Post-Stroke Pain: Difference between revisions

No edit summary
No edit summary
Line 13: Line 13:


* central post-stroke pain (CPSP)  
* central post-stroke pain (CPSP)  
* pain secondary to spasticity
* spasticity-related pain
* shoulder pain
* shoulder pain
* complex regional pain syndrome (CRPS)
* complex regional pain syndrome (CRPS)
Line 71: Line 71:
There is little evidence regarding the treatment of spasticity specifically after stroke <ref>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).</ref>  
There is little evidence regarding the treatment of spasticity specifically after stroke <ref>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).</ref>  


== Pathophysiology ==
== Musculoskeletal Pain: Glenohumeral Subluxation and Contractures ==
For more information:


== Clinical Presentation  ==
[[Hemiplegic Shoulder Subluxation]]


== Diagnosis and Assessment  ==
[[Shoulder Dysfunction Associated with Stroke]]


== Pharmacological Management ==
== Complex Regional Pain Syndrome ==
For


=== Physiotherapy Management ===
[[Complex Regional Pain Syndrome (CRPS)]]
=== Multi-disciplinary Approach ===
 
== Headache ==
== Multi-disciplinary Approach ==

Revision as of 09:24, 11 November 2023

Original Editor - Carina Therese Magtibay

Top Contributors - Carina Therese Magtibay and Kim Jackson

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (11/11/2023)

Introduction[edit | edit source]

Stroke is one of the primary causes of mortality and adult-onset disability globally.[1][2]Post-stroke 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]Current research shows that post-stroke pain is under-reported and poorly understood.

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

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.[4] It affects 11% of patients with stroke and it manifests in the first month after stroke in more than 50% of patients.[5]

Clinical Features for identification of CPSP:[3]

  • 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:

Management:

At present, both pharmacological and non-pharmacological management studies of CPSP is lacking of large randomized trials. The best current evidence is related to the use of amitriptyline and lamotrigine, but results are from small RCTs and not enough research is available to perform meaningful meta-analysis.[5]

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”[6] It is a prevalent occurrence after stroke, affecting anywhere from 30% to 80% of individuals who had stroke.[7]

Pathophysiology:

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.[8] Spasticity can cause changes in rheologic muscle properties, leading to fibrosis, and atrophy which can contribute to the experience of pain.[9]

Management:

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 [10]

Musculoskeletal Pain: Glenohumeral Subluxation and Contractures[edit | edit source]

For more information:

Hemiplegic Shoulder Subluxation

Shoulder Dysfunction Associated with Stroke

Complex Regional Pain Syndrome[edit | edit source]

For

Complex Regional Pain Syndrome (CRPS)

Headache[edit | edit source]

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. 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.
  5. 5.0 5.1 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.
  6. Bhimani R, Anderson L. Clinical understanding of spasticity: implications for practice. Rehabilitation research and practice. 2014 Oct;2014.
  7. 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.
  8. 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.
  9. Dietz V, Sinkjaer T. Spastic movement disorder: impaired reflex function and altered muscle mechanics. The Lancet Neurology. 2007 Aug 1;6(8):725-33.
  10. 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).