Post-stroke Pain

A clinical history and physical examination with judicious use of appropriate diagnostic modalities are mandatory in identifying what is the likely pain in stroke survivors.
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It is well recognized that the recovery and long-term health of stroke survivors can be adversely affected by a number of medical complications, including chronic pain. The medical literature estimate of the prevalence of chronic post-stroke pain ranges from 32-42% at four to six months and 11-21% at twelve to sixteen months after a stroke.1-3 Shoulder pain alone has been found to affect up to 72% of post-stroke survivors.4 If one were to include other causes of post-stroke pain, this number could be significantly higher.

The Post-Stroke Rehabilitation Out-comes Project studied the prescription of pain medications by providers at seven distinct inpatient rehabilitation facilities (six in the United States and one in New Zealand) for 1,122 stroke patients.4 The results of this study revealed the complexity of post-stroke pain: twelve distinct areas of pain in the human body were identified, eight distinct classes of medications used to treat pain were utilized, and twenty-nine different pain medications were prescribed.

Properly identifying the potential causes of pain should be a major focus in post-stroke care because the correct evaluation and treatment will be of significant benefit for the patient. The objective of this article is to provide a review in the available medical literature of potential causes and treatment of chronic post stroke pain, including neuropathic and musculoskeletal causes.

Neuropathic Pain Central Post-stroke Pain

Central post-stroke pain (CPSP) has been referred to as thalamic pain and was once thought to be synonymous with thalamic injury. However, it is now believed that the key factor in developing central post-stroke pain is a lesion in the spino-thalamo-cortical pathway and that this syndrome actually arises more often from non-thalamic than thalamic lesions.5 The condition is actually not as rare as once thought and has been reported at an 8% incidence in the first year after stroke, 63% of which develop pain within the first month.6

CPSP is characterized by an intense spontaneous or evoked pain localized in the affected extremities and can affect the entire side of the body with an aching and burning quality.7 Sensory disturbance is a major component of CPSP, including abnormal temperature sensation, dysesthesia and hypersensitivity to cutaneous stimuli.7 In contrast, there is often a normal response to light touch and vibration. The pain appears to be alleviated with relaxation and worsened with emotional and physical stress.7

Commonly prescribed oral medications for use in post-stroke pain include antidepressants and anticonvulsants, while opioids are not felt to be effective.4,8

The tricyclic antidepressant amitriptyline given at 75mg/day was found to be effective in improving the pain scores in 10 out of 15 patients with CPSP versus 1 of 15 in a placebo group of a double blinded placebo-controlled crossover study at 2 weeks and 4 weeks from the start of treatment.9 Amitriptyline is usually started at 10 or 25mg/day and titrated up to 75mg/day. The medication is commonly given at nighttime as it can cause sedation and thus interfere with daytime activities. Amitriptyline has a variety of adverse reactions including anti-cholinergic side effects and should be carefully considered and monitored when prescribing—especially for elderly patients.

Anticonvulsants have been used in clinical practice for a variety of neuropathic pain syndromes since the 1960s. Gabapentin has become commonly used for treating a variety of neuropathic pain conditions and was the most prescribed anti-convulsant in the Post-Stroke Rehabilitation Outcomes Project pain study which looked at medication usage for stroke patients at seven inpatient rehabilitation facilities.4 Gabapentin is a structural analog of the neurotransmitter gamma-aminobutyric acid (GABA), but its exact mechanism of action in the treatment of central neuropathic pain is unclear. Gabapentin is relatively safe, with the most common side effects being dizziness and sedation.

Specific research on gabapentin to treat CPSP is limited to case series and not large, randomized, well-controlled studies.4,8 One report described gaba-pentin as being effective for thalamic pain starting at 300mg two times/day and titrating up to 300mg three times/day, while a second case found effective treatment starting at 100mg three times/day and titrating up to 300mg three times/day lasting at least one year.12,13 There are no randomized clinical trials examining the effectiveness of gabapentin for CPSP on a larger scale at the present time, nor is there any literature on the use of gabapentin at higher doses such as 2400mg/day or 3600mg/day. Further study is recommended before justifying the wide-spread use of gabapentin for this condition.

Lamotrigine is an anti-epileptic medication with non-NMDA anti-glutamatergic activity and is relatively well-tolerated, although there is documented potential for severe dermatologic adverse reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis. It was found to be moderately effective and achieve greater reduction of pain than a placebo at maximum doses of 200mg/day.10 Higher doses of lamotrigine have been thought to provide even better relief of pain but have not been tested with larger controlled studies.11

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) type 1 is a sympathetically mediated pain disorder presenting with the qualities of neuropathic pain. CRPS type 1 is differentiated from CRPS type 2 in that type 1 cannot be defined by a peripheral nerve injury. Although established as a wellknown complication after stroke, it remains unclear exactly how common it is. Estimates of its prevalence have ranged from 12.5% to 30.5%.14-16 CRPS type 1 is most commonly seen one to three months after stroke and less often after five months. The exact mechanisms that precipitate the onset of CRPS after stroke are not precisely understood at this time. Spasticity and limited range of motion of the shoulder, especially external rotation, appear to be influential factors towards development of this condition.17 Conversely, adequate range of motion in the shoulder is felt to be a protective mechanism against the development of CRPS type 1.

The most common presentation of post-stroke CRPS is severe shoulder and hand pain with sparing of the elbow together with swelling, especially in the hand. CRPS is unique from other forms of neuropathic pain in that it is associated with vasomotor, sudomotor, and trophic changes. The diagnosis of CRPS is based on clinical criteria adopted by the International Association for the Study of Pain (see Table 1).

First published on: June 1, 2009