A growing amount of evidence suggests that OA pain has a neuropathic component in some patients. Deeper understanding of the likely multiple mechanisms of OA pain has led to the use of centrally acting drugs to alleviate osteoarthritic pain [12].
Several animal studies supported the hypothesis that neuropathic pain would be part of OA pathogenesis [13,14]. Histologic assessment of the morphology of nerves in knee OA animal model by sodium monoiodoacetate (MIA) injection showed changes to nerves suggestive of neuropathic pain. Such changes include reduced nerve fiber density, expression of activation transcription factor-3 (ATF-3; a marker of nerve damage) in the spinal cord [13]. The presence of lysophosphatidic acid (LPA) in joint synovium has been found to correlate with myelin thickness and ATF-3 in OA model by MIA injection [14]. However, these hypotheses have not been proved in the patients of OA.
Previous studies demonstrated that neuropathic pain localized to the knees, assessed using the PDQ, affected 5% to 32% of patients [4,11,15-18]. Possible neuropathic pain has been variously reported in 21% to 50% of cases (Table 4) [4,11,15-18]. The present study reported 6% and 22 % with neuropathic pain and possible neuropathic pain, respectively. This prevalence was lower than many studies; however, it was similar to Japanese report by Ohtori et al. [15]. Although, previous studies did not evaluate the outcomes after TKA in patients with neuropathic pain, the present study demonstrated the key role of preoperative possible neuropathic pain on postoperative pain. Using the Self-administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS) scale, Fitzsimmons et al. [19] reported that suspected neuropathic pain was present in 35.5% of pre-TKA patients, and in 23.6% of OA patients at 6 months post-TKA. Patients scoring 12 or greater on the scale were defined as having suspected neuropathic pain [19]. If surgeons recognize the presence of possible neuropathic pain before TKA, careful evaluation, including of spinal disease, is needed to avoid chronic postoperative knee pain. A recent study demonstrated that possible neuropathic pain with end-stage hip and knee OA was more strongly associated with pain at rest than pain on activity [20]. This indicates that the clinical presentation of pain at rest may warrant more thorough evaluation for potential neuropathic pain. Using S-LANSS, Razmjou et al. [21] showed that the prevalence of neuropathic pain was 14% at an average of 5 years after TKA. They also showed that patients with neuropathic pain (S-LANSS score of 12 or greater) remained more disabled, and with a higher level of depression and less satisfaction. Moreton et al. [4] evaluated PDQ and S-LANSS to determine agreement between the two assessment methods. PDQ assesses pain quality associated with augmented central pain processing in patients with OA. Although developed as a screening questionnaire, the PDQ may also function as a measure of characteristics that indicate augmented central pain processing. They found that agreement between PDQ and S-LANSS for pain classification was low, and it is currently unknown which tool may best predict treatment outcome. One of the important problems of PDQ is that when the patient has no pain, the patient is classified as nociceptive pain group. Nociceptive pain includes no pain.
Neuropathic pain is uncommon after TKA surgery. While approximately 20% of patients with advanced degenerative knee disease have elements of pain that test positive with a specific neuropathic pain, less than 3% of the patients assessed in this study continued to have similar pain symptoms noted after their surgery. The overlap of pain symptoms between osteoarthritis patients and this specific battery (PDQ), suggests that the inventory may not be a selective tool to assess for neuropathic pain. New onset neuropathic pain is uncommon after TKA, and may only impact 1-2% of patients. While the severity of pain may significantly impact these patients, it is not a likely explanation for up to 20% of patients who have reported dissatisfaction with TKA in a number of reported studies [22-24]. One of the reasons might be transformation of PDQ scores to category variable from continuous variable. When we used PDQ scores as continuous variable, postoperative NRS and PDQ scores showed positive correlation. We showed a nearly 9-fold decrease in the proportion of patients with neuropathic pain after TKA. However, knees with postoperative possible neuropathic pain had higher postoperative NRS scores than those with nociceptive pain. In addition, higher PDQ scores were associated with severe pain and might be resulted in worse outcome and less satisfaction after TKA.
Buvanendran et al. [25] reported that perioperative pregabalin administration reduces postoperative neuropathic pain. However, this remains controversial as two studies have generated conflicting results [26,27]. Although the causes and factors associated with neuropathic pain warrant further investigation, preoperative assessment, including by the PDQ, may be useful to reduce the prevalence of postoperative chronic knee pain.
Limitations of this study include the absence of evaluations of spinal disease and only a 6 month follow-up period.