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Sleep, Pain and Recovery

How sleep and pain affect each other, why surgery and shoulder problems disturb sleep, and what helps you rest and recover.

45 citationsUpdated Sep 2026

For patients: a plain-language version of this topic is available. See the patient guide.

Overview

Sleep disturbance is a prevalent and clinically significant component of the postoperative recovery trajectory across multiple orthopaedic conditions. In pediatric concussion, patients reporting difficulty falling asleep or excessive sleep are more likely to experience prolonged recovery [1]. Following total knee arthroplasty, sleep quality generally improves, though an initial phase of disturbance occurs immediately postoperatively [2]. This improvement is often domain-specific, with reductions in environmental disturbances suggesting meaningful gains in select aspects of rest [4]. Similarly, after rotator cuff repair, sleep quality typically worsens at two weeks before improving beyond baseline by six weeks [3], with disturbances resolving as early as three months post-repair [11]. Preoperative sleep disturbance is highly prevalent, affecting 84-97% of patients undergoing shoulder arthroplasty, with minimal improvement reported within the first six weeks [6]. Notably, patients with a history of sleep disorders do not report or objectively experience worse sleep patterns perioperatively following total knee arthroplasty [9].

Behavioral and environmental factors play a role in recovery outcomes. Maintaining consistent sleep timing is a modifiable factor that may support concussion recovery, as irregular sleep timing is associated with delayed recovery in adolescents [8]. Pharmacological interventions present a mixed evidence base. Melatonin did not significantly affect baseline, follow-up, or change in sleep quality (PSQI), pain (VAS), and quality of life (SF-36) scores compared to placebo in orthopaedic trauma patients [5], nor does it improve postoperative sleep quality measured with the VAS compared with placebo in adult patients [10]. However, melatonin is recommended for use postoperatively after arthroscopic rotator cuff repair to reduce early sleep disturbance and potentially aid longer-term functional outcomes [7], and its application is supported for improving postoperative sleep quality [24]. Other agents, including corticosteroids and anticonvulsants, provide inconsistent benefits for postoperative sleep in primary total joint arthroplasty patients [12]. Dexamethasone at doses of four, eight, and 16 mg effectively reduces pain and enhances sleep quality in total knee arthroplasty patients, with the 16 mg dose showing the most pronounced effects at 12, 24, and 48 hours postoperatively [15]. Overall, evidence for the effects of perioperative pharmacological approaches on postoperative sleep remains limited [17].

Anatomy & Pathophysiology

Sleep-Pain Inflammatory Mechanisms

Total knee arthroplasty (TKA) surgery triggers an inflammatory response involving the release of mediators such as IL-6 and C-reactive protein (CRP), which may exacerbate sleep disturbances [19]. This surgical stress creates an inflammatory "storm" that enhances pain sensitivity and impairs postoperative sleep quality in knee osteoarthritis patients [19]. Sleep disruption further increases IL-6 levels, a process associated with peripheral nociceptor sensitization and central or spinal sensitization during glial cell activation [19]. Decreased sleep quality amplifies pain perception because sleep deprivation reduces endogenous pain inhibition and increases pain sensitivity [19]. Consequently, a "sleep deprivation—pain sensitization" vicious cycle may be a key factor in long-term sleep dysfunction and persistent pain in some TKA patients [19].

Biopsychosocial Factors in Osteoarthritis

Chronic pain is an important component of osteoarthritis, with biopsychosocial factors mediating the complex interactions between noxious stimuli and peripheral and central nervous system responses [27]. The severity and character of an individual’s osteoarthritis pain depend on that individual’s unique social, cultural, and personal state [27]. Qualitative analyses have identified distinct patterns of intermittent versus background chronic pain, both of which negatively affect mood, sleep, and social participation [27]. Fatigue, psychological distress, and social context each augment the pain perceived in osteoarthritis [27]. Individuals with poor self-efficacy or pain catastrophizing experience greater pain and poorer outcomes [27]. Therapy remains inadequate due to the complexity involving nociceptive, neuropathic, and biopsychosocial aspects, which differ among individual patients [27].

