According to the International Association for the Study of Pain IASP, neuropathic pain is caused by a lesion or disease of the somatosensory nervous system.
After a stroke, patients can experience central post-stroke pain (CPSP), peripheral neuropathies, and spasticity-related shoulder pain. Pain can be assessed by patient-reported questionnaires and by physical examinations.
Approximately 7-10% of stroke patients develop central post-stroke pain characterized by abnormal activity of the thalamic ventral posterolateral nucleus, that play an important role in the maintenance of nociceptive hypersensitivity and allodynia (nociceptive perception of non-painful stimuli). Patients experience sensory touch abnormalities (dysaesthesia), cold allodynia, mechanical hypersensitivity, and low discrimination of temperature pain stimuli. Central post-stroke pain might become evident even 3-6 months after the acute stroke event.
The occurrence of Central post-stroke pain is rare and caused by the ischemic lesion within the spinal-thalamic circuit. Certain hypotheses suggest that CPSP might derive from the remodelling of cognitive and sensory networks following ischemic injury, and for that reason, it can be treated with non-pharmacological therapy (Hosomi et al. 2015).
Many patients experience no relief from pain management. This might be partially due to genetic variations of the molecular targets of analgesics or to differences in drug metabolism enzymes. A personalized approach to pain management provides the best option for pain care in patients.
Reference scientific publications for the pain management are:
- Finnerup et al. 2015 Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurology. 14(2):162-73. doi: 10.1016/S1474-4422(14)70251-0. Free access article
- Hosomi et al. 2015 Modulating the pain network -- neurostimulation for central poststroke pain. Nature Review in Neurology. 11(5):290-9. doi: 10.1038/nrneurol.2015.58. Abstract
- Colloca et al. 2017 Neuropathic pain. Nature Review in Disease Primers; 3: 17002. doi:10.1038/nrdp.2017.2. Free access article