Updating Assessment Of Neuralgia With Special Emphasis On Cranial Neuralgia

Abstract

Any of the cranial neuralgias may be primary (idiopathic) or secondary {symptomatic). Most of the cranial neuralgias share a common feature: the presence of trigger points • This may support the hypothesis that cranial neuralgias are due to temporal summation of afferent impulses evoking eventually an increased neuronal firing to a threshold which thereafter triggers an antidromic paroxysmal discharge in the distribution of the sensory nuclei of the cranial nerves. Impairments of the efficacy of the inhibitory mechanisms of pain in the nervous system may be an important factor for the genesis of many of the cranial neuralgias .This was supported by the . finding of (Strittmatter et al., 1997) that an increase in the concentration of hyperalgesic prostaglandins E2 and prostaglandins F2 alpha as well as the decrease in the hypoalgesic prostaglandins 02

concentration has an important role in the onset of neuralgic pain in

• patients with idiopathic trigeminal neuralgia {ITN). The serotonergic, noradrenergic, dopaminergic, and peptidergic systems have a role in development of idiopathic