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Post-Stroke Pain

Original Editor - Carina Therese Magtibay

Top Contributors - Umamah Ejaz, Carina Therese Magtibay, Chioma Clara Okeakpu, Alexandra Stead, Kim Jackson and Vidya Acharya

Introduction

Stroke is one of the primary causes of mortality and adult-onset disability globally, as it ranks third in mortality after coronary heart disease (13%) and cancer (12%) in developed countries.[1][2] Post-stroke pain is a common complication of stroke, reported in 10 to 45.8% of cases, that hinders recovery, impairs quality of life, and is also associated with the psychological state of patients with stroke.[3] Evidence has shown that causes of post-stroke pain may be due to a variety of sources, ranging from musculoskeletal problems to the peripheral nervous system and the central nervous system.[2]

Despite the estimated 30-40% of stroke survivors experiencing pain, current research shows that post-stroke pain is under-reported and poorly understood.[4] Early recognition of post-stroke is very vital, as the prognosis will be better if pain is treated early.[2]

[5]

Epidemiology

Risk factors for developing post-stroke pain[6]:

Demographic

  • Female sex
  • Older age at stroke onset

Premorbid

  • Alcohol use
  • Statin use
  • Peripheral vascular disease
  • Depression

Clinical features

  • Spasticity
  • Reduced upper extremity movement
  • Sensory deficits

Stroke-related

  • Ischaemic stroke
  • Thalamic localisation
  • Brainstem localisation

Diagnosis

According to the American Stroke Association (2022), the diagnosis of post-stroke pain relies on a thorough clinical history and a comprehensive physical examination. Patients must report continuous pain on the affected side following the stroke and must exhibit symptoms in at least three of the following pain categories[4]:

  • Increased sensitivity
  • Skin colour changes
  • Asymmetrical sweating
  • Decreased range of motion

Types of Post-Stroke Pain

Central Post-Stroke Pain (CPSP)

Central post-stroke pain is defined as the neuropathic pain accompanied by sensory hyposensitivity, like temperature dysesthesia, that arises either acutely or in the chronic phase of a cerebrovascular event and is a result of central lesions of the somatosensory tract.[7] It is the most common form of post-stroke pain, as one-third of post-stroke cases are disclosed with CPSP.[8] It affects 11% of patients with stroke, and it manifests in the first month after stroke in more than 50% of patients.[9]

Clinical Features for identification of CPSP

The clinical features for identifying CPSP are given below[6]:

  • Verbal Descriptors Used: lacerating, aching, burning, freezing, squeezing
  • Spontaneous dysesthesia
  • Allodynia to touch and mild temperatures
  • Variable pain quality
  • Abnormal sensitivity to pinprick and high temperatures
  • Raised thresholds for perception of touch and two-point discrimination
Pathophysiology of CPSP

CPSP is originally associated with thalamic stroke (Dejerine-Roussy syndrome), and the thalamus continues to be the most commonly documented and studied neural structure linked with this condition.[10] Aside from injury to the thalamus, it can also result from a lesion anywhere along the spinothalamic and thalamocortical tracts within the central nervous system. The reduced sensation can lead to CPSP because when the brain is not receiving the normal sensory inputs it is used to, the brain itself produces painful sensations.[10]

The theory of disinhibition, first proposed by Head and Holmes, suggests that injury to the sensory pathways would lead to a compensatory overactivation within the thalamus, thus causing spontaneous pain or allodynia.[11] This theory is still the most widely accepted explanation for CPSP.

