Anticonvulsant medications are often utilized in treating neurogenic or deafferent pain following SCI based on the theory that these drugs alter sodium conduction in uncontrolled hyperactive neurons (“convulsive environment”) in the spinal cord. Carbamazepine has been reported as being somewhat effective in the paroxysmal, sharp, shooting pain of trigeminal neuralgia (Swerdlow 1984). Gibson and White (1971) described relief resulting from carbamazepine treatment in two cases of L2 and T8 SCI with intractable pain below the level of SCI. A similar effect of Carbamazepine (200 mg 2x daily in combination with Amitriptyline 50 mg 3x daily) was reported in a complete C8 patient with dysesthesia below the level of the injury (Sandford et al. 1992). Again, controlled studies utilizing these drugs in SCI pain are lacking with the exception of gabapentin and pregabalin.
Gabapentin and pregabalin are now regarded as first-line treatments of neuropathic pain (Ahn et al. 2003; Moulin et al. 2007). Gabapentin and pregabalin have been recommended as first line treatments for neuropathic pain in Canadian and international guidelines (Gajraj 2007). The mechanism of action for Pregabalin and Gabapentin is through binding the alpha-2 delta receptors in the central nervous system. These receptors are present on the presynaptic nerve terminals. When bound by gabapentin or pregabalin they decrease the influx of calcium into the presynaptic terminal there by decreasing the release of excitatory neurotransmitters. Gabapentin and pregabalin appear to potentiate GABA effects centrally through enhancement of GABA synthesis and release. Levendoglu et al. (2004) noted that neuropathic pain is ultimately generated by excessive firing of pain-mediating nerve cells, insufficiently controlled by segmental and non-sequential inhibitory circuits. Gabapentin and pregabalin work by increasing GABA and reducing the release of glutamate thereby suppressing the sensitivity of N-methyl-D-asparate (NMDA) receptor. This has been shown to reduce neuronal hyper-excitability recorded at the spinal dorsal horn near the level of injury (Ahn et al. 2003). Gabapentin and pregabalin are relatively well tolerated with only a few transient side effects, lack of organ toxicity, and no evidence of significant interaction with other medications (Levendoghu et al. 2004; Gajraj 2007).