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Pain. 2018 Jul;159(7):1317-1324. doi: 10.1097/j.pain.0000000000001213.

How central is central poststroke pain? The role of afferent input in poststroke neuropathic pain: a prospective, open-label pilot study.

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Division of Clinical and Translational Research, Department of Anesthesiology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Washington University Pain Center, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Clinical Medicine, Danish Pain Research Center, Aarhus University, Aarhus, Denmark.
Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.
Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
The Center for Clinical Pharmacology, St. Louis College of Pharmacy, Washington University in St. Louis, St. Louis, MO, USA.


Central poststroke pain (CPSP) 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 CPSP is a result of misinterpretation of afferent sensory input by the sensitized neurons within the brain, rather than generated spontaneously by the damaged central nervous system (CNS) neurons. To test this hypothesis, we prospectively recruited 8 patients with definite CPSP affecting at least 1 extremity. In an open-label intervention, 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 7 of the 8 subjects within 30 minutes (the primary outcome measure of the study), and >50% pain relief in the remaining participant. Median (interquartile range) 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 CPSP is autonomously generated within the CNS. 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 CNS.

[Indexed for MEDLINE]

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