Postoperative neuropathic pain (PNP) falls within the broader category of neuropathic pain, defined by the International Association for the Study of Pain as pain “caused by a lesion or disease of the somatosensory nervous system”. This definition, proposed by Treede et al. (2008) [1] and further refined by the NeuPSIG group [2], is accompanied by a grading system (possible/probable/definite) that is useful for both research and clinical practice. In the surgical setting, PNP refers to pain that appears or worsens after an operation and is typically described as burning sensations, electric shocks, brush-evoked allodynia, and paresthesia, with focal sensory abnormalities on examination; screening is facilitated by validated tools such as the DN4 (Neuropathic pain in 4 questions) [1]-[3].

From an epidemiological standpoint, chronic postsurgical pain (CPSP) affects approximately 10% - 50% of operated patients, depending on the type of surgery, with 2% - 10% experiencing severe forms; a neuropathic component is common. Syntheses indicate that among patients with CPSP, the proportion of neuropathic pain is about 66% after thoracotomy and 68% after breast surgery, compared with about 31% after inguinal hernia repair and about 6% after hip/knee arthroplasty [4], while phantom limb pain affects nearly 60% of amputees [5]. More recent updates emphasize incorporating functional interference and quality of life into the definition of CPSP [4]-[7].

Risk factors for PNP are multifactorial and occur before, during, and after surgery. The most robust predictors are preoperative pain and the severity of acute postoperative pain [8][9]. Additional factors include psychological variables (anxiety, depression, catastrophizing) [10], female sex and younger age in several series, and the type of procedure (thoracotomy, mastectomy, amputation, gynecologic or abdominal wall surgery), which carries an increased risk of iatrogenic nerve injury [4][7]. Moreover, early identification of a neuropathic profile in the acute phase (positive DN4) increases the likelihood of persistence in the medium term [11].

The consequences of PNP are substantial: impaired quality of life, functional limitations, and sleep disturbances, with a psychological burden (anxiety, depression) greater than that observed in other chronic pain conditions [12][13]. PNP is also associated with increased healthcare use and analgesic consumption, including a risk of persistent opioid use after surgery [14], supporting multimodal approaches and targeted prevention for high-risk procedures [7][9]. Finally, despite progress, treatment efficacy for neuropathic pain remains partial, reinforcing the value of mechanistic stratification and complementary non-pharmacological options [15].

Local relevance. In Sub-Saharan Africa, postoperative pain is very common and often undertreated due to organizational and resource constraints; however, specific documentation of PNP remains scarce, and routine use of standardized tools (DN4, painDETECT, NPSI) is heterogeneous [16]. In Cameroon, the DN4 has demonstrated clinical utility in other contexts (e.g., diabetic neuropathy), but PNP has been little studied, preventing estimation of its burden and limiting the development of locally adapted prevention strategies [17]. Data from South Africa further highlight a high prevalence of chronic pain in the general population and a marked impact on quality of life, arguing for stronger pain surveillance and management systems [18][19]. The objective of our study was to determine the prevalence of PNP and its associated factors.

The prevalence of postoperative neuropathic pain (PNP) observed in our study (28%) falls within the range of prevalences reported in the early phase following certain high-risk surgeries, notably thoracic surgeries, where approximately one-third of patients exhibit a neuropathic component in the first days and weeks postoperatively [25]-[27]. This “early” prevalence is of prognostic interest, as a positive DN4 score early after surgery is associated with an increased risk of long-term neuropathic persistence [28]. The most common sensory profiles (burning, tingling, brushing) closely matched the descriptors and signs included in the DN4, which combines symptoms and clinical examination and is considered positive for a score ≥ 4/10 [3][29].

The independent associations identified with specific procedures are largely consistent with the literature. After thoracic surgery/thoracotomy, injury to intercostal nerves and central sensitization explain the high proportion of neuropathic components in persistent pain; retrospective series and critical reviews report that approximately 25% to 60% of patients develop chronic post-thoracotomy pain, with about one-third presenting neuropathic features [26][27]. Mastectomy is classically associated with injury to the intercostobrachial nerve, and reviews/meta-analyses report high rates of persistent pain with a substantial neuropathic component after breast cancer treatment [30]. Amputation is frequently accompanied by phantom limb pain and stump pain with a neuropathic phenotype; the meta-analysis by Limakatso et al. estimated a prevalence of approximately 6 out of 10 patients reporting phantom limb pain [31]. Finally, gynecological surgery is associated with a non-negligible risk of chronic pain, with studies showing rates around 30% one year after hysterectomy and a subset with a neuropathic phenotype [32]-[34].