The pain and loss of function associated with osteoarthritis, along with pharmacological side effects from medications, interfere with sleeping ability, mood, personality predispositions, and other core human traits [28]. The association between osteoarthritis and depression is related to lack of exercise, loss of independence, and a heightened awareness of one’s physical aging [28]. Depression can have severe downstream effects on sleep, hygiene, ability to cope with arthritis pain and postoperative pain, and ultimate functional capacity [28]. Insomnia in osteoarthritis can result from pain worsening with nocturnal nadirs in native cortisol production [28]. A 2018 study found that 53% of patients with osteoarthritis had insomnia symptoms and 66% had obstructive sleep apnea [28]. Pain and depression were associated with insomnia, while opioid use and depression were associated with obstructive sleep apnea in osteoarthritis patients [28]. The duration of sleep is strongly inversely correlated with osteoarthritis symptoms [28]. The chronic pain of osteoarthritis can lead to memory complaints, mood and anxiety disorders, multifocal pain, and fatigue [28].

Sleep Physiology and Recovery Processes

During deep sleep stages, the body releases human growth hormone, testosterone, and prolactin, which facilitate tissue repair and muscle growth [57]. During REM sleep, memory is consolidated, synaptic connections are built, and procedural memories are laid down [57]. Poor sleep impairs sensorimotor processes (balance), motor coordination, and retention of newly learned motor skills [57]. Reduced soft-tissue recovery rates combined with neuromuscular impairments from poor sleep increase the risk of injury for otherwise-healthy athletes [57]. Impaired sleep quantity or quality alters neurocognitive processes, impacting working memory function when awake [57].

Peripheral Nerve Injury Pathophysiology

Peripheral nerves consist of a mixture of myelinated and unmyelinated axons, with motor, sensory, and sympathetic fibers often traveling together in a single nerve [43]. Axons are grouped in bundles termed fascicles, which are surrounded by perineurium, with fine connective tissue between axons called endoneurium [43]. Fascicles are held together as a nerve by the epineurium, and nerves are classified as monofascicular, oligofascicular, or polyfascicular based on the number of fascicles [43]. Peripheral nerve injury disrupts a highly specialized structure that is part of a multisystem pathway by which consciousness interacts with the physical world [33]. Compression neuropathy can be considered a progressive metabolic failure of axonal conduction, followed by disruption of anatomical structures that physiologically enable axonal conduction [33]. Neuronal death is a fundamental issue that requires timely nerve repair and/or pharmacologic intervention [33].

After nerve injury, the somatosensory cortex reorganizes so the area represented by the injured nerve diminishes [43]. The cell body of the lacerated axon increases in size, production of materials for cytoskeleton repair increases, and production of neurotransmitters decreases [43]. In the axon distal to a laceration, Schwann cells phagocytose the axon, allowing the surrounding myelin tube to collapse [43]. Within 24 hours of injury, axonal sprouting occurs from the proximal stump, with multiple axons in a fascicle forming a regenerating unit [43]. Longitudinal growth of the regenerating nerve depends on the ability of axons to adhere to trophic factors in the basal lamina of the Schwann cell [43]. At the motor endplate, muscle fibers atrophy, and the sensitivity and number of acetylcholine receptors increase as their location expands from pits to the entire length of the muscle fiber [43]. Muscle reinnervation occurs only if the axon reaches the muscle within a year, whereas sensory receptors may be effectively reinnervated years after injury [43].

Injury classifications define the potential for recovery: Neurapraxia: A conduction block that occurs without axonal disruption, with recovery usually complete within days to a few months [43]. Axonotmesis: An injury in which axonal disruption occurs with the endoneurial tube remaining in continuity, providing a well-defined path for regenerating sprouting axons [43]. Neurotmesis: Transection of the nerve, where regenerating axons cannot find a suitable path and recovery does not occur unless the nerve is repaired [43]. In neurotmesis, frustrated sprouting axons form a neuroma at the distal end of the proximal segment of the lacerated nerve [43]. Neurotmesis is caused by sharp laceration or high-energy traction injury that ruptures the nerve, affecting all connective tissue layers as well as axons [32]. Recovery after neurotmesis is only possible by axonal regeneration after surgical repair, with function returning in a proximal to distal pattern [32]. The quality of functional recovery after neurotmesis is never normal due to the failure of correct "rewiring," where regenerating nerve fibers connect with different muscle and sensory organs from those they previously innervated [32].

