Clinical presentation of trigeminal neuralgia and the rationale of microvascular decompression.

Among the facial pain syndromes, trigeminal neuralgia has a special position for many reasons. Already described in the Romans age, the specific features of its severe symptoms, the therapeutic debate and the recent curative possibilities, make this complex pain syndrome a unique entity. The clinical onset is predominantly unilateral and is described as an electric, lancinating, focal and sharp pain. It can last seconds to minutes initially, and sometimes can last as long as 1 hour. Usually the patient is symptom-free between attacks. Later in the course of the disease, patients report dull, aching, constant pain in the same distribution as the paroxysms. The pain can be triggered by non-noxious stimuli like chewing, talking, swallowing, wind on the face, cold and light touch. Thought to be attributable to fifth cranial nerve dysfunction, the first surgical attempts aimed to interrupt nerve continuity by means of a rizothomy, with disappearance of both pain and sensory disturbances. Further investigations claimed nerve compression by vascular structures as responsible of nervous dysfunction. Hence the attempt to perform a decompression in order to relieve the symptoms and maintain physiologic nerve function. From the successful attempts of first microvascular decompression descends the now standardised and widespread technique that is commonly used today to treat trigeminal neuralgia.