Post-Stroke Pain

Original Editor - Carina Therese Magtibay

Top Contributors - Carina Therese Magtibay and Kim Jackson

Introduction[edit | edit source]

Stroke is one of the primary causes of mortality and adult-onset disability globally.[1][2] Pain is a common sequelae of stroke that can significantly reduce quality of life, potentially leading to depression, anxiety, sleep disorders and complicating rehabilitation.[3] Despite the estimated 30-40% stroke survivors experiencing pain, current research shows that post-stroke pain is under-reported and poorly understood.[4]

[5]

Common post-stroke pain subtypes:

  • central post-stroke pain (CPSP)
  • spasticity-related pain
  • shoulder pain
  • complex regional pain syndrome (CRPS)
  • headache

Epidemiology[edit | edit source]

Risk factors for developing post-stroke pain:[3]

  • 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
    • Ischemic stroke
    • Thalamic localization
    • Brainstem localization

Diagnosis[edit | edit source]

According to the American Stroke Association (2022), diagnosis of post-stroke pain include clinical history and physical examination. Patients must report symptoms in the following pain categories:[4]

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

Patients must also experience continuous pain on the affected side following stroke.

Types of Post-stroke Pain[edit | edit source]

Central Post-Stroke Pain[edit | edit source]

CPSP is defined as the neuropathic pain that arises either acutely or in the chronic phase of a cerebrovascular event and is a result of central lesions of the somatosensory tract.[6] It affects 11% of patients with stroke and it manifests in the first month after stroke in more than 50% of patients.[7]

Clinical Features for identification of CPSP[3][edit | edit source]

  • 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[edit | edit source]

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 CPSP. 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.[8] The reduced sensation can lead to CPSP because when the brain is not receiving normal sensory inputs it is used to, the brain itself produces painful sensations.

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.[9] This theory is still the most widely accepted explanation for CPSP.

Management[10][edit | edit source]

  • 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.
  • 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.

Spasticity-related Pain[edit | edit source]

Spasticity is defined as “disordered sensory-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”[11] It is a prevalent occurrence after stroke, affecting anywhere from 30% to 80% of individuals who had stroke.[12]

Pathophysiology[edit | edit source]

The connection between spasticity and pain is not fully understood. There are potential neuropathic and nociceptive mechanisms by which they are related. Abnormal loading on muscles and ligaments caused by spasticity may produce nociceptive pain.[13] Spasticity can cause changes in rheologic muscle properties, leading to fibrosis, and atrophy which can contribute to the experience of pain.[14]

Management[edit | edit source]

Generally, the goal of treatment is to reduce reflex activity, thus reducing muscle tone. The use of local neuromuscular blockade or pharmacological treatment must be carefully evaluated against the drawback of potentially losing functional benefits of increased muscle tone.

There is little evidence regarding the treatment of spasticity specifically after stroke [15]

Shoulder Pain[edit | edit source]

Shoulder pain.jpg

The shoulder is highly mobile and a less stable joint, contributing to its vulnerability to a variety of post-stroke secondary complications such as pain, subluxation and reduced joint range of motion. [16] Usually occurring 2-3 months following a stroke, shoulder pain has a prevalence of up to 12%-49%.[17][18]

Independent risk factors for developing shoulder pain after stroke[19][edit | edit source]

  • diabetes
  • limited shoulder joint activity
  • Brunnstrom grade I-III period
  • Ashworth scale 3- 4 grade
  • motor arm score of NIHSS 3-4 points
  • sensory disturbance.

Pathophysiology[edit | edit source]

The causes of shoulder pain after stroke can be broadly classified into 2 categories:[20]

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

Management[edit | edit source]

Treatment approaches include physiotherapy,  massage  therapy,  strapping,  slings and other supports to minimize glenohumeral subluxation,  and  local  interventions  such  as  nerve blocks and botulinum toxin type A (BTx-A) intra-muscular    injections    for    shoulder spasticity.[21] Due to being multifactorial in nature, optimal  treatment  modalities  for hemiplegic shoulder pain remain unclear in current literature.[20]

For more information on shoulder pain after stroke:

Complex Regional Pain Syndrome[edit | edit source]

CRPS after stroke is also known as Shoulder-hand Syndrome (SHS). It has been classified as type I as it lacks obvious peripheral nerve injury.[22] The reported incidence of post-stroke CRPS varies between 2 and 49%.[23][24]

Main symptoms of post-stroke CRPS[22][edit | edit source]

  • pain
  • hyperalgesia
  • allodynia
  • edema
  • swelling
  • limited range of motion of the shoulder, wrist, and hand joints
  • feverish sensation and redness of the wrists and hands.

Pathophysiology[edit | edit source]

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.[25][26] Trauma to the affected shoulder is also associated with the development of CRPS after stroke.[22] 

Management[edit | edit source]

  • Physiotherapy
  • Pharmacologic therapy
    • Non-steroidal anti-inflammatory drugs (NSAIDs)
    • oral corticosteroids
    • opioid analgesics

For more in-depth discussion on CRPS and SHS:

Headache[edit | edit source]

Post-stroke headache.jpg

Headache is a common symptom after stroke that usually begin on the day of stroke and last for a mean of 3.8 days. It is more often continuous, pressure-type, bilateral, located in the anterior region, and increased by movement and by cough.[28] In a study by Harriot et al (2020), headache occurred in 6%–44% of the ischemic stroke population, mostly having tension-type features, were moderate to severe, and became chronic in nature. [29]

Pathophysiology[edit | edit source]

  • Lack of adequate blood flow in the brain during and after stroke can lead to headaches or migraine episode.
  • Headaches can be a side-effect of medications such as pain relievers.
  • Headaches after subarachnoid hemorrhage may be caused by hydrocephalus wherein there is a buildup of cerebrospinal fluid around the brain.[30]
  • Other conditions such as obstructive sleep apnea or neck tightness, may contribute to a post-stroke headache or lead to it becoming persistent.

