[Advances in physiopathology and the treatment of neuropathic pain].
OBJECTIVE
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.


METHODS
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.
Caviedes
B E
BE
Servicio de Neuropediatría. Hospital Marqués de Valdecilla. Universidad de Cantabria, Santander, España. pedhfj@humv.es
Herranz
J L
JL
D000200:Action Potentials / Q000502:physiology; D000700:Analgesics / Q000627:therapeutic use*; D000927:Anticonvulsants / Q000627:therapeutic use*; D000928:Antidepressive Agents / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008953:Models, Anatomic; D009422:Nervous System Diseases / Q000503:physiopathology*; D009437:Neuralgia / Q000188:drug therapy* / Q000378:metabolism; D009619:Nociceptors / Q000378:metabolism*; D010146:Pain / Q000188:drug therapy* / Q000378:metabolism; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology; D026941:Sodium Channel Blockers / Q000627:therapeutic use; D015222:Sodium Channels / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000700:Analgesics; D000927:Anticonvulsants; D000928:Antidepressive Agents; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D002118:Calcium