Pharmacologic management

The majority of the literature is made up of case presentations and prospective and retrospective series. These have suggested efficacy of gabapentin,65,66,6768,69,70,71 lamotrigine,72, 73, 74, 75 topiramate,76 levetiracetam,77, 78, 79

oxcarbazepine,80 carbamazepine combined with ami-triptyline,81 phenytoin,82,83 valproate,84 nortriptyline (although this study is listed as for central pain, most are from peripheral nerve generators),85 mexiletine,86 and acupuncture.87 A small open label trial of topiramate for various central pain states (n = 7) showed no efficacy.88

Table 28.1 lists the grade II evidence (randomized, double-blind, placebo-controlled) for the pharmacologic treatment of central neuropathic pain. Included is a randomized, controlled, blinded, dose-response, but no placebo-controlled study on opioids for central pain.97 A couple of newer studies of cannabinoids for MS-related pain are included giving the level of the study structure and/or notable sample size, despite pain measurements being a secondary outcome.98,99 Unfortunately, most of these high quality studies stand alone (either as a positive or negative study) without further confirmatory or doseranging studies. Hence there is no grade I evidence (i.e. strong evidence from a systemic review of multiple grade II studies) for any of the pharmacologic treatments of central neuropathic pain.

In summary, the literature provides good support for the use of gabapentin (at least 1800 mg/day)91 and preg-abalin (mean dosage 460mg/day)92[II] for SCI central pain, lamotrigine (mean dosages 200-400 mg/day) for CPSP58[II] and incomplete SCI related at- and below-level central pain,59[II] amitriptyline (goal at least 75 mg/ day) for CPSP,60[II] (a study for SCI central pain with median dosages of 50 mg/day was negative94) and can-nabinoids for MS-related central pain.100,101[II] The data for carbamazepine for central pain states are mixed, but the positive study was poorly powered and, while supportive of probable efficacy, limited in the strength of its conclusions.89 As noted previously, given limited high quality data for these notoriously difficult to treat pain processes, it seems rational to extrapolate data suggesting efficacy in one central pain state to justify clinically treating a patient with another central pain state.

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