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The Occupational Therapist’s Role in Post Stroke Pain

By Mrs. Alison Louise Camp,

Occupational Therapy Clinician and Expert Physical/Neuro Practitioner, OTASA Professional Body

Post Stroke Pain (PSP) is found in up to 50-70% of stroke patients – there is variability in the literature, with differences in study designs and the definitions used. The consensus is that it is an under-reported and an under-treated phenomenon. The literature tells us that persons developing a chronic pain syndrome after stroke, have a greater likelihood of functional dependence, cognitive decline, depression and suicidality.

The reasons for the development of PSP are multifactorial:

  • Incidence increases with age at onset of stroke
  • Younger strokes are more specifically at an increased risk for central post stroke pain
  • Noted with increase in muscle tone post stroke
  • Those patients with an increase in sensory deficits
  • Reduced upper extremity movement
  • Ischemic stroke more frequently associated with pain than hemorrhagic stroke
  • Stroke localisation – higher incidence after thalamic and brainstem strokes
  • Premorbid peripheral vascular disease
  • Alcohol use
  • Statin use
  • History of depression
  • Pre-stroke anxious personality traits, and depressive symptoms are the overall predictor for post stroke complications and development of chronic pain post stroke.

Subtypes

PSP has neuropathic, nociceptive and nociplastic mechanisms. Within PSP there are subtypes that have been identified.

  • Central post stroke pain (CPSP)
  • Pain secondary to spasticity
  • Shoulder pain
  • Complex regional pain syndrome (CRPS)
  • Headache
  • More than one subtype is common e.g.: CPSP and spasticity + CPSP with shoulder pain
  • CRPS has features of neuropathic pain

Central Post stroke pain (CPSP)

Symptom onset is usually gradual, coinciding with the improvement of perceived sensory loss and appearance of dysesthesia. The risk factors include younger age (below 50), previous depression, current smoking and severity of stroke. Pain components with CPSP are reported as constant pain, spontaneous intermittent pain or hyperalgesia/allodynia. Once considered typical of thalamic stroke (Dejerine and Roussy), it is now recognized that CPSP can result from strokes ANYWHERE along the sensory tracts. The persistent over-activity and lack of inhibition of stimuli, leads to a central sensitization of pain. CPSP is difficult to manage medically, often with unsatisfactory outcomes. The focus is on symptom alleviation with pharmacological and non-pharmacological interventions. 

Spasticity related pain

The majority of patients with spasticity post stroke, experience pain. Nociceptive pain is produced by abnormal loading on muscles and ligaments. There are noted changes in rheologic muscle properties leading to fibrosis and atrophy. A low Barthel index score, hemiplegia at admission, left hemiplegia and a history of smoking, have all been identified as independent risk factors for development of spasticity. Pain is a definite indication for treatment of spasticity using Botox® or pharmacological treatment such as Baclofen®, but this must be weighed up against positive functional benefits of increased tone assisting with functional gains. 

Shoulder related pain

This is a common nociceptive pain syndrome post-stroke. It usually involves subluxation of the glenohumeral joint and contractures. Starts usually in the first three weeks of stroke.The risk factors are the following: upper extremity weakness and stroke severity, sensory abnormalities, premorbid rheumatological conditions, spasticity, right hemispheric lesions and a low Barthel score.

The OT’s Role in post stroke pain

The role of an occupational therapist within a comprehensive integrative pain management programme, uniquely focuses on function. This includes ADLs, instrumental activities of daily living (IADLs) (e.g., meal-prep, shopping, childcare), and other daily life activities. We need to be aware of the potential psychosocial factors that can contribute to nociplastic pain. Pain management begins in the ICU phase and continues through acute care, in- patient rehab, into the community and can be lifelong management. Education is paramount with the patient, family, nursing staff, and caregivers. There needs to be an ongoing supportive role, providing validation of the person’s pain and distress. This will also include physical management – -such as mobilizing, positioning, splinting, mirror therapy, hydrotherapy. Psycho-education which can include CBT, mindfulness, self-regulation and stress management strategies, is also important, as are aspects such as sleep management, pacing of activities and ergonomics at home and work to avoid flare ups. Advocacy for access to treatment is also part of the OT’s role.

Prevention is key! Post stroke, there is usually considerable laxity at the glenohumeral joint and it is vulnerable to injury. Positioning and support of the upper limb is key. In ICU, avoid the BP cuff on the hemi arm. Education of nursing staff is ongoing incorporating safety when doing bed baths and moving in bed – use a draw sheet. Subluxation usually does not resolve spontaneously.

Positioning in bed can be achieved with pillows, blocks and in the wheelchair with lap trays and hemi arm boards.

Taping – can work well but be careful of sensitive skin and frailty.

TENS – activating myelinated sensory fibers and disrupting pain signals of unmyelinated C-fibres (gate-control theory).

Movement can be both passive and active, including use of suspension therapy.

Use of slings Yes/No/ Maybe?

Always use clinical reasoning in your decision making, as to whether to make use of a sling or not. In my experience I find collar and cuff the best to use with transfers and mobilizing, and then remove with positioning /support when sitting or lying. Using the Give-Mohr® type sling has been beneficial for some patients.

The use of shoulder “rugby type” slings in my personal experience should not be used. They foster iinternal rotation at the glenohumeral joint which is not a wanted position for the glenohumeral joint. They are difficult to keep in position properly, as the arm slides out. The patient loses sight of their affected arm, which often when compounded with a perceptual difficulty, increases disuse and can upregulate the perceived pain.

Conclusion

OTs within their management of stroke patients need to take cognizance of the development and presence of pain and how to manage it within each patient’s individual pain experience, within a biopsychosocial framework.

References

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  • Neurological Evidence of a Mind-Body Connection: Mindfulness and Pain Control https://doi.org/10.1176/appi.ajp-rj.2018.130401
  • Pain and pain assessment in stroke patients with aphasia: a systematic review https://doi.org/10.1080/02687038.2016.1254150
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  • Songjin R. The management of poststroke thalamic pain: update in clinical practice. https://doi.org/10.3390/diagnositcs12061439

 

  • Caplan l, van Gijn J. Stroke syndromes 3rd ed 2013 ISBN -13 978-1-107-05556-8

Last Updated on 28 October 2024 by HPCSA Corporate Affairs