Management[edit | edit source]

  • Depending on the case, doctors may prescribe medications to alleviate post-stroke headaches.
  • Lifestyle modifications including regular exercise, healthy diet, and avoiding specific headache triggers may help in managing headaches following a stroke.
  • 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 occurrence 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.[31] If the body does not have sufficient fluid in the blood vessels, there is an increased risk for clots.


For more information about headache:

Resources[edit | edit source]

American Stroke Association - Pain After Stroke

Multi-disciplinary Approach[edit | edit source]

  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. ↑ Avan A, Digaleh H, Di Napoli M, Stranges S, Behrouz R, Shojaeianbabaei G, Amiri A, Tabrizi R, Mokhber N, Spence JD, Azarpazhooh MR. Socioeconomic status and stroke incidence, prevalence, mortality, and worldwide burden: an ecological analysis from the Global Burden of Disease Study 2017. BMC medicine. 2019 Dec;17(1):1-30.
  3. ↑ 3.0 3.1 3.2 Harrison RA, Field TS. Post stroke pain: identification, assessment, and therapy. Cerebrovascular diseases. 2015 Mar 5;39(3-4):190-201.
  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. ↑ Klit H, Finnerup NB, Jensen TS. Central post-stroke pain: clinical characteristics, pathophysiology, and management. The Lancet Neurology. 2009 Sep 1;8(9):857-68.
  7. ↑ 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.
  8. ↑ Treister AK, Hatch MN, Cramer SC, Chang EY. Demystifying poststroke pain: from etiology to treatment. PM&R. 2017 Jan 1;9(1):63-75.
  9. ↑ Head H, Holmes G. Sensory disturbances from cerebral lesions. Brain. 1911 Nov 1;34(2-3):102-254.
  10. ↑ 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.
  11. ↑ Bhimani R, Anderson L. Clinical understanding of spasticity: implications for practice. Rehabilitation research and practice. 2014 Oct;2014.
  12. ↑ 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.|Post-stroke spasticity: a review of epidemiology, pathophysiology, and treatments. International Journal of Gerontology. 2018 Dec 1;12(4):280-4.
  13. ↑ Lundström E, Smits A, Terént A, Borg J. Risk factors for stroke‐related pain 1 year after first‐ever stroke. European Journal of Neurology. 2009 Feb;16(2):188-93.
  14. ↑ Dietz V, Sinkjaer T. Spastic movement disorder: impaired reflex function and altered muscle mechanics. The Lancet Neurology. 2007 Aug 1;6(8):725-33.
  15. ↑ Demetrios M, Khan F, Turner‐Stokes L, Brand C, McSweeney S. Multidisciplinary rehabilitation following botulinum toxin and other focal intramuscular treatment for post‐stroke spasticity. Cochrane Database of Systematic Reviews. 2013(6).
  16. ↑ Brandstater EM. Stroke rehabilitation. In: DeLisa JA,  Gans  BM,  editors.  Physical  medicine  and rehabilitation.  Principles  and  practice.  4th  ed. Philadelphia:  Lippincott  Williams  and  Wilkins;2005. p. 1655–1676
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 20.0 20.1 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.
  21. ↑ 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.
  22. ↑ 22.0 22.1 22.2 Chae J. Poststroke complex regional pain syndrome. Topics in stroke rehabilitation. 2010 May 1;17(3):151-62.
  23. ↑ McLean DE. Medical complications experienced by a cohort of stroke survivors during inpatient, tertiary-level stroke rehabilitation. Archives of physical medicine and rehabilitation. 2004 Mar 1;85(3):466-9.
  24. ↑ Kocabas H, Levendoglu F, Ozerbil OM, Yuruten B. Complex regional pain syndrome in stroke patients. International Journal of Rehabilitation Research. 2007 Mar 1;30(1):33-8.
  25. ↑ Gokkaya NK, Aras M, Yesiltepe E, Koseoglu F. Reflex sympathetic dystrophy in hemiplegia. International Journal of Rehabilitation Research. 2006 Dec 1;29(4):275-9.
  26. ↑ Dursun E, Dursun N, Ural CE, Çakci A. Glenohumeral joint subluxation and reflex sympathetic dystrophy in hemiplegic patients. Archives of physical medicine and rehabilitation. 2000 Jul 1;81(7):944-6.
  27. ↑ Liu S, Zhang C, Cai Y, Guo X, Zhang A, Xue C et al. Acupuncture for Post-stroke Shoulder-Hand Syndrome: A Systematic Review and Meta-Analysis. Frontiers in Neurology. 2019;10.
  28. ↑ 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.
  29. ↑ Harriott AM, Karakaya F, Ayata C. Headache after ischemic stroke: a systematic review and meta-analysis. Neurology. 2020 Jan 7;94(1):e75-86.
  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. ↑ 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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