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Kumar i Clark:

Trigeminal neuralgia
Trigeminal neuralgia typically starts in the 6th and 7th decades; hypertension is the main risk factor. Compression of the trigeminal nerve at or near the pons by an ectatic vascular loop is the usual cause. High resolution MRI studies may demonstrate the vascular loop in contact with the nerve in a high proportion of cases. Younger patients are more likely to have multiple sclerosis or cerebellopontine angle tumours (acoustic schwannomas, meningiomas, epidermoids) as the cause.

Clinical features
Paroxysms of knife-like or electric shock-like pain, lasting seconds, occur in the distribution of the Vth nerve. Pain tends to commence in the mandibular division (V3) but may spread over time to involve the maxillary (V2) and occasionally the ophthalmic divisions (V1). Bilateral TN is rare (3%) and usually due to intrinsic brainstem pathology such as demyelination. Episodes occur many times a day with a refractory period after each. They may be brought on by stimulation of one or more trigger zones in the face. Washing, shaving, a cold wind or chewing are examples of trivial stimuli that provoke pain. The face may be screwed up in agony. Spontaneous remissions last months or years before (almost invariable) recurrence. There are no signs of Vth nerve dysfunction on examination.

Treatment
Carbamazepine (6001200 mg daily) reduces severity of attacks in the majority. Oxcarbazepine, lamotrigine and gabapentin are also used. If drugs fail or are not tolerated, a number of surgical options are available which in general are more effective than medical treatments. Percutaneous radiofrequency selective ablation of the trigeminal ganglion is performed as a day-case procedure; recurrence may occur after an average of two years. Microvascular decompression of the nerve in the posterior fossa has a high long-term success rate (approx. 90%).

Harrison:
Symptoms result from ectopic generation of action potentials in pain-sensitive afferent fibers of the fifth cranial nerve root just before it enters the lateral surface of the pons. Compression or other pathology in the nerve leads to demyelination of large myelinated fibers that do not themselves carry pain sensation but become hyperexcitable and electrically coupled with smaller unmyelinated or poorly myelinated pain fibers in close proximity; this may explain why tactile stimuli, conveyed via the large myelinated fibers, can stimulate paroxysms of pain. Compression of the trigeminal nerve root by a blood vessel, most often the superior cerebellar artery or on occasion a tortuous vein, is the source of trigeminal neuralgia in a substantial proportion of patients. In cases of vascular compression, age-related brain sagging and increased vascular thickness and tortuosity may explain the prevalence of trigeminal neuralgia in later life.

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http://www.neurology.org/content/71/15/1183.long

For patients with classic TN, does high-resolution MRI accurately identify patients with neurovascular compression?
Evidence.

Sixteen papers, the latest published in 2006, studied patients with TN with high-resolution MRI. Nine studies were graded Class IV because they relied on the unmasked findings of the operating surgeon to determine the presence of vascular contact. Table e-5 lists the characteristics of the seven higher-quality studies.1925 One study employed a case control design with a narrow spectrum of patients and another was retrospective (Class III).19,20 Five studies were masked cohort surveys with prospective data collection (Class I).2125 The most common reference standard in these Class I studies was the masked comparison of the MRI of the symptomatic side to the asymptomatic side. Sensitivities and specificities in the Class I through III studies varied widely (sensitivity 52 to 100%; specificity 29 to 93%) and in three Class I studies the association was not significant. The heterogeneity in results may have resulted from differences in the MRI techniques employed.
Conclusions.

Because of inconsistency of results, there is insufficient evidence to support or refute the usefulness of MRI to identify vascular contact in CTN or to indicate the most reliable MRI technique. ================
It would also be useful to determine if finding a neurovascular contact on high-resolution MRI accurately identifies patients who will respond to microvascular decompression. This question could be answered with a prospective study comparing long-term outcomes in patients with TN undergoing microvascular decompression with and without neurovascular contact identified on preoperative high-resolution MRI.

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