PAIN�

154 (2013) 189

w w w . e l s e v i e r . c o m / l o c a t e / p a i n

Commentary

Post-stroke shoulder pain: Nociceptive or neuropathic?

Acute rehabilitation after stroke can be adversely affected bycomplications such as pain in the hemiplegic shoulder. The onsetof hemiplegic shoulder pain (HSP) can compromise functionalgains, and has been shown to contribute to longer term disability[3]. The first systematic study of the incidence of post-strokeshoulder pain (PSSP) found that 40% of patients were affected dur-ing the 3–6 months following survival of a stroke [2]. In 25% of pa-tients, pain occurred during the first two weeks after stroke [1].The prognosis at six months, however, appears to be reasonablygood, with 80% of patients reporting improvement or completerecovery in the context of prompt appropriate acute management(physiotherapy, shoulder injection and low dose amitriptyline forsleep disturbance and nocturnal pain) [2].

However, it is still unclear what the mechanisms of post-strokeshoulder pain are and what the most appropriate treatment shouldbe. Answers to these questions could have a profound impact ondegree of the success in rehabilitation after a stroke and the poten-tial for long-term disability.

The scientific literature has tended to focus on associations ofPSSP with peripheral pathology, particularly in relation to tendinop-athies and capsulitis, with relatively few studies focusing on poten-tial neuropathic components to the pain. Gamble et al. [2], foundthat motor impairment, sensory loss and depression were moreassociated with patients with PSSP compared to those without pain.In this issue of PAIN [6], Zeilig et al. systematically assessed thirtypatients, either with or without hemiplegic shoulder pain (HSP),at least six months after stroke. Their analysis included detailedneurological examination, quantitative sensory testing and brainscans (CT/MRI). These two groups were compared to 15 normal vol-unteers. Those with HSP had higher heat pain thresholds and hyper-pathia to heat in the affected shoulder and leg compared to thosewithout HSP. The HSP group also more often reported pain through-out the affected side than did those without HSP and had moreextensive parietal lobe damage on their brain scans. The authorsappropriately suggest that the evidence of damage to the spino-thalamocortical system, the presence of chronic pain throughoutthe affected side, and greater parietal damage are consistent withthere being a central neuropathic component to this type of pain.

Patients in the study were recruited from two rehabilitationcentres and were only included if they had no previous history ofshoulder pain. The patients may, therefore, not be completely rep-resentative of this condition in the community. Nevertheless, the

0304-3959/$36.00 � 2012 Published by Elsevier B.V. on behalf of International Associahttp://dx.doi.org/10.1016/j.pain.2012.11.009

study’s findings are still consistent with findings from previoussystematic studies showing an association between post-strokeshoulder pain and the extent of neurological deficit on the affectedside [2–5]. Based on clinical evidence it therefore seems that post-stroke shoulder pain is likely be due to central sensitisation with avariable contribution from peripheral pathologies, such as capsuli-tis, which are common in this age group. In the study by Zeilig andcolleagues [6] patients were carefully selected to the exclusion ofprevious shoulder pain. Therefore, peripheral pathology is lesslikely to be a contributing factor to the pain in this group.

The challenge is now to understand the mechanisms of thistroublesome condition and to develop a rational basis for preven-tion and intervention. If successful, this is likely to result in a sub-stantial improvement in acute and chronic stroke rehabilitation.

Conflict of interest statement

The authors have no conflict of interest regarding thiscommentary.

References

[1] Gamble GE, Barberan E, Bowsher D, Tyrrell PJ. Post stroke shoulder pain: morecommon than previously realized. EJP 2000;4:313–5.

[2] Gamble GE, Barberan E, Laasch HU, Bowsher D, Tyrrell PJ, Jones AKP. Poststrokeshoulder pain: a prospective study of the association and risk factors in 152patients from a consecutive cohort of 205 patients presenting with stroke. EJP2002;6:467–74.

[3] Lindgren I, Jönsson AC, Norrving B, Lindgren A. Shoulder pain after stroke: aprospective population-based study. Stroke 2007;38:343–8.

[4] Ratnasabapathy Y, Broad J, Baskett J, Pledger M, Marshall J, Bonita R. Shoulderpain in people with a stroke: a population-based study. Clin Rehab2003;17:304–11.

[5] Roosink M, Renzenbrink GJ, Buitenweg JR, Van Dongen RTM, Geurts ACH,Ijzerman MJ. Somatosensory symptoms and signs and conditioned painmodulation in chronic post-stroke shoulder pain. J Pain 2011;12:476–85.

[6] Zeilig G, Rivel M, Weingarden H, Gaidoukov E, Defrin R. Hemiplegic shoulderpain: evidence of a neuropathic origin. PAIN� 2013;154:263–71.

Anthony K.P. Jones⇑Christopher A. Brown

Human Pain Research Group, University of Manchester,Clinical Sciences Building, Salford Royal Hospitals NHS Foundation Trust,

Eccles Old Road, Salford M6 8HD, United Kingdom⇑ Tel.: +44 0161 206 4265/4266.

E-mail address: kate.ryan@manchester.ac.uk (A.K.P. Jones)

tion for the Study of Pain.