Páll Karlsson

Central post-stroke pain is a neuropathic pain disorder, the underlying mechanisms of which are not well understood. It has been suggested that stroke-associated loss of inhibitory neurons in the spinothalamic tract causes disinhibition of thalamic neurons, which autonomously generate ectopic nociceptive action potentials responsible for the pain experience. We hypothesized that central post-stroke pain is a result of misinterpretation of afferent sensory input by the sensitized neurons within the brain, rather than generated spontaneously by the damaged CNS neurons. To test this hypothesis, we prospectively recruited eight patients with definite central post-stroke pain affecting at least one extremity. In an open-label interventions, an ultrasound-guided peripheral nerve block with lidocaine was performed to block afferent sensory input from a painful extremity. Spontaneous and evoked pain, neuropathic pain descriptors, and lidocaine plasma concentrations were measured. The blockade of peripheral sensory input resulted in complete abolition of pain in seven of the eight subjects within 30 minutes (the primary outcome measure of the study), and >50% pain relief in the remaining participant. Median (IQR) spontaneous pain intensity changed from 6.5 (4.3-7.0) at baseline to 0 (0-0) after the block (p=0.008). All mechanical/thermal hypersensitivity was abolished by the nerve block. The results suggest that it is unlikely that central post-stroke pain is autonomously generated within the central nervous system. Rather, this pain is dependent on afferent input from the painful region in the periphery, and may be mediated by misinterpretation of peripheral sensory input by sensitized neurons in the central nervous system.