Axons must exit the proximal nerve face by a phasic, staggered outgrowth, with very little significant progress achieved in humans until some 2 to 3 weeks have passed [41]. Neurites must cross the nerve repair site, which presents a significant barrier even if only 1 to 2 mm across [41]. Approximately 50% of fibers fail to cross the repair site, forming a neuroma in continuity instead [41]. Many fibers entering the distal nerve are effectively lost due to poor type specificity, such as motor axons entering an endoneurial tube previously occupied by a sensory axon [41]. Axons grow at an average of 1 mm/day, but growth may slow or peter out distally [41]. Regenerated axons exhibit a high degree of spontaneous activity and mechanosensitivity, accounting for the ubiquity of episodic lancinating pain and the physiologic basis of the Hoffman-Tinel sign [41]. After a brachial plexus injury, it may take over 12 to 18 months for axons to re-innervate distal nerve segments, muscles, or skin [41]. Sensory recovery is highly associated with significant reductions in neurogenic pain [41]. Regenerated axons remain abnormal with reduced fiber diameters and hence conduction velocity [41]. Denervation changes in muscle are partially reversed when regenerating axons connect with muscle fibers, resulting in increased diameter and muscle bulk [41]. The number of axons re-innervating a muscle is reduced due to neuronal loss, resulting in fewer but larger motor units [41]. Neurobiologic changes pertaining to the quality of nerve regeneration exhibit profound deterioration when the delay from injury to repair is extended beyond 1 to 2 months [41].

The repair site environment is not adequately conducive to bridging by neurite growth, resulting in the loss of many axons [33]. Nerve regeneration is far too slow for optimal salvage of much of the distal nerve, target muscles, and higher-order sensory organs from irreversible denervation atrophy [33]. Plasticity is initially disadvantageous during denervation and subsequently inadequate to make best use of re-innervation [33]. Neurobiologic determinants of regeneration are time-dependent and show profound worsening after some 1 to 2 months delay from injury to nerve repair [33].

Sensory loss usually follows a definite anatomic pattern, with a small area of complete sensory loss called the autonomous zone or isolated zone of supply [38]. A larger area of tactile and thermal anesthesia corresponds more closely to the gross anatomic distribution of the nerve and is known as the intermediate zone [38]. When a nerve is intact and adjacent nerves are blocked or sectioned, an area of sensibility exceeds the gross anatomic distribution of the nerve, known as the maximal zone [38]. The autonomous zone becomes smaller during the first few days or weeks after injury, long before regeneration is possible [38]. This decrease in the area of sensory loss is more plausibly explained by resumption of or increase in function in anastomotic branches from adjacent nerves rather than ingrowth of adjacent nerves [38]. In injury to the median and ulnar nerves, pinprick is the first perception to return, followed by 30 cycles/s vibratory stimulus, then moving touch [38]. The perception of constant touch and the perception of a 256 cycles/s vibratory stimulus are the last to return [38]. The early return of pain perception results from the faster regeneration of small-diameter pain fibers, while larger-diameter touch fibers regenerate more slowly [38]. The return of moving touch perception before constant touch is explained by differential maturation of the respective receptors rather than by the diameter of the fibers alone [38]. Two-point discrimination has been shown to directly correlate with return of hand function and object identification [38].

Sensory recovery progresses in time and space according to successive stages: perception of pain and temperature, perception of low frequency vibratory stimuli (30 Hz) and moving tact sense, perception of static tact sense and high frequency vibratory stimuli (256 Hz), and two point discrimination [52]. Motor recovery is always slower than sensory recovery [52]. The first sign of motor recovery is regression of the atrophy in the territory normally supplied by the injured nerve [52]. Early signs of neural regeneration are of limited prognostic value, suggesting a favourable outcome but offering no guarantee of functional recovery [52]. Regeneration can be halted at any stage, and there is frequently a marked difference between motor recovery and sensory recovery [52]. Pain usually appears before tactile sensation returns in sensory recovery [52]. Sensation returns first to the proximal margin of the anesthetic zone [52]. Regeneration can slow down or even cease before reaching the extremity of the limb [52]. Early electrodiagnosis is of limited value after a peripheral nerve lesion, as the process of wallerian degeneration can be recorded only from four to five weeks after the nerve division [52].

Electrodiagnostic studies essentially detect only two types of pathophysiology: axon loss (axonotmetic lesion) manifested as conduction failure, and focal demyelination (neuropraxic lesion) causing conduction slowing or block [53]. The severity of conduction slowing has no correlation with the severity of clinical symptoms, such as weakness or static large-fiber sensory loss [53]. High axonotmetic lesions may take 1 to 2 years for maximal recovery, whereas even lesions at the wrist may take 6 to 9 months for maximal recovery of nerve function [53]. An advancing Tinel's sign can be monitored and is a good prognostic sign [53].

