Herman et al. (1992) note that baclofen, an α-aminobutyric acid (GABA)B receptor agonist, acts to suppress spasticity in SCI patients centrally within the spinal cord itself. GABA is known to be involved in several analgesics pathways (Sawynok 1987) and experimentally induced allodynia has been shown to be suppressed by baclofen (Henry 1982). However, baclofen, by treating spasticity, may reduce the musculoskeletal pain associated with spasticity. Continuous intrathecal infusion of baclofen can be effective, when oral baclofen is ineffective, in further reducing post-SCI spasticity and/or pain (dysesthetic, musculoskeletal, neurogenic; Boviatsis et al. 2005; Herman & D’Luzansky 1991; Penn & Kroin 1987; Plassat et al. 2004). For an in-depth discussion of intrathecal baclofen and its effects on spasticity in SCI, please refer to the Spasticity chapter.
Boviatsis et al. (2005) and Plassat et al (2004) presented case series data that reflected improvements in self-reported pain ratings after intrathecal baclofen administration. Herman et al. (1992) in a RCT found that intrathecal baclofen significantly suppressed the dysesthetic (burning) pain among six of the seven subjects (p<0.001). Only one of the placebo patients noted the dysesthetic pain was abolished. Intrathecal baclofen did not have a significant impact on pinch induced pain. Therefore, in this study, intrathecal baclofen appeared to have an impact on post-SCI dysesthetic pain in addition to treating the spasticity. Loubser and Akman (1996) performed a before and after study of implanted Baclofen infusion pumps provided for spasticity. Twelve of sixteen patients described pre-existing chronic pain but there was no significant difference in the VAS neurogenic pain symptoms at 6 and 12 months (p=0.26) while musculoskeletal pain symptoms and pain severity decreased in conjunction with control of spasticity in 5 of 6 patients. In this study, it appeared musculoskeletal pain was reduced more with intrathecal baclofen, presumably by reducing spasticity.
Hence, it would appear that intrathecal baclofen improves chronic post-SCI pain but the actual mechanism has not been adequately established. There is evidence that baclofen infusion pumps may be helpful for both neuropathic and musculoskeletal pain after SCI (Loubser & Akman 1996). However, studies have shown that intrathecal baclofen only reduces SCI pain when pain is related to muscle spasms (Coffey et al. 1993; Meythaler et al. 1992). Suppression of central pain through baclofen antagonism of substance P has been postulated (Herman et al. 1992).
Motor Point Phenol Block
In a case series, Uchikawa et al. (2009) followed seven spinal cord injury individuals with spastic shoulder pain underwent a motor point phenol block procedure. A significant improvement in VAS shoulder pain was seen post injection (p<0.05).
In a double blind placebo study, Han et al. (2016) found BTX-A significantly improved post SCI neuropathic pain based on average pain ratings on the VAS at 4 and 8 weeks. The study found no significant improvements in quality of life. Marciniak et al. (2008) treated 29 SCI patients with Botulinum toxin type A injections to treat focal spasticity. Pain was improved by 83.3%.
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 1 evidence (from one RCT: Han et al. 2016) that local botulinum toxin injections may reduce neuropathic pain post SCI.