Central poststroke pain

The median annual incidence of first stroke for all ages is 183 per 100,000 with the risk of stroke roughly doubling with each decade during adulthood.12 In the United States in 2007, the incidence of first stroke would be estimated at approximately 551,000 cases per year (based on 301 million US population). Stroke is the third leading cause of death in the United States and a leading cause of dis-ability.26 Based on the prevalence of stroke in the population (compared with that of SCI or MS), CPSP is the most common cause of central neuropathic pain.9,27 Interestingly, the median age of patients who develop CPSP appears to be younger than the median age of patients having strokes.27,28,2930,31,32,33 However, Andersen et al.34 found no statistically significant difference in age between those with and without somato-sensory deficits or pain.

The classic CPSP example is the thalamic pain syndrome described by Dejerine and Roussy.35 However, CPSP can occur with both ischemic and hemorrhagic lesions at any level: infratentorial/brain stem, thalamic, or various supratentorial, extra-thalamic sites. It does not appear that either ischemic or hemorrhagic insult is more likely to induce CPSP.8,27,30,36 Reported percentages of patients with CPSP in these series are in keeping with the relative proportion of ischemic versus hemorrhagic strokes in the population. As such, given that ^80 percent of strokes are ischemic,12 more patients have CPSP from ischemic strokes. A pain series focusing on CPSP in len-ticulo-capsular hemorrhages has been published.37

More important than what causes the lesion is where the lesion occurs and what deficits are associated. The incidence of CPSP varies based on the location of the stroke. Lateral medullary infarctions (Wallenberg's syndrome - i.e. the loss of pain and temperature function of the face ipsilateral and body contralateral to the lateral medullary stroke, vestibular dysfunction, hoarseness and dysphagia, and an ipsilateral Horner's syndrome), which selectively affect the spino- and trigeminothalamic pathways and spare lemniscal ("large fiber'') pathways, has one of the highest incidences of CPSP at 25 percent within six months of the stroke.31 The incidence of CPSP after thalamic infarction also appears to be high, particularly when it involves the ventral posterior nuclei. One literature review noted the frequency of pain after any thalamic stroke to be 11 percent (range, 8-16 percent), but confining analysis to strokes in the geniculothalamic arterial territory (the ventral posterior thalamus) the frequency was 24 percent (range, 13-59 percent).28 However, in a study evaluating the clinical syndromes associated with 40 thalamic infarcts, only three patients developed CPSP, suggesting a lower incidence.38 Thalamic infarcts are well represented in most unselected CPSP series (25-33 percent of CPSP cases),34,36 but importantly do not represent the majority of CPSP cases, stressing that while thalamic pain is the quintessential CPSP syndrome, strokes elsewhere can have the same consequences. A CPSP-MRI correlation study found a high percentage of CPSP patients had thalamic lesions (^60 percent), particularly involving the ventroposterior thalamus, although most patients had multiple lesions and were imaged well after the stroke making it impossible to know if this was the CPSP-causing lesion.30

Unselected prospective stroke series have demonstrated a lower incidence of CPSP when all patients with stroke are considered. The most cited study of CPSP is that of Anderson et al.34 which prospectively evaluated an unselected stroke population for the first year poststroke (within the first week, at one month, six months, and one year poststroke). Of 267 patients, 207 were still alive and could communicate at six months and an additional seven patients were lost to follow up over the next year leaving the final cohort at 200 patients. Sixteen patients (8 percent) had developed CPSP by the end of one year (only 4/16 had thalamic infarcts, clearly demonstrating that CPSP can occur with lesions at many levels). Interestingly, the incidence of CPSP in this cohort of those whose stroke deficits included somatosensory deficits was 18 percent. Bowsher39 retrospectively reviewed the experience with 400 patients with stroke of various types and found ^25 percent had somatosensory deficits, but only ^2 percent developed CPSP. He acknowledged that poor documentation of clinical encounters poststroke may have underestimated the frequency of CPSP. Based on these studies, the incidence of CPSP from non-lateral medullary, non-thalamic strokes is commonly cited at 2-8 percent.

Stroke-related pain can occur at stroke onset, but more commonly begins over the coming months, with most evident in the first month. In thalamic strokes, 18 percent had pain from stroke onset, 18 percent within the first week, 20 percent between one week and one month (in total 56 percent occurred within the first month), 15 percent between one and three months, 12 percent between four and six months, 6 percent between six and twelve months, and 11 percent greater than one year after the stroke.28 Looking at CPSP in a prospective, unselected stroke population, onset within the first month was seen in 63 percent, one to six months in 19 percent, and six to twelve months in 19 percent (series limited follow up to one year and therefore would have missed those taking more one year to present).34 Seventy-five percent of those developing CPSP after a lateral medullary infarct do so within the first month.31 It has been reported, however, that CPSP may present up to three years after stroke.36 Given patients with cerebrovascular disease are at risk for future, sometimes silent, events, one might wonder whether these seemingly rarer late presentations of CPSP are related to new, otherwise clinically silent, strokes. Modern imaging has not addressed this, but may be useful in further assessing these cases.

An interesting phenomenon, not reported with other central neuropathic pain types, has been noted in some forms of CPSP. In thalamic infarcts, CPSP appears to be more commonly associated with right-sided lesions. One hundred and eighty cases were pulled via a review of the literature with imaging or autopsy confirmed evidence of a thalamic infarction and clinical evidence of contralateral pain. Of these, 114 (63 percent) had right thalamic lesions, whereas only 66 (37 percent) had left-sided lesions. This laterality predominance was greatest among males. It was speculated that this is in keeping with interesting experimental evidence demonstrating right-hemisphere specialization for mediation of pain and internal representation of body image.28 These retrospective results need to be confirmed prospectively and evaluated in nonthalamic pain types. Notably, there was no significant difference in the stroke side in relationship to development of CPSP in the lateral medullary infarct study31 or the prospective, unselected stroke cohort of Andersen et al.34

As in other central neuropathic pain types, pain severity in CPSP can be significant and dysfunctioning. Of those with CPSP in Andersen's series, 10/16 (63 percent) reported their pain as moderate to severe.34 All of the lateral medullary infarct cohort reported their pain severe and required treatment.31 Allodynia is common to cold and to light touch (generally ^25-75 percent of CPSP patients).27,29,34,40,41 Approximately 50 percent of CPSP patients report disturbed sleep, fatigue, and/or stress in relationships and 87 percent report mood changes.42

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