Tinel's sign is the first detectable clinical sign of recovery, where percutaneous percussion of the nerve trunk distal to the lesion produces a "pins and needles" sensation distally [37]. The "pins and needles" sensation resulting from percussion is caused by regeneration of the sensory axons, which are very sensitive to pressure [37]. Tinel's sign signifies a favorable prognosis and enables one to follow the progress of the regenerating nerve [37]. Only percussion of the tactile fibers (not those transmitting pain, heat, and cold) triggers the pins and needles sensation [37]. Axonal regrowth usually occurs at a rate of 1–2 mm per day after nerve suturing [37]. Tinel's sign is absent in the early stages following injury or nerve suturing, appearing only four to six weeks after the injury [37]. The sign may be difficult to elicit if the nerve lies deep to a large mass of muscle [37]. Tinel's sign cannot be demonstrated when the lesion is proximal to the posterior root ganglion [37]. A false positive result for Tinel's sign is elicited when sensory fibers grow into motor sheaths [37]. The test has no quantitative value and can be positive with only a few fibers regenerating, hence its limited functional significance [37]. Steady distal progression of Tinel's sign suggests a good prognosis, even though the sign gives little information concerning the functional quality of reinnervation [37].

Tension at a nerve repair site is detrimental to healing, and direct repair should only be carried out if tension can be avoided [50]. Small nerve gaps (<5 to 10 mm) can be treated with autograft, allograft, or conduit [50]. Larger nerve gaps benefit from autograft or allograft reconstruction, with little comparative data available [50]. Autograft is likely superior to allograft in long nerve gaps (>7 cm) [50]. Nerve transfers are useful when direct or indirect repair is not feasible [50]. Tendon transfers and selective arthrodesis are alternatives when nerve repair or reconstruction is unlikely to succeed [50].

Nerve-fiber regeneration occurs at the rate of approximately 1 mm/day following a latent period of 30 days [35]. The maximum recovery time for the first signs of motor recovery can be estimated by measuring the distance from the fracture site to the point of innervation of the brachioradialis muscle [35]. In most midshaft humerus fractures, this distance is 90 to 120 mm, indicating regeneration times of between 17 and 21 weeks [35]. Evidence of reinnervation on electromyography may precede the clinical appearance of motor function by approximately 4 weeks [35]. It is logical to wait 4 to 5 months before proceeding with exploration if there is no return of nerve function in nonoperatively treated radial nerve palsy [35]. Historically, delays of 12 months or longer were not considered likely to jeopardize functional motor return after nerve repair, but this view is now challenged by suggestions of 3-month or shorter windows of opportunity [35].

The mechanisms responsible for muscle repair and regeneration are tightly regulated by timely events that prepare the injury site for wound healing by clearing necrotic debris and synthesizing extracellular matrix [51]. Muscle stem cells (satellite cells) migrate to populate the extracellular matrix, then undergo fusion, primary tube formation, tube elongation, and hypertrophy to form mature fibers that become innervated [51]. When any portion of these events is disrupted by severe injury or disease, the results can detrimentally impact muscle regeneration, maturity, and homeostasis [51]. The ability of muscle to regenerate is largely dependent on the preexisting status of the muscle at the time of injury or disease onset [51]. Current treatments for injuries and diseases resulting in permanent cosmetic and functional deficits are able to mitigate some negative effects but are largely ineffective to fully regenerate skeletal muscle form and function [51].

Classification

Sleep Disturbance Prevalence and Baseline Status

Preoperative sleep disturbance is highly prevalent, affecting 84-97% of patients undergoing shoulder arthroplasty [6]. In athletic populations, approximately one in four student-athletes report sleep difficulty [25]. Among adolescents, those with a concussion demonstrate worse sleep quality than uninjured controls [22].

Postoperative Sleep Trajectory by Procedure

Sleep quality trajectories vary by procedure. Following total knee arthroplasty, sleep quality improves overall, although an initial stage of sleep disturbance occurs immediately postoperatively [2]. After rotator cuff repair, sleep quality worsens at 2 weeks and improves beyond baseline by 6 weeks [3], with improvements in sleep disturbances occurring as early as 3 months post-repair [11]. In contrast, minimal improvement in sleep quality is reported within the first 6 weeks following shoulder arthroplasty [6]. Carpal tunnel release leads to substantial improvements in both subjective and standardized patient-reported sleep quality in patients with carpal tunnel syndrome [14].

