Summary
Pain following SCI is quite common. The most common type of pain post SCI is central or neuropathic in nature characterized by a dysesthetic, burning pain below the level of SCI. Borderzone or segmental pain is much less common; occurring along the border between normal and absent sensation. The precise etiology of central/neuropathic or borderzone segmental pain is not known. There is some evidence suggesting an association may exist between the central or neuropathic dysesthetic burning pain and abnormalities of the sympathetic nervous system. Musculoskeletal pain, either secondary to the original trauma or to overuse is both common and well understood. Unfortunately, the management of central or neuropathic pain remains difficult and largely ineffective.
For many SCI patients, pain has a significant impact on quality of life.
Over 50% of SCI patients develop chronic pain. Severe pain is more common the lower down the lesion in the spinal cord. Pain post SCI most often begins within the first 6-12 months post-SCI.
The most common types of pain post SCI are: 1) a burning pain (likely neuropathic) usually localized to the front of torso, buttock or legs or 2) an aching pain (likely musculoskeletal) usually localized to the neck, shoulders and back.
There is level 2 evidence (from one randomized controlled trial and one prospective controlled trial; Chase et al. 2012; Norrbrink & Lundeberg 2011) that massage therapy may not improve neuropathic and musculoskeletal pain intensity post SCI.
There is level 1b evidence (from one randomized controlled trial: Arienti et al. 2011) that osteopathy alone is not effective in improving neuropathic pain post SCI.
There is level 1a evidence (from two randomized controlled trials: Dyson-Hudson et al. 2001, 2007) that in general acupuncture is no more effective than Trager therapy or sham acupuncture in reducing nociceptive musculoskeletal shoulder pain post SCI.
There is level 1b evidence (from one randomized controlled trial: Yeh et al. 2010) that acupuncture and electroacupuncture reduces neuropathic pain of patients with SCI.
There is level 1b evidence (from one randomized controlled trial: Ginis et al. 2003) that a regular exercise program significantly reduces post-SCI neuropathic and musculoskeletal pain.
There is level 2 evidence (from one prospective controlled trial and one pre-post study: Nawoczenski et al. 2006; Serra-Ano et al. 2012) that a shoulder exercise protocol reduces the intensity of nociceptive shoulder pain post-SCI.
There is level 4 evidence (from one pre-post study: Finley & Rodgers 2007) that the MAGIC wheels 2-gear wheelchair results in less nociceptive shoulder pain.
There is level 2 and level 4 evidence (from one randomized controlled trial and one pre-post study: Jensen et al. 2009, 2000) that hypnosis reduces neuropathic and musculoskeletal pain intensity post SCI.
There is level 4 evidence (from one pre-post study: Jensen et al. 2013) that biofeedback may reduce neuropathic and musculoskeletal pain intensity post SCI.
There is level 2 evidence (from one prospective controlled trial: Perry et al. 2010) that a cognitive behavioural pain management program with pharmacological treatment may improve secondary outcomes among SCI individuals with chronic pain post SCI.
There is level 1b evidence (from one randomized controlled trial one prospective controlled trial, and one pre-post study: Heutink et al. 2012; Norrbrink et al. 2006; Burns et al. 2013) that cognitive-behavioural therapy alone does not change post-SCI pain intensity.
There is conflicting level 1b evidence (from one randomized controlled trial, a chohort study and two pre-post studies: Soler et al. 2010; Kumru et al. 2013; Gustin et al. 2008; Moseley 2007) that visual imagery may reduce at level neuropathic pain post SCI for a short period.
There is strong evidence level 1a evidence (from four randomized controlled trials: Capel et al. 2003; Fregni et al. 2006; Soler et al. 2010; Tan et al. 2006) for the benefits of transcranial electrical stimulation in reducing neuropathic and neuropathic and musculoskeletal post-SCI pain.
There is level 4 evidence (from one pre-post study: Panagos et al. 2004) that using a static field magnet helps to reduce reports of sharp, stabbing nociceptive shoulder pain but does not significantly reduce the VAS score of pain in individuals with a SCI.
There is level 4 evidence (from one case series study: Davis & Lentini 1975) that transcutaneous electrical nerve stimulation reduced at-the-injury site pain in only a minority of patients with thoracic or cauda equina SCI, but not those with cervical SCI.
There is level 1a evidence (from two randomized controlled trials: Jette et al. 2013; Defrin et al. 2007) that transcranial magnetic stimulation significantly reduced post-SCI neuropathic pain significantly over the long-term.
There is level 1a evidence (from two randomized controlled trials, and one case series, pre-post, and observational study: Levendoglu et al. 2004; Tai et al. 2002; To et al. 2002; Ahn et al. 2003; Putzke et al. 2002) that the Gabapentin and pregabalin improve neuropathic pain post SCI.