Management of CPSP

Pharmacotherapy

The use of amitriptyline and lamotrigine is a reasonable first line of treatment, while pregabalin, gabapentin, carbamazepine, or phenytoin may be considered as second-line treatments.[12]

Surgical and Neuromodulatory Interventions

Motor cortex stimulation may provide relief for CPSP for up to 2 years after surgical implantation. It is used for intractable central post-stroke pain that is not responsive to other treatments.[12]

Spasticity-related Pain

Spasticity is defined as “disordered sensory-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles." [13] It is a prevalent occurrence after a stroke, affecting anywhere from 30% to 80% of individuals who have had a stroke.[14]

Pathophysiology of Spasticity-related Pain

The exact connection between spasticity and pain is not fully understood, though it involves both neuropathic and nociceptive mechanisms.[15] Involuntary, sustained muscle contractions cause abnormal mechanical loading on peripheral muscles, tendons, and ligaments, producing nociceptive pain. Over time, persistent spasticity alters the rheological properties of muscle tissue, causing progressive fibrosis, contractures, and disuse atrophy, which further intensify chronic pain behaviours.[15]

Management of Spasticity-related Pain

Injections & Medication
  • Botulinum Toxin A: Best for stiffness in specific muscles.
  • Intrathecal Baclofen: Best for severe, full-body stiffness.
  • Dry Needling: Helps relax tight muscle spots.[16]
Physical Therapy & Splints
  • Stretching: Keep it short, intense, and frequent. Do not exceed 2.5 hours a day, and rest at least 60 minutes between sessions.
  • Splints (Orthoses): Do not wear them for more than 9–12 hours a day, as they do not prevent frozen joints.
  • Vibration: Whole-body vibration tools help improve recovery.[16]
Brain & Nerve Stimulation

Use these electrical or magnetic therapies alongside daily rehab:

  • Shock wave therapy (ESWT)
  • TENS (electrical nerve stimulation)[16]

Shoulder Pain

The shoulder is a highly mobile and stable joint, contributing to its vulnerability to a variety of post-stroke secondary complications such as pain, subluxation, and reduced joint range of motion.[17] Usually occurring 2-3 months following a stroke, shoulder pain has a prevalence of up to 12%-49%.[18][19]

Independent Risk Factors For Developing Shoulder Pain After Stroke

Independent risk factors for developing shoulder pain after stroke[20]:

  • Diabetes
  • Limited shoulder joint activity
  • Brunnstrom grade I-III period
  • Ashworth scale 3rd- 4rth grade
  • Motor arm score of NIHSS 3-4 points
  • Sensory disturbance

Pathophysiology of Shoulder Pain

The causes of shoulder pain after stroke can be broadly classified into 2 categories[21]:

  • Neurological (paralysis, spasticity, altered sensation and neuropathic pain)   
  • Mechanical   factors (glenohumeral  subluxation,  rotator  cuff  injury, muscle imbalance and altered scapula position)

Management of Shoulder Pain

Treatment approaches include physiotherapy,  massage  therapy, strapping, slings and other supports to minimise glenohumeral subluxation and local interventions such as  nerve blocks and botulinum toxin type A (BTx-A) intramuscular injections for    shoulder spasticity[22] Due to being multifactorial in nature, optimal treatment modalities for hemiplegic shoulder pain remain unclear in current literature.[21]

For more information on shoulder pain after stroke:

Complex Regional Pain Syndrome

Complex regional pain syndrome after a stroke is also known as Shoulder-Hand Syndrome (SHS). It is a chronic severe pain believed to be a result of damage to both the peripheral and central nervous systems that affects the limbs and is accompanied by increased sensitivity to tactile stimulation, changes in skin temperature and colour, limited range of motion, and osteopenia.[15] It is of two types (Type I and Type II), where Type I is known as CRPS following a stroke, as it lacks obvious peripheral nerve injury.[23] The reported incidence of post-stroke CRPS ranges from 2% to 49%.[15]

Main symptoms of Post-Stroke CRPS

The main symptoms of post-stroke CRPS are given below[23]:

  • Pain
  • Hyperalgesia
  • Allodynia
  • Oedema
  • Swelling
  • Limited range of motion of the shoulder, wrist, and hand joints
  • Pyrexic sensation and redness of the wrists and hands

