Indications and Clinical Considerations
Trigeminal neuralgia is an episodic pain that affects the areas of the face supplied by the trigeminal nerve. The pain is unilateral in 97% of cases reported. When it does occur bilaterally, it is in the same division of the nerve. The second or third division of the nerve is affected in the majority of patients, with the first division affected less than 5% of the time. The pain develops on the right side of the face in unilateral disease 57% of the time. The pain is characterized by paroxysms of electric shocklike pain lasting from several seconds to less than 2 minutes. The progression from onset to peak is essentially instantaneous.
The patient with trigeminal neuralgia will go to great lengths to avoid any contact with trigger areas. Persons with other types of facial pain, such as temporomandibular joint dysfunction, tend to constantly rub the affected area or apply heat or cold to it. Patients with uncontrolled trigeminal neuralgia frequently require hospitalization for rapid control of pain. Between attacks, the patient is relatively pain free. A dull ache remaining after the intense pain subsides may indicate a persistent compression of the nerve by a structural lesion. This disease is almost never seen in people younger than age 30 unless it is associated with multiple sclerosis.
The patient with trigeminal neuralgia will often have severe and at times even suicidal depression with high levels of superimposed anxiety during acute attacks. Both of these problems may by exacerbated by the sleep deprivation that often occurs during episodes of pain. Patients with coexisting multiple sclerosis may exhibit the euphoric dementia characteristic of that disease.
The mainstay of the treatment of trigeminal neuralgia is pharmacologic, with carbamazepine and baclofen the drugs of first choice. Other anticonvulsants, including pregabalin, gabapentin, and oxcarbazepine, may also be beneficial. For patients whose condition fails to respond to pharmacologic treatment, trigeminal nerve block via the coronoid approach may be the next reasonable step. If conservative treatment fails, more invasive options including radiofrequency lesioning, balloon compression, gamma knife radiosurgery, and microvascular decompression may be considered with a careful assessment of the risk-to-benefit ratio for each procedure.
Clinically Relevant Anatomy
The maxillary division (V2) of the trigeminal nerve is a pure sensory nerve ( Figure 16-1 ). It exits the middle cranial fossa via the foramen rotundum and crosses the pterygopalatine fossa ( Figure 16-2 ). Passing through the inferior orbital fissure, it enters the orbit, emerging on the face via the infraorbital foramen. The maxillary nerve can be selectively blocked by placing a needle just above the anterior margin of the lateral pterygoid plate.
The maxillary nerve provides sensory innervation for the dura of the middle cranial fossa, the temporal and lateral zygomatic region, and the mucosa of the maxillary sinus. The nerve also provides sensory innervation for the upper molars, premolars, incisors, canines, and associated oral gingiva as well as the mucous membranes of the cheek. The nasal cavity, lower eyelid, skin of the side of the nose, and the upper lip are also subserved by the maxillary nerve.
The mandibular division (V3) is composed of a large sensory root and smaller motor root. Both leave the middle cranial fossa together via the foramen ovale and join to form the mandibular nerve. Branches of the mandibular nerve provide sensory innervation to portions of the dura mater and the mucosal lining of the mastoid sinus. Sensory innervation to the skin overlying the muscles of mastication, the tragus and helix of the ear, the posterior temporomandibular joint, the chin, and the dorsal aspect of the anterior two thirds of the tongue and associated mucosa of the oral cavity is also provided by the mandibular nerve (see Figure 16-1 ). The smaller motor branch provides innervation to the masseter, external pterygoid, and temporalis muscles.