There is level 1b evidence (from one randomized controlled trial: Arienti et al. 2011) that combined pregabalin and osteopathy treatment improves pain post SCI.
There is level 4 evidence (from one pre-post study: Ahn et al. 2003) that the anticonvulsant Gabapentin is more effective when SCI pain is<6 months than >6 months.
There is level 1b evidence (from one randomized controlled trial: Finnerup et al. 2002) that lamotrigine improves neuropathic pain in incomplete spinal cord injury
There is level 1b evidence (from one randomized controlled trial: Finnerup et al. 2009) that Levetiracetam is not effective in reducing neuropathic pain post SCI.
There is level 2 evidence (from one randomized controlled trial: Drewes et al. 1994) that valproic acid does not significantly relieve neuropathic pain post SCI.
There is level 1b evidence (from one randomized controlled trial: Rintala et al. 2007) that amitriptyline is effective in the treatment of post-SCI neuropathic pain in individuals only when there is concomitent depression.
There is level 1b evidence (from one randomized controlled trial: Vranken et al. 2011) that duloxetine may improve neuropathic pain post SCI.
There is level 1b evidence (from one randomized controlled trial: Davidoff et al. 1987b) that trazodone does not reduce post-SCI neuropathic pain.
There is level 1b evidence (from one randomized controlled trial: Loubser & Donovan 1991) that Lidocaine delivered through a subarachnoid lumbar catheter provides short-term relief of pain greater than placebo.
There is level 1a evidence (from two randomized controlled trials: Kvarnstrom et al. 2004; Eide et al. 1995) that intravenous Ketamine significantly reduces allodynia when compared to placebo.
There is level 1b evidence (from one randomized controlled trial: Chiou-Tan et al. 1996) that mexilitene (a derivative of lidocaine) does not improve SCI dysesthetic pain when compared to placebo.
There is conflicting level 4 evidence (from two case series studies and one pre-post study: Boviatsis et al. 2005; Plassat et al. 2004; Loubser & Akman 1996) that intrathecal baclofen reduces dysesthetic pain post-SCI.
There is level 4 evidence (from one pre-post study: Loubser & Akman 1996) that intrathecal baclofen reduces musculoskeletal pain post-SCI in conjunction with spasticity reduction.
There is level 4 evidence (from one case series study: Uchikawa et al. 2009) that motor point phenol block is effective in reducing short term spastic shoulder pain post SCI.
There is level 4 evidence (from one case series study: Marciniak et al. 2008) that local botulinum toxin injections to treat focal spasticity reduces pain.
There is level 1b evidence (from one randomized controlled trial; Attal et al. 2002) that intravenous morphine significantly reduces mechanical allodynia more than placebo.
There is level 1b evidence (from one randomized controlled trial: Norrbrink & Lundeberg 2009) that tramadol is effective in reducing neuropathic pain post SCI.
There is level 1b evidence (from one randomized controlled trial: Eide et al. 1995) that alfentanil reduces overall post SCI pain.
There is level 1b evidence (from one randomized controlled trial: Eide et al. 1995) that alfentanil is more effective at reducing wind up like pain than ketamine.
There is level 4 evidence (from one pre-post study: Barrera-Chacon et al. 2010) that oxycodone and anticonvulsants may be effective in improving SCI neuropathic pain.
There is conflicting level 2 evidence (from one randomized controlled trial: Hagenbach et al. 2007) for the use of delta-9-tetra hydrocannabinol in reducing spastic pain in SCI individuals.
There is level 2 evidence (from one randomized controlled trial: Rintala et al. 2010) that dronabinol is not effective in reducing pain intensity post SCI.
There is level 1b evidence (from one randomized controlled trial: Siddall et al. 2000) that intrathecal clonidine alone does not provide pain relief greater than placebo.
There is level 2 evidence (from one prospective controlled trial: Uhle et al. 2000) that the combination of intrathecal morphine and clonidine provides pain relief greater than placebo.
There is level 4 evidence (from one case series study: Sandford & Benes 2000) that topical capsaicin reduces post-SCI radicular pain.
There is level 4 evidence (from one case series study: Ciono et al. 1995) that spinal cord stimulation improves post-SCI pain.
There is level 3 evidence (from one case control study: Livshits et al. 2002) to support the use of dorsal longitudinal T-myelotomy procedures, in particular Pourpre’s technique, to reduce spastic pain post SCI.
There is level 2 evidence (from one prospective controlled trial, one pre-post study, and seven case series studies: Falci et al. 2002; Chun et al. 2011; Sindou et al. 2001; Spaic et al. 1999 2002; Rath et al. 1997; Sampson et al. 1995; Bashold et al. 1990; Friedman & Nashold 1986) to support the use of the DREZ surgical procedure to reduce pain post SCI. It may be that some populations (segmental pain) are more likely to benefit from this procedure.
