSA can worsen the central amplification of pain that characterizes fibromyalgia, while the non-restorative sleep of both conditions feeds a vicious cycle of increased pain, fatigue, and reduced function. Screening these patients for OSA (including asking about nocturia) and treating confirmed apnea can therefore reduce overall symptom burden, sometimes improving pain control, energy, and quality of life when fibromyalgia-directed therapies alone have been only partially successful. In practice, identifying and treating sleep apnea becomes another targeted tool: It addresses a physiological amplifier of pain sensitivity rather than simply adding another analgesic, and it is particularly worth pursuing in patients with fibromyalgia or those who report frequent nighttime urination alongside chronic pain.
Sleep disturbances beyond obstructive sleep apnea are highly prevalent in chronic pain patients and form a strong bidirectional relationship that complicates pain management. Approximately 50 to 88 percent of people with chronic pain report sleep difficulties, and roughly 44 percent meet criteria for a diagnosable sleep disorder. Among these, insomnia is the most common (around 72 percent in meta-analyses of chronic pain populations), followed by restless legs syndrome (around 32 percent). Non-restorative sleep (feeling unrefreshed despite adequate time in bed) is especially frequent in conditions such as fibromyalgia. These problems amplify pain intensity, lower pain thresholds, increase disability, and worsen mood, while pain itself fragments sleep and perpetuates the cycle.
Evidence consistently supports a two-way interaction, though sleep impairment often appears to be the stronger predictor of future or worsening pain than the reverse. Longitudinal studies show that sleep problems at baseline raise the risk of developing or intensifying chronic musculoskeletal pain. Conversely, chronic pain increases the short-term risk of sleep problems. Experimental sleep disruption (including selective reduction of deep sleep) reliably heightens pain sensitivity the next day, while good nights of continuous deep (N3) sleep are associated with lower next-morning pain.
Shared mechanisms include:
- Reduced endogenous pain inhibition and heightened central sensitization
- Increased inflammatory cytokines
- Dysregulation of monoaminergic (serotonin, dopamine, norepinephrine), opioid, and HPA-axis systems
- Fragmentation of slow-wave sleep and alpha-wave intrusions into deep sleep (particularly noted in fibromyalgia)
- Hyperarousal that maintains both insomnia and amplified pain signaling
Insomnia
Difficulty falling asleep, staying asleep, or waking too early is extremely common. Patients with both chronic pain and insomnia typically report higher pain intensity, longer pain duration, greater disability, more anxiety/depression, and lower physical activity than those with pain alone. Insomnia predicts the onset of new musculoskeletal pain and can maintain existing pain. Treating insomnia (especially with cognitive behavioral therapy for insomnia, or CBT-I) often yields improvements in both sleep and pain outcomes, sometimes more reliably than pain-focused therapy alone for the sleep component.
Restless legs syndrome
Restless legs syndrome (RLS) involves an urge to move the legs (often with uncomfortable or painful sensations) that worsens at rest and in the evening/night and is temporarily relieved by movement. Prevalence rises sharply with the number of pain sites and pain severity, reaching over 50 percent in some cohorts with widespread pain. RLS shares features with chronic pain states, including elevated central sensitization scores even in the absence of other pain diagnoses, reduced pain thresholds, and enhanced temporal summation of pain. Sleep disruption from RLS contributes to next-day pain amplification; the conditions appear linked through dopaminergic, opioid, and inflammatory pathways. Treating RLS can improve sleep continuity and may help with secondary pain symptoms.
Non-restorative sleep
Patients report sleeping enough hours yet waking unrefreshed, fatigued, and more sensitive to pain. This is classic in fibromyalgia, where polysomnography often shows reduced slow-wave sleep, frequent arousals, and alpha-delta sleep patterns. Non-restorative sleep impairs recovery processes, elevates next-day pain, and contributes to the fatigue-pain-mood cycle. Improving the continuity and depth of slow-wave sleep (through behavioral strategies, addressing concurrent disorders, or selected medications) is associated with better pain control.
Because these sleep problems act as modifiable amplifiers of pain sensitivity and suffering, routine screening is warranted in chronic pain evaluations. Simple questions about difficulty initiating/maintaining sleep, urge-to-move symptoms in the evening, or feeling unrefreshed on waking can identify candidates for further assessment (sleep diary, validated questionnaires, or referral for polysomnography when indicated). Effective approaches are multimodal:
- Behavioral: CBT-I has the strongest evidence for improving sleep in pain populations and can secondarily reduce pain interference.
- Pharmacologic: Agents that address both domains (e.g., certain gabapentinoids or low-dose agents targeting sleep architecture) may be useful; pure sedatives or long-term opioids often worsen sleep architecture or breathing.
- Addressing co-occurring mood disorders, which frequently mediate the sleep-pain link.
- Lifestyle measures supporting sleep continuity and circadian alignment.
In short, untreated sleep apnea can make chronic pain harder to control, while diagnosing and effectively treating it often contributes to better pain relief, improved function, and reduced suffering. Beyond OSA, insomnia, restless legs syndrome, and non-restorative sleep are not merely secondary complaints in chronic pain. They actively worsen pain perception, reduce treatment responsiveness, and perpetuate disability. Systematically evaluating and treating them expands the therapeutic toolbox and frequently yields meaningful gains in both sleep quality and pain control.
Kayvan Haddadan is a physiatrist and pain management physician, and president and medical director of Advanced Pain Diagnostic & Solutions, a multidisciplinary pain management practice in California that he founded in 2012. A physician and surgeon licensed by the Medical Board of California, he is double board-certified in pain medicine and physical medicine and rehabilitation. He is also certified in controlled substance registration through the DEA and serves as a qualified medical examiner through California’s Department of Industrial Relations Division of Workers’ Compensation.
Dr. Haddadan earned his Bachelor of Science degree from the College of Alborz in Tehran, Iran, and his medical degree from Shahid Beheshti University of Medical Sciences. He later received his Educational Commission for Foreign Medical Graduates certification in Philadelphia, completed an internship in medical surgery at Loyola University Medical Center’s Stritch School of Medicine in Illinois, and finished his residency in physical medicine and rehabilitation at the same institution. He completed his fellowship in pain medicine at California Pacific Medical Center’s Pacific Pain Treatment Center and also trained in medical acupuncture for physicians at the University of California, Los Angeles David Geffen School of Medicine.
Dr. Haddadan has contributed to 29 research publications across multiple specialties, including pain management, cardiology, pulmonology, endocrinology, gastroenterology, and infectious disease. His work has examined topics such as hyperlipidemia in high cardiovascular risk patients, hyperuricemia and gout management, type 2 diabetes and hypertension, chronic obstructive pulmonary disease and asthma therapies, influenza treatment, irritable bowel syndrome, and opioid related complications in chronic pain care. His research has also included clinical outcome studies in spinal cord stimulation and award-winning presentations on neuropathic pain management and neuromuscular disorders.
