Trigeminal neuralgia (TN) is defined by the International Headache Society (IHS) as “unilateral disorder characterized by brief electric shock-like pains, abrupt in onset and termination, and limited to the distribution of one or more divisions of the trigeminal nerve” [International Headache Society, 2004]. The IHS suggests a classification of TN as either classic (essential or idiopathic) TN (CTN) or symptomatic TN (STN; pain indistinguishable from that of CTN, but caused by a demonstrable structural lesion other than vascular compression). The diagnosis of CTN requires the absence of a clinically evident neurological deficit. CTN starts in the second or third divisions, affecting the cheek or the chin [International Headache Society, 2004]. The ophthalmic division alone is involved in less than 5% of cases [De Simone et al. 2005]. The single attack generally lasts from less than a second to a few seconds, but it may present in clusters of variable intensity with up to 2 minutes duration. In many cases it is followed by a brief refractory period during which a new stimulation is not able to evoke another attack. Between paroxysms the patient is usually pain free, but a dull background pain may persist in some cases [International Headache Society, 2004]. Growing neurosurgical data advocate the distinction of these two subtypes of TN into type 1 as defined as >50% episodic onset of TN pain and type 2 defined by >50% constant pain [Tatli et al. 2008; Limonadi et al. 2006]. The mechanisms associated with the development of this persistent pain are not well understood but concomitant background pain is associated with poor medical and surgical outcome [Obermann et al. 2008; Sandell and Eide, 2008; ]. Recent investigations focused on the suspected central component in the pathophysiology of TN, which could involve central allodynic mechanisms that may also engage the nociceptive neurons at thalamic and cortical level .