Sensitization and Impaired Habituation of Somatosensory Evoked Potentials in Central Post-stroke Pain

Central post-stroke pain (CPSP) is associated with hyperpathia and allodynia, and neurophysiological biomarkers may help to clarify these mechanisms. We report sensitization and impaired habituation of median somatosensory evoked potentials (MSEPs) in CPSP and examine their association with quantitative sensory testing (QST) and clinico-radiological features.

Thirty-four CPSP patients and 18 matched healthy controls were prospectively included. Clinical evaluation, QST, Visual Analog Scale (VAS), Pittsburgh Sleep Quality Index (PSQI), and magnetic resonance imaging (MRI)-based stroke location were recorded. Five consecutive MSEP blocks were obtained bilaterally. N19 latency and amplitude from block 1, as well as habituation across blocks 1 to c5, were analyzed. Impaired habituation was defined as failure of amplitude reduction in blocks 2-5 compared with block 1.

CPSP patients showed significantly prolonged N19 latency (21.7 ± 2.25 ms vs 18.8 ± 1.26 ms) and reduced amplitude (3.1 ± 1.57 µV vs 6.2 ± 2.58 µV) compared with controls. N19 amplitude was also reduced on the unaffected side. Tactile threshold correlated with higher pain intensity ( P = 0.04), inversely with allodynia ( P = 0.01), and with extra-thalamic lesions ( P = 0.01). Impaired habituation occurred in 64.7% of CPSP patients and was significantly associated with hyperalgesia ( P = 0.008).

CPSP is marked by altered somatosensory processing, reduced cortical excitability, and impaired habituation, reflecting maladaptive thalamocortical plasticity.