Pathophysiology of CRPS

SHS is multifactorial, although altered mechanics of the glenohumeral joint have been implicated in its development. Studies suggest that hemiplegic patients with more severe shoulder subluxation were significantly more likely to develop CRPS, and the degree of weakness and inactivity in the shoulder can influence its onset.[24] Trauma to the affected shoulder is also associated with the development of CRPS after a stroke.[23] 

Managementof CRPS

The managements are given below[25]:

Rehabilitative Therapies

Physical and occupational therapies serve as the cornerstone of CRPS management to restore range of movement (ROM) and lower long-term disability. Key modalities include manual exercise to boost endogenous analgesia, desensitisation techniques to down-regulate hyperactive peripheral nociceptors, and Graded Motor Imagery (GMI) or mirror therapy to target maladaptive cortical neuroplastic changes.

Pharmacological Management

A multimodal drug approach targets the inflammatory, neuropathic, and vasomotor components of the condition. Treatment includes short-course oral corticosteroids to arrest early-stage neurogenic inflammation, bisphosphonates to inhibit painful bone resorption, and neuropathic agents (anticonvulsants like gabapentin or tricyclic antidepressants) to modulate central pain processing.

Interventional and Behavioural Support

When baseline therapies plateau, advanced interventional and psychological strategies are deployed. Interprofessional protocols include sympathetic ganglion blocks or spinal cord stimulation (SCS) to intercept ascending pain signals, paired with structural behavioural therapy and psychological support to lower sympathetic nervous system amplification and curb fear-avoidance behaviours.

Headache

Headache is a common symptom after a stroke that usually begins on the day of the stroke and last for a mean of 3.8 days.[26] It is more often continuous, pressure-type, bilateral, located in the anterior region, and increased by movement and by cough.[26] In a study by Harriot et al. (2020), headache occurred in 6%–44% of the ischaemic stroke population, mostly having tension-type features, was moderate to severe, and became chronic in nature.[27]

Pathophysiology of Headache

  • Lack of adequate blood flow in the brain during and after a stroke can lead to headaches.[28]
  • Headaches can be a side effect of medications such as pain relievers.[29]
  • Headaches after subarachnoid haemorrhage may be caused by hydrocephalus, wherein there is a build-up of cerebrospinal fluid around the brain.[30]

Management of Headache

  • Depending on the case, doctors may prescribe medications to alleviate post-stroke headaches.[31]
  • Lifestyle modifications including regular exercise, healthy diet, and avoiding specific headache triggers may help in managing headaches following a stroke.[31]
  • Hydrocephalus can be treated with an operation to drain the fluid by inserting a thin tube, called a shunt, to drain the fluid away from the brain.[30]
  • Staying hydrated may reduce the re-ocurrence of headaches. A study by Cortés-Vicente et al (2019) states that approximately 9% of people who had a stroke were dehydrated at the time.[32] If the body does not have sufficient fluid in the blood vessels, there is an increased risk for clots.

For more information about headaches:

Conclusion

Post-stroke pain is a frequent yet often under-recognized complication that significantly affects recovery and quality of life. It presents in several distinct forms: central post-stroke pain, spasticity-related pain, shoulder pain, complex regional pain syndrome, and headache, each with its own underlying mechanisms, whether neuropathic, musculoskeletal, or vascular in origin. Because these subtypes can overlap and share risk factors, accurate diagnosis requires careful clinical assessment. Early identification and a tailored, often multidisciplinary approach combining pharmacological treatment, physiotherapy, and targeted interventions are essential for effective pain management. Given the variability in presentation and the current gaps in evidence for optimal treatment, continued research and individualized care remain key to improving outcomes for stroke survivors experiencing pain.