Sleep Disturbance and Recovery Outcomes

Sleep parameters correlate with recovery timelines. Patients reporting trouble falling asleep or sleeping more than usual are more likely to experience prolonged recovery from pediatric concussion [1]. Additionally, irregular sleep timing is associated with delayed recovery following adolescent concussion [8].

Measurement Tools and Definitions

Pittsburgh Sleep Quality Index (PSQI): This tool assesses sleep quality over the previous month, with scores ranging from 0 to 21 points [16]. A cutoff point of 7 is used, with scores exceeding 7 indicating the presence of sleep disorders [16].

AIS: The AIS is a self-rated psychometric questionnaire consisting of eight items with item scores ranging from 0 to 3, for a total score of 0 to 24 [29]. An AIS total score of 6 points or higher reflects a diagnosis of sleep disturbance [29].

NRS: The NRS is an 11-point scale where 0 represents the best possible sleep and 10 represents the worst possible sleep [29]. Postoperative sleep disturbance is identified by either an NRS score of 6 or more or an AIS score of 6 or more [29].

Pain Interference Score: This score is calculated as the mean of items 9A-9G, which measure the interference of pain with general activity, mood, walking, normal work, relations, sleep, and enjoyment of life [20].

Environmental and Behavioral Factors

Maintaining consistent sleep timing during recovery may represent a modifiable behavioral factor to support concussion recovery [8].

Physiological Mechanisms

The release of inflammatory mediators, such as IL-6 and C-reactive protein (CRP), triggered by surgical trauma may exacerbate sleep disturbances after total knee arthroplasty [19]. Sleep deprivation reduces endogenous pain inhibition and increases pain sensitivity, creating a "sleep deprivation—pain sensitization" vicious cycle [19]. REM sleep returns to normal after 2 weeks at altitude, but impaired breathing does not improve [13].

Clinical Presentation

Sleep Disturbance in Orthopaedic Conditions and Postoperative Settings

Severe pain that wakes the patient nightly is a particularly debilitating symptom of severe arthritis and leads to sleep deprivation [48]. In the later stages of knee osteoarthritis, rest pain and night pain develop [48]. Preoperative sleep disturbance is highly prevalent, affecting 84-97% of patients undergoing shoulder arthroplasty [6]. Among student-athletes, approximately one in four reports sleep difficulty and one in seven reports fatigue [25]. In patients with rotator cuff tears and night pain, 46% have insomnia [58]. Sleep disturbances due to rotator cuff tears cannot be captured by the JOA or VAS scores alone [58].

Association with Recovery and Outcomes

Sleep timing interventions may represent a modifiable behavioral factor to support concussion recovery [8]. Lower Injury Psychological Readiness to Return to Sport (IPRRS) ratings are associated with longer symptom resolution time and the occurrence of subsequent injury after concussion [21]. Carpal tunnel release leads to substantial improvements in both subjective and standardized patient-reported sleep quality in CTS patients [14]. Minimal improvement in sleep quality is reported within the first 6 weeks postoperatively after shoulder arthroplasty [6].

Mechanisms and Pathophysiology

Inflammatory mediators may regulate pain sensitivity in knee osteoarthritis patients, and the inflammatory "storm" triggered by surgical stress could further enhance pain sensitivity, severely impairing postoperative sleep quality [19]. Decreased sleep quality can amplify pain perception, as sleep deprivation reduces endogenous pain inhibition and increases pain sensitivity [19]. A "sleep deprivation—pain sensitization" vicious cycle may be a key factor in long-term sleep dysfunction and persistent pain experienced by some total knee arthroplasty patients after surgery [19]. Central Sensitization Index (CSI) and Pain Catastrophizing Scale (PCS) scores are higher in patients with rotator cuff tears, night pain, and sleep disturbances [58].