The psychological factors that showed an effect in our model, particularly anxiety disorders, were consistent with quantitative syntheses: the systematic review and meta-analysis by Theunissen et al. demonstrated that preoperative anxiety and catastrophizing increased the risk of chronic postoperative pain, and a more recent meta-analysis confirms the association (albeit moderate) between anxiety, depression, catastrophizing, and chronic postoperative pain [35][36]. These data support the hypothesis that psychological vulnerability potentiates the transition from acute to persistent pain; this continuum has been extensively discussed in reference reviews [25][37].

In terms of mechanisms, our findings can be explained by a combination of peripheral nerve injury (intercostal/intercostobrachial, trunk nerves) and central sensitization, phenomena well documented in surgical cohorts and mechanistic reviews [4][37]. Furthermore, multicentric studies such as GENDOLCAT have highlighted the combined influence of surgery type and clinical/psychological factors on the risk of medium-term chronic pain [34].

In our study, female sex was associated with PNP in bivariate analysis, but this association disappeared after multivariable adjustment. This pattern is compatible with the literature: meta-analyses suggest that female sex is often linked to a higher risk of chronic postsurgical pain, but with modest effect sizes, and the association may attenuate when adjusting for more proximal factors (preoperative pain, type of surgery, psychological factors) [38]. A plausible explanation is confounding by procedure type: some surgeries, more frequent in women (e.g., breast/mastectomy and gynecological surgery), are more likely to involve neuropathic mechanisms and persistent pain, which may create a crude association with sex that is subsequently absorbed by surgical variables in the model [4][34]. Finally, recent syntheses emphasize that risk factors for persistent postsurgical pain are multifactorial and strongly procedure-dependent, which helps explain why sex does not always remain an independent predictor after adjustment [7].

Although depressive disorders were strongly associated with PNP in bivariate analysis (p = 0.001), they were no longer significant after adjustment in the multivariable model. A plausible explanation is the frequent co-occurrence and strong correlation between anxiety and depressive symptoms in the perioperative setting: when anxiety is included in the model, it may capture part of the shared variance (negative effect), making the association with depression non-independent. This interpretation is consistent with evidence showing that preoperative anxiety and/or state anxiety are robust predictors of persistent postoperative pain, sometimes more consistent than depression after adjustment for clinical and surgical factors [36]. Moreover, the effect of psychological factors may vary by surgical model; in some procedures, anxiety emerges as the main determinant, whereas depression loses its independent effect once covariates are considered [39]. Finally, syntheses on persistent postsurgical pain note that anxiety and depression both belong to “negative affective constructs”, and their independent contributions depend on the covariates selected (type of surgery, intensity of acute pain, complications) and on the structure of the statistical model [25][38].

Our study presented several limitations: First, the cross-sectional nature of our study did not allow us to infer the chronicity of specific categories of pain, such as chronic postoperative pain, which is defined as pain persisting beyond three months after surgery. Second, the DN4 is a validated screening tool (cutoff ≥ 4/10) with good sensitivity and specificity, but it is distinct from a formal neurophysiological diagnosis. Third, the precision of some estimates may have been limited by the size of subgroups and unmeasured confounding factors (surgical techniques, analgesic protocols, complications). Finally, the absence of longitudinal follow-up did not allow a direct link to be established between early PNP and persistent pain, although the literature suggests an increased risk when early neuropathic symptoms are present.

In conclusion, our results showed that slightly more than one quarter of postoperative patients experienced PNP, with a phenotype consistent with DN4 descriptors and associated factors dominated by high-risk surgeries (thoracic surgery/thoracotomy, mastectomy, amputation, gynecological surgery) and anxiety. These findings, in line with the literature, support systematic DN4 screening during hospitalization and risk stratification integrating psychological factors and surgical type. Practically, a positive screen (DN4 ≥ 4) or identification of a high-risk patient should prompt: 1) a structured pain assessment (pain mapping, intensity, functional impact, brief neurological examination, and assessment of allodynia/hyperalgesia) and, where available, early input from a pain/anesthesia team; 2) initiation or optimization of multimodal analgesia with adjuvants targeting neuropathic mechanisms according to local protocols and contraindications; 3) implementation, when feasible, of nerve-sparing techniques and/or targeted regional analgesia (peripheral nerve blocks, epidural/paravertebral/interfascial plane techniques depending on the surgical site) for patients undergoing high-risk procedures; and 4) management of psychological factors, particularly anxiety (education, reassurance, non-pharmacological strategies, referral when needed). Finally, a scheduled follow-up at 3 - 12 months is warranted to document persistence, adapt treatment, and classify persistent pain according to the 11th revision of the International Classification of Diseases published by the World Health Organization.