Post-Stroke Pain: Difference between revisions
No edit summary |
No edit summary |
||
| Line 17: | Line 17: | ||
* complex regional pain syndrome (CRPS) | * complex regional pain syndrome (CRPS) | ||
* headache | * headache | ||
== Epidemiology == | == Epidemiology == | ||
| Line 39: | Line 37: | ||
** Thalamic localization | ** Thalamic localization | ||
** Brainstem localization | ** Brainstem localization | ||
== Central Post-Stroke Pain == | |||
CPSP is defined as the [[Neuropathic Pain|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.<ref>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.</ref> It affects 11% of patients with stroke and it manifests in the first month after stroke in more than 50% of patients.<ref name=":1">Liampas A, Velidakis N, Georgiou T, Vadalouca A, Varrassi G, Hadjigeorgiou GM, Tsivgoulis G, Zis P. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7467424/ Prevalence and management challenges in central post-stroke neuropathic pain: a systematic review and meta-analysis.] Advances in therapy. 2020 Jul;37:3278-91.</ref> | |||
'''Clinical Features for identification of CPSP:<ref name=":0" />''' | |||
* 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 | |||
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 still deriving from small RCTs and not enough research to perform meaningful meta-analysis.<ref name=":1" /> | |||
== 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”<ref>Bhimani R, Anderson L. [https://downloads.hindawi.com/journals/rerp/2014/279175.pdf?_gl=1*1oxjvj8*_ga*NTAyMjU5MTAxLjE2OTk1MTM4NDQ.*_ga_NF5QFMJT5V*MTY5OTUxMzg0My4xLjAuMTY5OTUxMzg0My42MC4wLjA.&_ga=2.240198531.1825854506.1699513844-502259101.1699513844 Clinical understanding of spasticity: implications for practice.] Rehabilitation research and practice. 2014 Oct;2014.</ref> It is a prevalent occurrence after stroke, affecting anywhere from 30% to 80% of individuals who had stroke.<ref>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.</ref> | |||
== Pathophysiology == | == Pathophysiology == | ||
Revision as of 09:17, 9 November 2023
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]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)
- pain secondary to spasticity
- 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
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 still deriving from small RCTs and not enough research to perform meaningful meta-analysis.[5]
[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[edit | edit source]
Clinical Presentation[edit | edit source]
Diagnosis and Assessment[edit | edit source]
Pharmacological Management[edit | edit source]
Physiotherapy Management[edit | edit source]
Multi-disciplinary Approach[edit | edit source]
- ↑ 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.
- ↑ 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.
- ↑ 3.0 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.
- ↑ 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.
- ↑ 5.0 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.
- ↑ Bhimani R, Anderson L. Clinical understanding of spasticity: implications for practice. Rehabilitation research and practice. 2014 Oct;2014.
- ↑ 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.