Measurement and Assessment

A PSQI cutoff point of 7 is used, with scores exceeding 7 indicating the presence of sleep disorders and higher scores suggesting poorer sleep quality [16]. The Pain Interference Score is calculated as the mean of items assessing interference of pain with general activity, mood, walking, normal work, relations, sleep, and enjoyment of life [20]. Postoperative sleep disturbance (PSD) can be identified by either a Numeric Rating Scale (NRS) score of 6 or more or an AIS score of 6 or more [29]. The AIS is a self-rated psychometric questionnaire consisting of eight items with scores ranging from 0 to 24, where a total score of 6 points or higher reflects a diagnosis of sleep disturbance [29]. The NRS for sleep is an 11-point scale where 0 = best possible sleep and 10 = worst possible sleep [29]. Concordance between subjective sleep and PSQI/ISI increases over time in carpal tunnel syndrome patients after surgery [14].

Environmental and Physiological Factors

Patients who have a history of sleep disorders did not report nor objectively experience worse sleep patterns perioperatively after total knee arthroplasty [9]. While sleep benefits after total knee arthroplasty were more domain-specific, reductions in environmental disturbances suggest meaningful improvements in select aspects of rest [4]. REM sleep returns to normal after 2 weeks at altitude, but impaired breathing does not improve in young elite soccer players [13]. Sleep quality returned to normal by the end of the first week at altitude, but sleep quantity had still not stabilised at its normal level after 2 weeks in elite athletes [18].

Investigations

Sleep Assessment Tools and Metrics

Standardized Scales: The Pittsburgh Sleep Quality Index (PSQI) assesses sleep quality over the previous month, with scores ranging from 0 to 21 points [16]. A PSQI score exceeding 7 indicates the presence of sleep disorders, with higher scores suggesting poorer sleep quality [16]. The Epworth Sleepiness Scale (ESS) is used to measure overall postoperative sleep quality following total hip arthroplasty [62].

Pain, Fatigue, and Mood: The Widespread Pain Index (WPI) measures pain or tenderness in 19 different body parts over the 7 days preceding assessment, with scores ranging from 0 to 19 [16]. The Multidimensional Fatigue Inventory (MFI) comprises 20 items scored on a 5-point Likert scale, with a total score range of 20 to 100 points where higher scores indicate more severe fatigue [16]. The Beck Depression Inventory (BDI) consists of 13 items with a score range of 0–39 points, where scores between 5 and 39 indicate the presence of depression [16].

Statistical Considerations: The calculation of the Minimal Clinically Important Difference (MCID) needs to be correlated with changes in scores on the rating scale and external anchors [26].

Preoperative Sleep Status

Preoperative sleep disturbance was highly prevalent in patients undergoing shoulder arthroplasty, with rates reported between 84% and 97% [6]. Approximately one in seven student-athletes reported fatigue [25].

Postoperative Sleep Trajectories

Carpal tunnel release leads to substantial improvements in both subjective and standardized patient-reported sleep quality in carpal tunnel syndrome patients, with increasing concordance over time [14].

Sleep and Recovery Outcomes

Patients reporting trouble falling asleep or sleeping more than usual after pediatric concussion were more likely to have prolonged recovery from their concussion [1]. Patients with obstructive sleep apnea may experience higher rates of medical complications in the short term following total shoulder arthroplasty, but no difference in orthopedic or mortality outcomes in the long term [23].

Environmental and Physiological Factors

Sleep quality returned to normal by the end of the first week at altitude, but sleep quantity had still not stabilised at its normal level after 2 weeks [18].

Treatment

Sleep Disturbance and Recovery Trajectory

Postoperative sleep quality varies by procedure. Following rotator cuff repair, sleep quality worsens at 2 weeks but improves beyond baseline levels by 6 weeks [3]. In total knee arthroplasty, sleep benefits are more domain-specific; reductions in environmental disturbances suggest meaningful improvements in select aspects of rest rather than global sleep enhancement [4].

Pharmacological Interventions

Melatonin: A systematic review and meta-analysis supports the application of melatonin for improving postoperative sleep quality [24].

Behavioral and Environmental Factors

Sleep Timing: Maintaining consistent sleep timing during recovery is a modifiable behavioral factor that may support concussion recovery [8].

Mechanisms and Comorbidities

Inflammatory Pathways: Inflammatory mediators such as IL-6 and C-reactive protein (CRP) released by surgical trauma may exacerbate sleep disturbances in total knee arthroplasty patients [19]. Sleep disruption increases IL-6 levels, which are associated with peripheral nociceptor sensitization and central/spinal sensitization during glial cell activation, contributing to increased pain severity and sensitivity [19].

