UNASSIGNED: Postoperative pain and analgesic use after arthroscopic rotator cuff repair remain important issues that affect rehabilitation and overall outcomes.
UNASSIGNED: To evaluate the pre- and intraoperative factors that may cause prolonged duration of postoperative pain and analgesic use.
UNASSIGNED: Case-control study; Level of evidence, 3.
UNASSIGNED: We included 443 patients who underwent arthroscopic rotator cuff repair and subacromial decompression. Visual analog scale (VAS) scores for pain were obtained preoperatively and at 30 and 90 days postoperatively. Patients were divided into a group who had prolonged postoperative pain (duration ≥1 and <3 months; n = 86 patients) and a group with nonprolonged pain (duration <1 month; n = 357 patients). The following factors were compared between groups: age, sex, body mass index, repair technique, tear size, retraction amount, repair tension, tendon degeneration, preoperative pseudoparesis, symptom duration, application of microfracture to the rotator cuff footprint for marrow stimulation, smoking, degree of fatty degeneration, preoperative narcotic analgesic use, diabetes, acromioclavicular joint degeneration, and preoperative Douleur Neuropathique 4 (DN4) and American Shoulder and Elbow Society (ASES) scores.
UNASSIGNED: Significant differences were seen between the prolonged and nonprolonged groups regarding the median duration of pain (54 vs 27 days, respectively; P < .001) and analgesic use (42 vs 28 days, respectively; P < .001). Significant differences were noted between the groups for symptom duration (P = .007), smoking status (P = .001), degree of fatty degeneration (P = .009), preoperative narcotic analgesic use (P < .001), preoperative DN4 and ASES scores, 30-day VAS score (P < .001), duration of opioid and nonopioid analgesic use (P < .001), tear size (P = .026), and retraction stage (P = .032). Tear size (P = .009), retraction amount (P = .005), preoperative narcotic analgesic use (P < .001), degree of fatty degeneration (P < .001), and preoperative DN4 score (P = .024) were factors independently associated with prolonged postoperative pain and analgesic use.
UNASSIGNED: Patients with larger size tears, retracted tendons, preoperative use of narcotic analgesics, higher tensioned tendon after repair, and Goutallier grade 3 or 4 fatty degeneration faced an increased risk of prolonged postoperative pain and analgesic use after arthroscopic rotator cuff repair. These factors might be mitigated by psychosocial support; gentle, controlled, and individualized postoperative rehabilitation approaches; detailed preoperative evaluation; and closer follow-up of patients who are treated operatively.

Previous research has observed that the speed of alpha band oscillations (8-12 Hz range) recorded during resting electroencephalography is slowed in chronic pain patients. While this slowing may reflect pathological changes that occur during the chronification of pain, an alternative explanation is that healthy individuals with slower alpha oscillations are more sensitive to prolonged pain, and by extension, more susceptible to developing chronic pain. To test this hypothesis, we examined the relationship between the pain-free, resting alpha oscillation speed of healthy individuals and their sensitivity to two models of prolonged pain, Phasic Heat Pain and Capsaicin Heat Pain, at two visits separated by 8 weeks on average (n = 61 Visit 1, n = 46 Visit 2). We observed that the speed of an individual\'s pain-free alpha oscillations was negatively correlated with sensitivity to both models and that this relationship was reliable across short (minutes) and long (weeks) timescales. Furthermore, the speed of pain-free alpha oscillations can successfully identify the most pain sensitive individuals, which we validated on data from a separate, independent study. These results suggest that alpha oscillation speed is a reliable biomarker of prolonged pain sensitivity with potential for prospectively identifying pain sensitivity in the clinic.

The infrapatellar fat pad (IFP) contains nerve fiber endings and is considered to play an important role in the perception of knee pain. However, it is unclear whether and to what degree prolonged pain influences the nociceptive role of the IFP. To answer this question, we established a novel rat model of knee pain in which inflammation is restricted to the IFP. Rats received a single intra-IFP injection of monoiodoacetic acid (MIA) (0.2 mg/10 µL or 1.0 mg/10 µL) in the left knee and a phosphate-buffered saline (10 µL) injection in the right knee as a control. Pain-avoidance behavior and histological changes of the knee joint were measured at multiple time points up to 28 days after MIA injection. Histological analysis showed a transient inflammatory response in the IFP body in the 0.2-mg model, whereas prolonged inflammation followed by fibrotic changes was observed in the 1.0-mg model. Subtle histological alterations were observed in the articular cartilage and IFP surface regardless of the dose. The pain-avoidance behavior test indicated the development of prolonged knee pain throughout the experimental period in the 1.0-mg group. Histological assessments showed a significant increase in calcitonin gene-related peptide (CGRP)-positive nerve fiber endings inside IFPs with fibrosis in newly vascularized surrounding regions. These data suggest that irreversible fibrotic changes in the IFP induce the formation of new vessels and CGRP-positive nerve fiber endings that associate prolonged pain in the joint.

Kinesin superfamily proteins (KIFs) are molecular motors that typically alter the subcellular localization of their cargos. However, the atypical kinesin KIF26A does not serve as a motor but can bind microtubules and affect cellular signaling cascades. Here, we show that KIF26A maintains intracellular calcium homeostasis and negatively regulates nociceptive sensation. Kif26a-/- mice exhibit intense and prolonged nociceptive responses. In their primary sensory neurons, excessive inhibitory phosphorylation of plasma membrane Ca2+ ATPase (PMCA) mediated by focal adhesion kinase (FAK) rendered the Ca transients resistant to termination, and the peripheral axonal outgrowth was significantly enhanced. Upstream, KIF26A is directly associated with a FERM domain of FAK and antagonizes FAK function in integrin-Src family kinase (SFK)-FAK signaling, possibly through steric hindrance and localization to cytoplasmic microtubules.

A framework for defining pain terms such as acute, persistent, prolonged or chronic pain to newborns was derived from the scientific literature on neonatal pain assessments, previous attempts to define chronic pain and the clinical and neurophysiological features of neonatal pain. This novel framework incorporates the temporal features, localising characteristics, and secondary effects of the pain experienced, as well as the behavioural and physiological response patterns of newborns.
CONCLUSIONS: Although not evidence-based, this framework provides an initial starting point for defining commonly used neonatal pain terms. It will require future revision/refinement based on the accumulating evidence for non-acute pain.