Different Modalities in Management of Trigeminal Neuralgia

Abstract

Trigeminal neuralgia (TN), also called tic douloureux, is the most common of the cranial neuralgias. The first known clinical description of TN was written at the end of the first century by Aretaeus of Cappadocia. In the era preceding the description of TN, studies of the anatomy of the cranial nerves led to a better understanding of facial pain. In 1829, the Scottish anatomist Sir Charles Bell (1774-1842) described the anatomy of the fifth cranial nerve and its motor and sensory functions, establishing the trigeminal nerve as the cranial nerve responsible for sub-serving facial sensation as well as motor innervations to the masticator muscles. In the 19th century, Trousseau suggested that TN was related to abnormal impulse conduction analogous to epilepsy. Even it was referred for a time as “neuralgia epileptiform” An important breakthrough in the management of TN was when Bergouignan in 1942, use the newly introduced anticonvulsant, Dilantin, for treatment of trigeminal neuralgia. In 1962, When carbamazepine (Tegretol), a promising new medication for epilepsy, was introduced, it showed great effect and good results in curing patients with trigeminal neuralgia. Tegretol was found to have greater efficacy and less toxicity than Dilantin, and remains the mainstay in therapy today. Other anticonvulsants are also frequently used, including oxcarbazepine (Trileptal), gabapentin (Neurontin), Lyrica (pregapalin) and Keppra(levetiracetam). The trigeminal nerve leaves the midlateral surface of the pons as a large sensory root (portio major) and a smaller anteromedial motor root (portio minor). It enters the subarachnoid space in the cerebellopontine angle cistern. It travels anterolaterally then pierces the dura mater at the petrous apex to enter Meckel’s cave. The trigeminal nerve has three major divisions-ophthalmic (cranial nerve [CN] V 1), maxillary (CN V 2), and mandibular (CN V 3). These divisions traverse the foramina of the skull to exit the cranial vault on their way to reach the structures they innervate. The ophthalmic division is purely sensory and innervates the upper part of the face; the maxillary division is also purely sensory (although there may be some exceptions) and innervates the middle part of the face. The mandibular division is mixed, that is it carries sensory innervation to the muscles of mastication (temporalis, masseter, medial pterygoid, lateral pterygoid), and the mylohyoid, anterior belly of the digastric, tensor tympani, and tensor veliemicran muscles. The only robust epidemiological data on TN was from the U.S. and demonstrated an annual incidence of between 4-5 per 100,000. However, recent studies from both the UK and Netherlands show far higher incidence rates of 26.8 and 28.9 per 100,000 respectively. Most of trigeminal neuralgia cases are due to compression of the root of the trigeminal nerve, usually within a few millimeters of its entry into the pons, especially the root entry zone Less commonly, trigeminal neuralgia is due to a primary demyelinating disorder. Other, rare causes include infiltration of the trigeminal nerve root, ganglion or nerve by a tumor or amyloid, and small infarcts or angioma in the pons or medulla. In a few cases the etiology is unknown. The pathophysiology of trigeminal neuralgia remains controversial whether the pathogenesis of trigeminal neuralgia involving the central or the peripheral nervous system. there are large proportion of patients with trigeminal neuralgia show evidence of external vascular compression, with focal demyelination near the compression site. Defined by the International Association for the Study of Pain trigeminal neuralgia is known as ‘a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. The International Headache Society (IHS) classified trigeminal neuralgia into two types: classical and symptomatic. Classical trigeminal neuralgia is a unilateral disorder characterized by brief electric, shock-like pains. They have acute onset and termination and limited to the distribution of one or more divisions of the trigeminal nerve. Small areas in the nasolabial fold and/or chin may be particularly susceptible to the precipitation of pain known to be trigger zones. Pain may remit for variable periods of time. The symptomatic type is indistinguishable from the classical type which is caused by a structural lesion or vascular compression. The IHS suggested criteria for the diagnosis of trigeminal neuralgia. The first attack of trigeminal neuralgia is often sudden in onset and can mimic dental pain. Patients often assume that their pain is due to dental causes and seek dental therapy as a first line of treatment. Trigeminal neuralgia may also present exclusively intraorally, which can be confusing for patients and clinicians. Zakrzewska lists some of the types of orofacial pain that need to be considered. The American Academy of Neurology (AAN) and the European Federation of Neurological Societies (EFNS)decided to develop scientifically sound, clinically relevant guidelines to aid specialists and non-specialists in the management of trigeminal neuralgia (TN), by addressing its diagnosis, pharmacological treatment, and surgical treatment. The first line of therapy for trigeminal neuralgia is pharmacological, if for no other reason than in most cases it is immediately available and usually effective. Introduction of phenytoin in the 1940s and carbamazepine in the 1960s changed the management of TN considerably, which previously had been almost exclusively surgical. When medical treatment fails either due to poor pain control or because of intolerable side effects surgery is often considered the next option. The timing of surgery and choice of surgery then becomes the next issue to face the patient. Surgical interventions are varied and are best classified according to the principal target: percutaneous Gasserian ganglion techniques targeting the ganglion itself; gamma knife radiosurgery targeting the trigeminal root, and posterior fossa vascular decompression techniques.