Stroke remains one of the leading causes of long-term disability worldwide. According to the Global Burden of Disease Study 2019, the global incidence of stroke was 12.2 million cases, with a prevalence of 101 million and 143 million disability-adjusted life-years (DALYs) lost. 1,2 In India, the estimated adjusted prevalence of stroke ranges from 84 to 262 per 100,000 population in rural and urban settings, and India contributes a disproportionately large share of global stroke-related DALYs. 3,4

Hemiplegic shoulder pain (HSP) is among the most frequent complications following stroke. A systematic review of 18 studies estimated the incidence of HSP at 10 - 22% and its prevalence at 22 - 47% among stroke survivors, with wide variation attributable to differences in study population, timing of assessment, and case definition.⁵ A hospital-based Indian study reported a prevalence of approximately 54% among post-stroke patients.⁶ HSP has traditionally been attributed to peripheral musculoskeletal and neurological factors, including rotator cuff pathology, glenohumeral subluxation, spasticity, adhesive capsulitis, subacromial impingement, and brachial plexopathy. 7

An increasing body of evidence, however, suggests that alterations in central pain processing termed central sensitization (CS) may also be present in HSP, and more broadly in central post-stroke pain syndromes.8 CS is defined as an increased responsiveness of nociceptive neurons in the central nervous system to normal or sub-threshold afferent input, manifesting as hypersensitivity to stimuli, pain evoked by non-noxious input, and an expanded receptive field extending beyond the site of original injury. 9,10 The International Association for the Study of Pain (IASP) subsequently introduced the concept of nociplastic pain to describe pain arising from altered nociceptive function despite the absence of clear tissue injury or disease of the somatosensory nervous system, as a third mechanistic pain descriptor alongside nociceptive and neuropathic pain, emphasizing altered nociceptive processing as a distinct pain mechanism relevant across musculoskeletal pain conditions.

11-13 Because CS cannot be measured directly, it is inferred indirectly through psychophysical testing  most commonly pressure pain threshold (PPT) assessment at both the symptomatic site and distant, uninvolved sites  and through validated self-report screening instruments such as the Central Sensitization Inventory (CSI), a 25-item questionnaire with a suggested cut-off score of 40 for identifying patients at high probability of a central sensitivity syndrome. 14,15 The CSI is a screening tool rather than a diagnostic instrument, and a positive screen should be interpreted as indicating a high probability of a centrally mediated pain phenotype rather than as a confirmed diagnosis. This interpretation is consistent with previous work demonstrating that CSI scores reflect pain sensitivity and central pain-related constructs rather than constituting a definitive diagnosis of central sensitization.14,15,19

Identifying a centrally sensitized pain phenotype in HSP is not merely of academic interest. Patients demonstrating features suggestive of central sensitization may respond less predictably to interventions directed solely at peripheral pathology, such as local injections, positioning, or peripheral electrical stimulation. Multimodal pain management strategies including pain neuroscience education, graded exercise, cognitive-behavioural approaches, centrally acting pharmacotherapy, and selected neuromodulatory interventions; have been proposed for patients with nociplastic pain phenotypes, although evidence specific to post-stroke shoulder pain remains limited. 11,12 Establishing how common this phenotype is among patients with HSP is therefore a necessary first step before such targeted strategies can be evaluated in this population.

CS has been reported across a range of chronic musculoskeletal and inflammatory pain conditions, with prevalence estimates by CSI criteria varying by population and by the chronicity and severity of the underlying condition. 16 Reviews of musculoskeletal shoulder pain more generally have also found evidence of central sensitization in the majority of studies examined, based on PPT or other somatosensory testing. 17 Despite this, the specific prevalence of CSI-defined CS in hemiplegic shoulder pain, and the degree to which it can be corroborated by objective psychophysical testing, has been sparsely studied, particularly in South Asian populations. Hemiplegic shoulder pain has a variable natural history and may persist for months to years after stroke if not adequately managed, underscoring the clinical relevance of better characterizing its underlying pain mechanisms

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This study was therefore undertaken, as an exploratory hospital-based investigation, to estimate the prevalence of features suggestive of central sensitization among patients with hemiplegic shoulder pain attending a tertiary care rehabilitation department, using the CSI as the primary case-ascertainment instrument and PPT testing as a corroborating objective measure.

Study design and setting: This study was a cross-sectional observational study conducted in the Departments of Physical Medicine and Rehabilitation at a tertiary care teaching hospital in New Delhi, India. The study was approved by the institutional ethics committee, and written informed consent was obtained from all participants in their preferred language (Hindi or English).