Resources

American Stroke Association - Pain After Stroke

References

  1. ↑ Feigin VL, Abajobir AA, Abate KH, Abd-Allah F, Abdulle AM, Abera SF, Abyu GY, Ahmed MB, Aichour AN, Aichour I, Aichour MT. Global, regional, and national burden of neurological disorders during 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. The Lancet Neurology. 2017 Nov 1;16(11):877-97.
  2. ↑ 2.0 2.1 2.2 Khairunnisah SZ, Muchsin AH, Mardiana M. Characteristics of Post-Stroke Pain. Journal La Medihealtico. 2024 Jun 6;5(2):399-407.
  3. ↑ Zhang Z, Ma S, Feng B, Li X, Zhang Y, Pei L. Relationship between stroke injury sites and incidence of post-stroke pain: a systematic review and meta-analysis. Systematic Reviews. 2025 Oct 14;14(1):192.
  4. ↑ 4.0 4.1 American Stroke Association. Post-Stroke Pain. 2022 (https://www.stroke.org/-/media/Stroke-Files/Support-Group-Resources/Post-Stroke-Pain-Presentation.pdf)
  5. ↑ American Heart Association. Pain After Stroke. Available from: https://www.youtube.com/watch?v=nowPWzVsoFQ [last accessed 19/11/2023]
  6. ↑ 6.0 6.1 Harrison RA, Field TS. Post stroke pain: identification, assessment, and therapy. Cerebrovascular diseases. 2015 Mar 5;39(3-4):190-201.
  7. ↑ Zhou J, Fangma Y, Chen Z, Zheng Y. Post-Stroke Neuropsychiatric Complications: Types, Pathogenesis, and Therapeutic Intervention. Aging Dis. 2023 Dec 1;14(6):2127-2152. doi: 10.14336/AD.2023.0310-2. PMID: 37199575; PMCID: PMC10676799.
  8. ↑ Mohanan AT, Nithya S, Nomier Y, Hassan DA, Jali AM, Qadri M, Machanchery S. Stroke-induced central pain: Overview of the mechanisms, management, and emerging targets of central post-stroke pain. Pharmaceuticals. 2023 Aug 4;16(8):1103.
  9. ↑ Liampas A, Velidakis N, Georgiou T, Vadalouca A, Varrassi G, Hadjigeorgiou GM, Tsivgoulis G, Zis P. Prevalence and management challenges in central post-stroke neuropathic pain: a systematic review and meta-analysis. Advances in therapy. 2020 Jul;37:3278-91.
  10. ↑ 10.0 10.1 Treister AK, Hatch MN, Cramer SC, Chang EY. Demystifying poststroke pain: from etiology to treatment. PM&R. 2017 Jan 1;9(1):63-75.
  11. ↑ Vilela-Filho O, Cavalcante RB, Moura MU, Morais BA, Dalle CR, Grandi FT. Pathophysiology of the constant burning, tingling element of neuropathic pain: A new hypothesis. Medical Hypotheses. 2014 Oct 1;83(4):441-9.
  12. ↑ 12.0 12.1 Winstein CJ, Stein J, Arena R, Bates B, Cherney LR, Cramer SC, Deruyter F, Eng JJ, Fisher B, Harvey RL, Lang CE. Guidelines for adult stroke rehabilitation and recovery: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2016 Jun;47(6):e98-169.
  13. ↑ Bhimani R, Anderson L. Clinical understanding of spasticity: implications for practice. Rehabilitation research and practice. 2014 Oct;2014.
  14. ↑ Kuo CL, Hu GC. Kuo CL, Hu GC. Post-stroke spasticity: a review of epidemiology, pathophysiology, and treatments. International Journal of Gerontology. 2018 Dec 1;12(4):280-4.
  15. ↑ 15.0 15.1 15.2 15.3 Yang S, Chang MC. Poststroke pain. InSeminars in neurology 2021 Feb (Vol. 41, No. 01, pp. 067-074). Thieme Medical Publishers, Inc.
  16. ↑ 16.0 16.1 16.2 Suputtitada A, Chatromyen S, Chen CP, Simpson DM. Best practice guidelines for the management of patients with post-stroke spasticity: a modified scoping review. Toxins. 2024 Feb 10;16(2):98.
