Anti-convulsants and anti-depressants.

摘要: Damage to a nerve should only lead sensory loss. While this is common, the incidence of spontaneous pain, allodynia and hyperalgesia indicate marked changes in nervous system that are possible compensations for loss normal function arises from Neuropathic pain damaged which then alter spinal cord brain plasticity areas adjacent those directly influenced by neuropathy. The peripheral drive central so mechanisms involved multiple located at number sites. Nerve damage increases excitability both undamaged fibres, neuromas cell bodies dorsal root ganglion. These substrates ongoing efficacy blockers such as carbamazepine, lamotrigine mexiletine, all anti-convulsants. A better understanding ion channels sites injury has shown important roles particular sodium, potassium calcium genesis neuropathic pain. Within cord, activity receptors glutamate, especially N-methyl-D-aspartate (NMDA) receptor, trigger wind-up hyperexcitability. Increases transmitter release, neuronal receptive field size result nerves. Ketamine gabapentin/pregabalin, again with anticonvulsant activity, may interact these mechanisms. acts on whereas gabapentin subunit responsible release transmitters into cord. In addition hyperexcitability, cells participate spinal-supraspinal loop involves parts affective responses but also engages descending excitatory inhibitory systems use monoamines. pathways become more active after site action anti-depressants. This chapter reviews evidence drugs, anti-depressants anticonvulsants, believed be effective control, major emphasis state.