Participants and sampling approach: All post-stroke patients attending the Department of Physical Medicine and Rehabilitation outpatient clinic during the study period were assessed for eligibility. Inclusion criteria were: shoulder pain contralateral to a unilateral stroke lesion; age > 18 years; either gender; pain duration >3 months; worst pain severity in the preceding week ≥ 4 on a 0 - 10 scale; and willingness to participate. Patients were excluded if they had joint or overlying skin infection, another chronic pain syndrome, prior shoulder surgery on the affected limb, cognitive or communicative impairment precluding participation (e.g., hemineglect, aphasia), or a history of shoulder osteoarthritis, rheumatoid arthritis, fracture, tumor, or infection.

A non-probability convenience sample of 50 consecutive eligible patients presenting to the outpatient department during the study period were enrolled. Eligible patients underwent a structured evaluation. Pain intensity was first confirmed using the Numeric Pain Rating Scale (NPRS, 0–10) to verify the ≥ 4/10 severity threshold. Patients meeting this threshold then completed the Central Sensitization Inventory (CSI; Part A, 25 items, score range 0–100) in either Hindi or English, per the participant's preference; a formally validated, cross-culturally adapted Hindi version of the CSI was not specifically used, which is noted as a limitation below. A CSI score > 40 was used to classify patients as screening positive for central sensitization; a score ≤ 40 classified patients as screening negative. ¹⁴,¹⁵

Pressure pain threshold was measured, as a corroborating objective measure, using a handheld digital algometer (Wagner Instruments) with a 1 cm² probe, applying mechanical force at a target rate of 1 kg/second until the participant first reported a change from pressure to pain. Testing was performed over the mid-belly of the deltoid muscle and over the tibialis anterior, bilaterally. Three measurements were taken at each site, alternating sides between measurements to minimize habituation or temporal summation effects, and the average of the three was used for analysis.

Statistical analysis: Data were entered in Microsoft Excel and analyzed using SPSS version 25.0 (IBM Corp., Chicago, USA). Categorical variables were expressed as number and percentage; quantitative variables were expressed as mean ± standard deviation or median with interquartile range (IQR), depending on distribution, assessed using the Kolmogorov–Smirnov test. Quantitative variables were compared between patients with and without CS using the independent t-test (normally distributed data) or the Mann–Whitney U test (non-normally distributed data). Categorical variables were compared using Fisher's exact test where any expected cell count was <5. A two-tailed p-value <0.05 was considered statistically significant. The Kolmogorov–Smirnov test is a less powerful choice than the Shapiro–Wilk test for assessing normality in samples of this size (n=50); this is noted as a methodological limitation, as re-analysis was not possible without access to patient-level raw data.

Fifty patients with post-stroke shoulder pain satisfying the eligibility criteria were enrolled. The mean age was 60.48 years, with the largest proportion of patients (38%) aged 61–70 years. Thirty-three patients (66%) were male and 17 (34%) females (male: female ratio ≈ 2:1). Twenty-nine patients (58%) belonged to the upper-middle or lower-middle socioeconomic status on the Kuppuswamy scale. The mean duration of stroke was 15.48 ± 6.19 months. Forty-one patients (82%) had an ischemic (infarct) stroke and 9 (18%) a hemorrhagic stroke. Thirty-two patients (64%) had a right-sided and 18 (36%) a left-sided brain lesion, Figure 1 Summarizes the enrolment and classification of participants.

Features suggestive of central sensitization (CSI score >40) were identified in 39 of 50 patients a prevalence of 78% (95% CI 64.8–87.2%, Wilson score method; Table 1). The remaining 11 patients (22%) screened negative (CSI ≤ 40).

Table 1. Prevalence of CSI-defined features suggestive of central sensitization in the study cohort (95% CI calculated using the Wilson score method).

Baseline demographic and stroke-related characteristics did not differ significantly between CSI-positive and CSI-negative patients (all p>0.05; Table 2), indicating that the observed prevalence was not explained by imbalances in age, gender, socioeconomic status, stroke duration, stroke type, or side of lesion, as far as these variables were assessed.

Table 2. Baseline characteristics of CSI-negative and CSI-positive patients.

Pressure pain threshold was significantly lower in CSI-positive patients at both the affected deltoid (median 1.23 kg/cm² vs. 3.0 kg/cm²; p<0.0001) and the affected tibialis anterior (median 2.8 kg/cm² vs. 3.1 kg/cm²; p=0.008) compared with CSI-negative patients. No significant difference was observed at the non-affected deltoid (p=0.699) or non-affected tibialis anterior (p=0.121) (Table 3). This pattern reduced thresholds at both the affected site and a remote, pain-free site, with sparing of the corresponding unaffected side is consistent with widespread central hypersensitivity and provides objective, though not fully independent, support for the CSI-based classification.

