Pain and rehabilitation after spinal cord injury: the case of sensory spasticity?
Sixty percent of patients with posttraumatic para- or tetraplegia suffer from severe, continuous burning and/or lancinating pain. Multiple sclerosis produces pain in more than 30%. This pain can be as important as the absent mobility or sexual function as a cause of lowered quality of life. Two unique types of longstanding neuropathic pain can be recognized in persons with spinal cord injury: (1). segmentally distributed pain at the lesion; and (2). pain in the body below the lesion, often with late onset. The first type could be produced by nerve root entrapment or by direct segmental deafferentation. The second type probably contains several forms of central pain, evoked either by the original spinal lesion, by an expanding syrinx in the spinal cord or by secondary changes at higher levels of the somatosensory systems. Patients with central pain almost always have stimulus-independent pain. Its intensity may vary independently, be related to the presence of visceral activity/inflammation or be constant. In addition, stimulus-dependent pain is sometimes present, usually because skin areas or viscera below the lesion are allodynic. Partial spinal lesions, especially centrally in the cervical spinal cord, may be more prone to produce pain than are complete lesions. There is limited analgesic effectiveness in controlled studies of serotonin reuptake inhibitors, of sodium channel blockers (lidocaine, tetracaine), of the GABA receptor agonist baclofen (one study) and of the NMDA-receptor antagonist ketamine (one study). There are anecdotal reports on oral carbamazepine, on gabapentin, on intrathecal opiates and also on the alpha(2)-agonist clonidine, being effective in central neuropathic pain. Neurostimulation is effective only if it evokes paraesthesia in the painful area; hence TENS may give relief of segmental pain. Neurodestructive procedures and central neurostimulation have been largely unsuccessful. As in other longstanding pain, improved coping through cognitive-behavioural rehabilitation may be helpful for the clinical outcome.
Sjölund
Bengt H
BH
Department of Rehabilitation Medicine, Umeå University, Building 9A, NUS, S-901 85, Umeå, Sweden. bengt.sjolund@rehabmed.umu.se
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D009128:Muscle Spasticity / Q000503:physiopathology*; D009475:Neurons, Afferent / Q000502:physiology*; D010146:Pain / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology* / Q000534:rehabilitation*