Aims: In this paper we review the most significant studies on the treatment of neuropathic pain over the last few decades, as well as the most recent research work in which the physiopathological mechanisms of pain, with the intention of looking for evidence based criteria that can help us to choose the most appropriate treatment.

Method: The physiopathological bases of neuropathic pain are founded, peripherally, on alterations in the neuronal excitability mediated by voltage dependent sodium channels; from the central point of view, the chief neurotransmitter involved is glutamate, which allows calcium to enter through the N-methyl D-aspartate receptor and conditions a more prolonged depolarisation and the activation of secondary messengers. This determines the chronification of the pain. Thanks to these physiopathological findings about pain, some of the new antiepileptics, which inhibit the sodium channels or the calcium channels, increase the GABA or reduce the level of glutamate in the synapses, have been added to the already existing classic forms of medication.

Conclusions: Different neurophysical alterations induce the most diverse clinical manifestations, such as paresthesia, hyperalgesia or allodynia, regardless of the etiological processes that condition them. The efficiency of tricyclic antidepressants and of carbamazepine is made clear in different clinical studies, but the new antiepileptics (with the exception of gabapentin) have frequently been used in open clinical studies, which means there is a need for double blind controlled clinical trials in order to determine the efficiency and the tolerability of the different therapeutic alternatives in each of the clinical manifestations of neuropathic pain.