Table 3. Pressure pain threshold (kg/cm²) by CSI-based classification.

In this hospital-based cohort of patients with chronic hemiplegic shoulder pain, features suggestive of central sensitization were identified in 78% of participants. Because this study included only patients with established chronic HSP, this proportion should not be interpreted as the prevalence of central sensitization among all stroke survivors or among all patients with HSP. Rather, features suggestive of central sensitization were common in this selected cohort of patients with established, at least moderately severe, chronic symptoms.

This prevalence estimate is supported by the PPT findings: patients classified as CS-present demonstrated significantly reduced thresholds not only at the affected shoulder but also at the tibialis anterior a site remote from the original site of injury while PPT at the corresponding non-affected sites did not differ between groups. This pattern of localized plus remote hypersensitivity, with sparing of homologous unaffected tissue, is considered the classical psychophysical signature of widespread central hypersensitivity rather than purely local, peripheral nociceptor sensitization,⁸,²² and provides convergent psychophysical evidence supporting the CSI-based classification rather than relying on self-report alone.

Comparable prevalence was reported by Walankar et al. ¹⁸, in which 38 of 80 patients (47.5%) with chronic unilateral shoulder pain of mixed aetiology were classified as having central sensitization by CSI; a lower proportion than observed here, though drawn from a general chronic shoulder pain population rather than a specifically post-stroke one. A review by Borstad and Woeste¹⁷ of six studies on musculoskeletal shoulder pain found evidence of central sensitization, based on PPT or other somatosensory testing, in five of the six studies reviewed, reinforcing that central sensitization is frequently though not universally reported across shoulder pain populations, with the prevalence in this post-stroke cohort toward the higher end of that range.

The relatively high prevalence observed here should be interpreted in light of the study's inclusion criteria, which required a pain duration of more than three months and a worst-pain severity of at least 4/10 that is, the sample consisted of patients with established, at least moderately severe, chronic HSP, rather than an unselected post-stroke population assessed soon after stroke onset. Central sensitization is understood to develop and consolidate with persistent nociceptive input,¹⁰ so prevalence in a cohort selected for chronicity would be expected to be higher than in an unselected sample. This is consistent with findings from Soo Hoo et al.⁸, who similarly found evidence of widespread PPT hypersensitivity in patients with chronic hemiplegic shoulder pain using a comparable dual-site testing approach. Roosink et al. also demonstrated widespread somatosensory abnormalities during the early months after stroke, supporting the concept that altered pain processing may develop in post-stroke shoulder pain. 21 These findings are consistent with case-ascertainment approaches used in other chronic pain populations where CSI-based classification has been applied with the same cut-off of 40. 14.15

Notably, other groups using PPT testing to compare post-stroke patients with and without shoulder pain rather than stratifying an HSP cohort by CSI status, as in the present study have not consistently found significant PPT differences.16,20 This discrepancy likely reflects differences in study design and case definition rather than a true absence of central sensitization in HSP, and highlights that prevalence estimates for CS are sensitive to how the sensitized and non-sensitized groups are defined and stratified. Martín-Martín et al. similarly reported associations between objective pain sensitivity measures and subjective pain characteristics in post-stroke patients with shoulder pain, further supporting a link between psychophysical findings and the clinical pain experience in this population. 22

Limitations

• The relatively small sample size (n = 50) widens the confidence interval around the prevalence estimate and limits subgroup analyses.
• The absence of a comparator group of post-stroke patients without shoulder pain limits the ability to determine whether the observed prevalence is specific to HSP or reflects post-stroke central nervous system changes more broadly.
• The cross-sectional design precludes conclusions about the temporal course over which central sensitization develops in relation to the onset and chronicity of HSP.
• This was a single-centre, hospital-based sample, which may limit generalizability to community-dwelling stroke survivors who do not access tertiary rehabilitation services.

Central sensitization, identified using a CSI score > 40, was present in 78% of patients with chronic hemiplegic shoulder pain in this hospital-based cohort, toward the higher end of prevalence figures reported for central sensitization in other chronic shoulder pain populations. This CSI-based classification was supported by a pattern of reduced pressure pain thresholds at both the affected shoulder and a remote, pain-free site, consistent with widespread central hypersensitivity. These findings support central sensitization as a common feature of established hemiplegic shoulder pain in this selected population. The CSI may be a useful screening instrument for identifying patients with features suggestive of central sensitization in chronic HSP; however, prospective multicentre studies using standardized quantitative sensory testing are needed before routine clinical implementation can be recommended.