Pain-Sleep Cycle: Decreased sleep quality amplifies pain perception because sleep deprivation reduces endogenous pain inhibition and increases pain sensitivity, creating a "sleep deprivation—pain sensitization" vicious cycle [19].

Osteoarthritis Comorbidities: Osteoarthritis pain and loss of function, as well as pharmacological side effects from medications, interfere with sleeping ability, mood, and personality predispositions [28]. In a 2018 study of patients with osteoarthritis, 53% had insomnia symptoms and 66% had obstructive sleep apnea [28]. Pain and depression were associated with insomnia, while opioid use and depression were associated with obstructive sleep apnea in patients with osteoarthritis [28]. Chronic pain of osteoarthritis can lead to memory complaints, mood and anxiety disorders, multifocal pain, and fatigue [28].

Opioid Considerations: Opioid administration in some patients may cause a hyperalgesic effect, potentially worsening postoperative pain [45].

Complications

Pediatric Concussion

No evidence is provided for this category.

Total Knee Arthroplasty

Inflammatory Response: TKA surgery triggers an inflammatory response involving the release of IL-6 and C-react protein (CRP), which may exacerbate sleep disturbances [19]. Inflammatory mediators may regulate pain sensitivity in knee osteoarthritis patients, and the inflammatory response triggered by surgical stress can enhance pain sensitivity and impair postoperative sleep quality [19].

Sleep-Immune Interaction: Sleep disruption increases IL-6 levels, which are associated with peripheral nociceptor sensitization and central/spinal sensitization during glial cell activation [19].

Pre-existing Sleep Disorders: Patients with a history of sleep disorders did not report or objectively experience worse sleep patterns perioperatively after total knee arthroplasty [9].

Postoperative Sleep Benefits: Sleep benefits after TKA were more domain-specific, with reductions in environmental disturbances suggesting meaningful improvements in select aspects of rest [4].

Rotator Cuff Repair

No evidence is provided for this category.

Shoulder Arthroplasty

Obstructive Sleep Apnea: Patients with obstructive sleep apnea may experience higher rates of medical complications in the short term following total shoulder arthroplasty [23]. There is no difference in orthopedic or mortality outcomes in the long term for patients with obstructive sleep apnea following total shoulder arthroplasty [23].

Carpal Tunnel Syndrome

Subjective-Objective Concordance: Concordance between subjective sleep and standardized measures (PSQI/ISI) increases over time after carpal tunnel release [14].

Pharmacological Interventions

Melatonin: The use of melatonin is recommended postoperatively after arthroscopic rotator cuff repair to reduce sleep disturbance in the early postoperative period and potentially help with longer term functional outcome [7].

Altitude Exposure

Recovery Timeline: Sleep quality returned to normal by the end of the first week at altitude, but sleep quantity had not stabilized at its normal level after 2 weeks in elite athletes [18].

Recovery

Pediatric Concussion

Other Considerations: Lower Injury Psychological Readiness to Return to Sport (IPRRS) ratings are associated with longer symptom resolution time and the occurrence of subsequent injury [21].

Rotator Cuff Repair

Functional milestones: Sleep quality worsens at 2 weeks after rotator cuff repair and improves beyond baseline by 6 weeks [3]. Pharmacological Interventions: Melatonin use is recommended postoperatively after arthroscopic rotator cuff repair to reduce sleep disturbance in the early postoperative period and potentially help with longer term functional outcome [7].