  17. ↑ Alqahtani M. Physical therapy intervention in post stroke shoulder subluxation: a narrative review. Majmaah Journal of Health Sciences. 2018;6(1):48-60.Physical Therapy Intervention in Post Stroke Shoulder Subluxation: A Narrative Review Mazen Alqahtani
  18. ↑ Nadler M, Pauls M, Cluckie G, Moynihan B, Pereira AC. Shoulder pain after recent stroke (SPARS): hemiplegic shoulder pain incidence within 72 hours post-stroke and 8–10 week follow-up (NCT 02574000). Physiotherapy. 2020 Jun 1;107:142-9.
  19. ↑ Anwer S, Alghadir A. Incidence, prevalence, and risk factors of hemiplegic shoulder pain: a systematic review. International journal of environmental research and public health. 2020 Jul;17(14):4962.
  20. ↑ Hao N, Zhang M, Li Y, Guo Y. Risk factors for shoulder pain after stroke: A clinical study. Pakistan Journal of Medical Sciences. 2022 Jan;38(1):145.
  21. ↑ 21.0 21.1 Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Physical Medicine and Rehabilitation Clinics. 2014 May 1;25(2):411-37.
  22. ↑ Viana R, Pereira S, Mehta S, Miller T, Teasell R. Evidence for therapeutic interventions for hemiplegic shoulder pain during the chronic stage of stroke: a review. Topics in Stroke Rehabilitation. 2012 Nov 1;19(6):514-22.
  23. ↑ 23.0 23.1 23.2 Chae J. Poststroke complex regional pain syndrome. Topics in stroke rehabilitation. 2010 May 1;17(3):151-62.
  24. ↑ Mountford R, Mattocks G, Rittner HL, Gierthmühlen J, de Andrade DC, Moon JY, Packham T, Bultitude JH, Ferraro MC, Drummond PD, Tamasauskas A. Clinical Presentation of Shoulder‐Hand Syndrome: A Systematic Review. European Journal of Pain. 2026 Feb;30(2):e70205.
  25. ↑ Guthmiller K, Dua A, Dey S, Varacallo M. Complex regional pain syndrome. StatPearls. 2025 May 4.
  26. ↑ 26.0 26.1 Verdelho A, Ferro JM, Melo T, Canhao P, Falcao F. Headache in acute stroke. A prospective study in the first 8 days. Cephalalgia. 2008 Apr;28(4):346-54.
  27. ↑ Harriott AM, Karakaya F, Ayata C. Headache after ischemic stroke: a systematic review and meta-analysis. Neurology. 2020 Jan 7;94(1):e75-86.
  28. ↑ Verywellhealth.com. Available at: https://www.verywellhealth.com/how-a-headache-may-be-a-sign-of-a-stroke-1719596?__cf_chl_f_tk=WajjWaUhTvFgFZZT4k2dJ4NPTjOHAFjRYRX1RJdHDSM-1783442441-1.0.1.1-.8JRkiDnocvFXcPRDSduPwYx.x8iGRzTcFPmDSVsRaU (Accessed: July 7, 2026).
  29. ↑ Rebound headaches (2017) Cleveland Clinic. Available at: https://my.clevelandclinic.org/health/diseases/6170-rebound-headaches (Accessed: July 7, 2026).
  30. ↑ 30.0 30.1 Hochstetler A, Raskin J, Blazer-Yost BL. Hydrocephalus: historical analysis and considerations for treatment. European journal of medical research. 2022 Sep 1;27(1):168.
  31. ↑ 31.0 31.1 Maher, D. (2011) Should you worry about headaches after stroke?, HealthCentral. Available at: https://www.healthcentral.com/article/headache-stroke (Accessed: July 7, 2026).
  32. ↑ Cortés-Vicente E, Guisado-Alonso D, Delgado-Mederos R, Camps-Renom P, Prats-Sánchez L, Martínez-Domeño A, Martí-Fàbregas J. Frequency, risk factors, and prognosis of dehydration in acute stroke. Frontiers in neurology. 2019 Mar 29;10:305.
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