1. GBD 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet Neurol. 2021;20(10):795-820.
2. Coupland AP, Thapar A, Qureshi MI, Jenkins H, Davies AH. The definition of stroke. J R Soc Med. 2017;110(1):9-12.
3. Sudharsanan N, Deshmukh M, Kalkonde Y. Direct estimates of disability-adjusted life years lost due to stroke: a cross-sectional observational study in a demographic surveillance site in rural Gadchiroli, India. BMJ Open. 2019;9(11):e028695.
4. Pandian JD, Sudhan P. Stroke epidemiology and stroke care services in India. J Stroke. 2013;15(3):128-34.
5. Anwer S, Alghadir A. Incidence, prevalence, and risk factors of hemiplegic shoulder pain: a systematic review. Int J Environ Res Public Health. 2020;17(14):4962.
6. Joy A, Ozukum I, Nilachandra L, Khelendro T, Nandabir Y, Kunjabasi W. Prevalence of hemiplegic shoulder pain in post-stroke patients – a hospital-based study. Indian J Phys Med Rehabil. 2012;23(1):15-9.
7. Kalichman L, Ratmansky M. Underlying pathology and associated factors of hemiplegic shoulder pain. Am J Phys Med Rehabil. 2011;90(9):768-80.
8. Soo Hoo J, Paul T, Chae J, Wilson RD. Central hypersensitivity in chronic hemiplegic shoulder pain. Am J Phys Med Rehabil. 2013;92(1):1-9.
9. Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983;306(5944):686-8.
10. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895-926.
11. Kosek E, Clauw D, Nijs J, Baron R, Gilron I, Harris RE, Mico JA, Rice ASC, Sterling M. Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain. 2021;162(11):2629-2634.
12. Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W. Nociplastic pain: towards an understanding of prevalent pain conditions. Lancet. 2021;397(10289):2098-2110.
13. International Association for the Study of Pain. IASP Terminology. Available from: https://www.iasp-pain.org/resources/terminology/. Accessed 15 July 2026.
14. Mayer TG, Neblett R, Cohen H, Howard KJ, Choi YH, Williams MJ, et al. The development and psychometric validation of the central sensitization inventory. Pain Pract. 2012;12(4):276-85.
15. Neblett R, Cohen H, Choi Y, Hartzell MM, Williams M, Mayer TG, et al. The Central Sensitization Inventory (CSI): establishing clinically significant values for identifying central sensitivity syndromes in an outpatient chronic pain sample. J Pain. 2013;14(5):438-45.
16. Roosink M, Renzenbrink GJ, Buitenweg JR, van Dongen RT, Geurts AC, IJzerman MJ. Somatosensory symptoms and signs and conditioned pain modulation in chronic post-stroke shoulder pain. J Pain. 2011;12(4):476-85.
17. Borstad J, Woeste C. The role of sensitization in musculoskeletal shoulder pain. Braz J Phys Ther. 2015;19(4):251-7.
18. Walankar PP, Panhale VP, Patil MM. Psychosocial factors, disability and quality of life in chronic shoulder pain patients with central sensitization. Health Psychol Res. 2020;8(2):8874.
19. Coronado RA, George SZ. The Central Sensitization Inventory and Pain Sensitivity Questionnaire: an exploration of construct validity and associations with widespread pain sensitivity among individuals with shoulder pain. Musculoskelet Sci Pract. 2018;36:61-7.
20. Lindgren I, Ekstrand E, Lexell J, Westergren H, Brogårdh C. Somatosensory impairments are common after stroke but have only a small impact on post-stroke shoulder pain. J Rehabil Med. 2014;46(4):307-13.
21. Roosink M, Van Dongen RT, Buitenweg JR, Renzenbrink GJ, Geurts AC, IJzerman MJ. Multimodal and widespread somatosensory abnormalities in persistent shoulder pain in the first 6 months after stroke: an exploratory study. Arch Phys Med Rehabil. 2012;93(11):1968-74.
22. Martín-Martín L, Membrilla-Mesa MD, Lozano-Lozano M, Galiano-Castillo N, Fernández-Lao C, Arroyo-Morales M. Association between physiological and subjective aspects of pain and disability in post-stroke patients with shoulder pain: a cross-sectional study. J Clin Med. 2019;8(8):1093.