Lien vers les tableaux de données probantes et la liste des références (en Anglais)
Central post-stroke pain (CPSP) is a rare neurological disorder, in which the body becomes hypersensitive to pain, resulting from damage to the thalamus, the part of the brain that affects sensation. The condition is rare, occurring in an estimated 2% to 5% of all stroke cases. Antidepressants including tricyclic antidepressants, serotonin–norepinephrine reuptake inhibitors and selective serotonin reuptake inhibitors are used most frequently for the treatment of neuropathic pain, although there is little published evidence of their effectiveness in CPSP. Vranken et al. (2011) randomized 48 patients with severe neuropathic pain resulting from cerebrovascular lesions or spinal cord lesions to receive escalating doses of either duloxetine (60 and 120mg/day) or placebo for 8 weeks. At the end of treatment, the mean pain scores, assessed using a 10-point visual analogue scale were reduced from 7.1 to 5.0 (duloxetine) vs. 7.2 to 6.1 (placebo), p=0.06. There were no differences between groups in Patient Disability Index or EQ-5D scores but patients in the duloxetine group reported better pain scores on the bodily pain sub section of the SF-36 (p=0.035).
Several RCTs have been published evaluating the effectiveness of the anticonvulsant drugs, pregabalin and gabapentin, most of which included patients with neuropathic pain of varying etiology. A single RCT included patients who were suffering exclusively from CPSP. In this study (Kim et al. 2011) randomized 220 patients to receive either 150-600 mg of pregabalin or placebo over 13 weeks. At the end of treatment, the mean pain scores were reduced from 6.5 to 4.9 in the pregabalin group and from 6.3 to 5.0 in the placebo group, although the difference was not statistically significant. (p=0.578). Treatment with pregabalin resulted in significant improvements, on secondary endpoints including some aspects of sleep, anxiety and clinician global impression of change. Adverse events were more frequent with pregabalin causing the discontinuation of treatment in 8.2% of patients compared with 3.7% of placebo patients. Vranken et al. (2008) randomized 40 patients (19 with stroke) suffering from severe neuropathic pain, to receive a 4-week course of treatment with escalating doses of pregabalin (max 600 mg/day) or placebo. At the end of treatment, patients in the pregabalin group experienced significantly greater pain relief on a 10-point visual analogue scale (mean=7.6 to 5.1 vs. 7.4 to 7.3, p=0.01) and had significant improvement in EQ-5D scores and in the bodily pain domain of the SF-36. There was no significant difference in Pain Disability Index scores between groups. Serpell et al. (2002) randomized 307 patients with a wide range of neuropathic pain syndromes (9 with post stroke pain) to receive either gabapentin or placebo for 8-weeks. Gabapentin was given in three divided doses to a maximum of 2400 mg/day. Patients in the treatment group experienced a significantly greater reduction in pain over the study period (mean reduction of 21% vs. 14%, p=0.048). Significant differences were shown in favour of gabapentin for the clinician and patient Global Impression of Change Scale, and some domains of the Short Form-McGill Pain Questionnaire.
One RCT has evaluating the potential benefit of the anti-epileptic agent, levetiracetam in patients with CPSP. Jungehulsing et al. (2013) included 42 patients with CPSP resulting from stroke, of duration greater than 3 months and a score of 4 or greater on 10-point pain intensity scale. Participants were randomized to receive levetiracetam at a maximum dose of 3000 mg or a placebo over a 24-week study period which included two, 8-week treatment periods. Treatment with levetiracetam was not associated with significantly greater improvement in spontaneous or evoked pain, or any of the secondary measures including the McGill Pain Questionnaire, revised Beck Depression Inventory, or the Short Form-12 Health Survey, with increased frequency of reported side-effects.