Key Evidence

  • [L3] This study provides further insight into the association between patient-reported sleep disturbances and prolonged recovery in pediatric concussion after controlling for known sociodemographic and clinical predictors of prolonged recovery –those patients reporting trouble falling asleep or sleeping more than usual were more likely to have prolonged recovery from their concussion. [1] (10.1177/2325967126s00067)
  • [L3] We observed an overall improvement in sleep quality after total knee arthroplasty, although there was an initial stage of sleep disturbance immediately postoperatively. [2] (10.1016/j.jisako.2024.100373)
  • [L3] Sleep disturbance is common after rotator cuff repair, with sleep quality worsening at 2 weeks and improving beyond baseline by 6 weeks. [3] (10.1016/j.jse.2026.02.011)
  • [L3] While sleep benefits after TKA were more domain-specific, reductions in environmental disturbances suggest meaningful improvements in select aspects of rest. [4] (10.1016/j.arth.2025.05.020)
  • [L1] Compared to placebo, melatonin did not significantly affect baseline, follow-up, or change in sleep quality (PSQI), pain (VAS), and quality of life (SF-36) scores. [5] (10.1016/j.injury.2022.10.011)
  • [L4] Preoperative sleep disturbance was highly prevalent (84-97%), and minimal improvement was reported within the first 6 weeks postoperatively. [6] (10.1177/17585732261450975)
  • [L1] Based on this investigation, we recommend the use of melatonin postoperatively after aRCR to reduce sleep disturbance in the early postoperative period and potentially help with longer term functional outcome. [7] (10.1177/2325967125s00014)
  • [L3] These results highlight the potential importance of maintaining consistent sleep timing during recovery and indicate that sleep timing interventions may represent a modifiable behavioral factor to support concussion recovery. [8] (10.1177/2325967126s00094)
  • [L3] Patients who have a history of sleep disorders did not report nor objectively experience worse sleep patterns perioperatively. [9] (10.1016/j.arth.2026.03.072)
  • [L1] Our results indicate that melatonin supplementation does not improve postoperative sleep quality measured with the VAS compared with placebo in adult patients (GRADE: moderate). [10] (10.1007/s12630-023-02442-1)
  • [L1] The present study shows that improvement in sleep disturbances in patients with RCTs occurred as early as 3 months after RCR. [11] (10.1177/23259671251397512)
  • [L1] Melatonin, corticosteroids, and anticonvulsants provide inconsistent benefits, underscoring the need for more rigorous, standardized, and longer-term studies to establish optimal pharmacological strategies for enhancing postoperative recovery. [12] (10.1016/j.arth.2025.08.071)
  • [L4] REM sleep returns to normal after 2 weeks at altitude, but impaired breathing does not improve. [13] (10.1136/bjsports-2013-092829)
  • [L2] Carpal tunnel release leads to substantial improvements in both subjective and standardized patient-reported sleep quality in CTS patients, with increasing concordance over time. [14] (10.1016/j.jhsg.2025.100870)
  • [L1] Dexamethasone at doses of four, eight, and 16 mg effectively reduces pain and enhances sleep quality in patients undergoing TKA, with the 16 mg dose showing the most pronounced effects at 12, 24, and 48 hours postoperatively. [15] (10.1016/j.arth.2024.09.006)
  • [L4] [16] (10.1186/s12891-025-08323-6)
  • [L1] Evidence for the effects of perioperative pharmacological approaches on postoperative sleep are limited. [17] (10.4103/joacp.joacp_428_23)
  • [L4] Sleep quality returned to normal by the end of the first week at altitude, but sleep quantity had still not stabilised at its normal level after 2 weeks. [18] (10.1136/bjsports-2013-092843)
  • [L4] [19] (10.1186/s13018-025-06416-5)
  • [L3] [20] (10.1016/j.arth.2024.06.054)
  • [L3] Lower Injury Psychological Readiness to Return to Sport (IPRRS) ratings were associated with longer symptom resolution time and the occurrence of subsequent injury. [21] (10.1177/2325967126s00178)
  • [L3] Adolescents with a concussion demonstrated worse sleep quality than uninjured controls. [22] (10.1177/23259671251330571)
  • [L3] The findings of this study suggest that patients with OSA may experience higher rates of medical complications in the short term, but no difference in orthopedic or mortality outcomes in the long term. [23] (10.1016/j.jse.2025.03.003)
  • [L1] This study supports the application of melatonin for improving postoperative sleep quality. [24] (10.2147/nss.s381918)
  • [L4] Approximately one in four student-athletes reported sleep difficulty and one in seven reported fatigue, indicating a need for follow-up and potential referral to a sleep specialist. [25] (10.1177/2325967126s00114)
  • [L5] The calculation of the MCID needs to be correlated with changes in scores on the rating scale and external anchors. [26] (10.1177/03635465231193411)
  • [L1] [29] (10.1016/j.arth.2025.06.009)
  • [L5] [57] (10.1016/j.asmr.2025.101077)
  • [L3] Sleep disturbances due to rotator cuff tears cannot be captured by the JOA or VAS scores alone. 46% of patients with rotator cuff tears and night pain had insomnia, and CSI and PCS scores were higher in patients with sleep disturbances. [58] (10.1016/j.jse.2025.01.009)
  • [L1] Melatonin may not improve overall postoperative sleep quality following THA as measured by the ESS. [62] (10.1016/j.arth.2025.05.038)

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