Anaesthetic medication such as lidocaine and ketamine are sodium channel blockers and can be delivered by a number of routes. Ketamine is a non-competitive N-methyl-D-Aspartate (NMDA) receptor antagonist that can be administered epidurally, intrathecally, and orally to treat neuropathic pain syndromes (Hocking & Cousins 2003).
Given the severity of post-SCI pain, treatments such as lumbar epidural and subarachnoid infusions or anaesthetics are sometimes utilized and there is some evidence for these treatments. Loubser and Donovan (1991) conducted an RCT of 21 patients who were provided 2 separate lumbar subarachnoid injections of placebo and 5% lidocaine in dextrose. Following the lidocaine injection (n=13) there was a significant mean reduction in pain (p<0.01) for an average of 2 hours despite the fact that 8 patients showed no changes. However, this treatment provided short-term relief of pain only. The authors regarded the value of this treatment as more a diagnostic procedure than a therapeutic one.
Attal et al. (2000) reported on 15 patients who received lidocaine intravenously and experienced a greater reduction in pain than those who received placebo, with an effect lasting up to 45 minutes post injection, and a reduction in the intensity of brush-induced allodynia and mechanical hyperalgesia. In a RCT study by Finnerup et al. (2005) those patients who received lidocaine intravenously (n=24) in two treatment sessions 6 days apart reported significantly less pain than those who did not receive intravenous lidocaine.
Kvarnstrom et al. (2004) found no evidence for the effectiveness of intravenous lidocaine in reducing neuropathic pain when compared to placebo.
Chiou-Tan et al. (1996) provided 15 SCI individuals with either oral mexiletine (an orally administered derivative of lidocaine) or placebo (150mg 3x daily) in a double-blind cross-over RCT. There was no appreciable improvement in pain severity, as measured either on a VAS or using the McGill Pain Questionnaire, within either group.
In one RCT of 10 subjects, Kvarnstrom et al. (2004) found ketamine was successful in reducing spontaneous neuropathic pain post SCI. Eideet al. (1995)in an RCT of intravenous ketamine hydrochloride (NMDA receptor antagonist), alfentanil (m-opioid receptor agonist) or placebo were provided as combination of bolus and continuous intravenous infusions. There was a significant benefit to ketamine or alfentanil vs. placebo for allodynia. Alfentanil reduced wind-up pain compared toplacebo but not ketamine overall; however, there was a high correlation between the serum concentration of ketamine and the reduction in continuous pain and wind-up pain. The effects of ketamine and alfentanil were significant when compared to placebo.
There is level 1b evidence (from one randomized controlled trial; Loubser & Donovan 1991) that Lidocaine delivered through a subarachnoid lumbar catheter provides short-term relief of pain greater than placebo.
There is level 1a evidence (from two randomized controlled trials; Kvarnstrom et al. 2004; Eide et al. 1995) that intravenous Ketamine significantly reduces allodynia when compared to placebo.
There is level 1b evidence (from one randomized controlled trial; Chiou-Tan et al. 1996) that mexilitene (a derivative of lidocaine) does not improve SCI dysesthetic pain when compared to placebo.
Lidocaine through a subarachnoid lumbar catheter and intravenous Ketamine improve post-SCI neuropathic pain short term.
Mexilitene does not improve SCI dysesthetic pain.