5 research outputs found
Dissecting central post-stroke pain:a controlled symptom-psychophysical characterization
Central post-stroke pain affects up to 12% of stroke survivors and is notoriously refractory to treatment. However, stroke patients often suffer from other types of pain of non-neuropathic nature (musculoskeletal, inflammatory, complex regional) and no head-to-head comparison of their respective clinical and somatosensory profiles has been performed so far. We compared 39 patients with definite central neuropathic post-stroke pain with two matched control groups: 32 patients with exclusively non-neuropathic pain developed after stroke and 31 stroke patients not complaining of pain. Patients underwent deep phenotyping via a comprehensive assessment including clinical exam, questionnaires and quantitative sensory testing to dissect central post-stroke pain from chronic pain in general and stroke. While central post-stroke pain was mostly located in the face and limbs, non-neuropathic pain was predominantly axial and located in neck, shoulders and knees (Pâ<â0.05). Neuropathic Pain Symptom Inventory clusters burning (82.1%, nâ=â32, Pâ<â0.001), tingling (66.7%, nâ=â26, Pâ<â0.001) and evoked by cold (64.1%, nâ=â25, Pâ<â0.001) occurred more frequently in central post-stroke pain. Hyperpathia, thermal and mechanical allodynia also occurred more commonly in this group (Pâ<â0.001), which also presented higher levels of deafferentation (Pâ<â0.012) with more asymmetric cold and warm detection thresholds compared with controls. In particular, cold hypoesthesia (considered when the threshold of the affected side was <41% of the contralateral threshold) odds ratio (OR) was 12 (95% CI: 3.8â41.6) for neuropathic pain. Additionally, cold detection threshold/warm detection threshold ratio correlated with the presence of neuropathic pain (Ïâ=ââ0.4, Pâ<â0.001). Correlations were found between specific neuropathic pain symptom clusters and quantitative sensory testing: paroxysmal pain with cold (Ïâ=ââ0.4; Pâ=â0.008) and heat pain thresholds (Ïâ=â0.5; Pâ=â0.003), burning pain with mechanical detection (Ïâ=ââ0.4; Pâ=â0.015) and mechanical pain thresholds (Ïâ=ââ0.4, Pâ<â0.013), evoked pain with mechanical pain threshold (Ïâ=ââ0.3; Pâ=â0.047). Logistic regression showed that the combination of cold hypoesthesia on quantitative sensory testing, the Neuropathic Pain Symptom Inventory, and the allodynia intensity on bedside examination explained 77% of the occurrence of neuropathic pain. These findings provide insights into the clinical-psychophysics relationships in central post-stroke pain and may assist more precise distinction of neuropathic from non-neuropathic post-stroke pain in clinical practice and in future trials