Trigeminal Neuralgia

Trigeminal neuralgia is recurrent, unilateral, brief electric-shock-like pain in one or more divisions of the trigeminal nerve, triggered by innocuous stimuli such as touching the face, eating, talking or brushing teeth. The current classification distinguishes classical trigeminal neuralgia (due to neurovascular compression with morphological change of the nerve root), secondary trigeminal neuralgia (due to an identifiable disease such as multiple sclerosis or a tumour) and idiopathic trigeminal neuralgia. Each may be purely paroxysmal or have concomitant continuous pain^[1].

In 1967 Jannetta described arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia, establishing the rationale for microvascular decompression^[2]. Compression at the root entry zone, where central (oligodendrocyte) myelin gives way to peripheral (Schwann cell) myelin, causes focal demyelination and ectopic, ephaptic discharges. The superior cerebellar artery is the commonest offending vessel, followed by the anterior inferior cerebellar artery and veins (such as the superior petrosal venous complex).

MRI with high-resolution, heavily T2-weighted (CISS/FIESTA) and time-of-flight sequences identifies neurovascular contact and excludes secondary causes such as tumours (epidermoid, meningioma, schwannoma) and multiple sclerosis. Neurovascular contact is common in asymptomatic people, so imaging supports but does not establish the diagnosis; contact with morphological change (displacement or atrophy of the root) is more meaningful^[1]. Bilateral symptoms, sensory loss or onset in a young patient are red flags for a secondary cause.

Carbamazepine or oxcarbazepine is first-line treatment and controls pain initially in most patients^[1]. Surgery is considered when medication fails or causes intolerable side effects.

• Microvascular decompression (MVD): a retrosigmoid craniotomy to move the compressing vessel off the nerve. It is the only treatment that addresses the cause, and it preserves facial sensation. In 1185 patients treated by Jannetta, about 70% were pain-free off medication at ten years, and the annual rate of recurrence fell over time^[3].
• Stereotactic radiosurgery: non-invasive, with delayed onset of relief and a higher rate of recurrence and facial numbness; suited to older or high-risk patients.
• Percutaneous procedures through the foramen ovale (radiofrequency thermocoagulation, glycerol rhizolysis, balloon compression): quick, with immediate relief, but recurrence is common and some degree of numbness is expected.

• Lateral or park-bench position; retrosigmoid craniotomy exposing the junction of the transverse and sigmoid sinuses.
• Release CSF and approach along the superolateral (tentorial) surface of the cerebellum to the trigeminal nerve, dividing the arachnoid and preserving the petrosal vein where possible.
• Inspect the whole nerve from the root entry zone to Meckel's cave; multiple vessels and veins are common.
• Mobilise the artery and keep it away with Teflon felt, or transpose it with a sling; avoid kinking perforators.
• Brainstem auditory evoked potentials monitor the eighth nerve during cerebellar retraction.

MVD has the best long-term pain-free rates of any treatment^[3]. Risks include hearing loss, CSF leak, facial numbness, cerebellar injury and, rarely, stroke or death. Outcomes are best in classical trigeminal neuralgia with purely paroxysmal pain and clear arterial compression; continuous pain and venous compression predict a worse result.