The Clinical journal of pain
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Microvascular decompression (MVD) remains the only treatment of trigeminal neuralgia that directly addresses the presumed pathogenesis. It is a proven therapy, associated with the longest duration of pain relief while preserving facial sensation. ⋯ In an effort to more successfully select candidates for MVD, the authors have incorporated high-resolution magnetic resonance imaging into our preoperative algorithm, since it has proven extremely accurate in defining the neurovascular relations at the trigminal nerve complex. Microvascular decompression can only be recommended when it is performed with low rates of morbidity.
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The efficacy of the anticonvulsant drug carbamazepine in the management of trigeminal neuralgia is evidenced in several controlled trials, and the numbers needed to treat to obtain one patient with at least 50% pain relief (NNT) is 1.7. Single small trials have shown that baclofen alone provides pain relief (NNT = 1.4) and that lamotrigine has an additional effect in patients with insufficient relief using carbamazepine or phenytoin (NNT = 2.1). Uncontrolled observations and clinical practice indicate that phenytoin, clonazepam, sodium valproate, gabapentin, and lidocaine will also relieve trigeminal neuralgia. ⋯ Acute exacerbation has successfully been treated with intravenous loading with phenytoin or lidocaine, but again these procedures have not been tested in controlled trials. In conclusion, carbamazepine is the mainstay of pharmacotherapy of trigeminal neuralgia, and secondary drug choices are baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin, and sodium valproate. Controlled trials testing the effect of some of these drugs, new drugs, and drug combinations are needed.
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There are no satisfactory animal models of trigeminal neuralgia, and it is difficult to obtain essential data from patients. However, trigeminal neuralgia presents with such idiosyncratic signs and symptoms, and responds to so distinctive a set of therapeutic modalities, that scientific deduction can be used to generate likely hypotheses. The ignition hypothesis of trigeminal neuralgia is based on recent advances in the understanding of abnormal electrical behavior in injured sensory neurons, and new histopathologic observations of biopsy specimens from patients with trigeminal neuralgia who are undergoing microvascular decompression surgery. ⋯ The hyperexcitable afferents, in turn, give rise to pain paroxysms as a result of synchronized afterdischarge activity. The ignition hypothesis accounts for the major positive and negative signs and symptoms of trigeminal neuralgia, for its pathogenesis, and for the efficacy of treatment modalities. Proof, however, awaits the availability of key experimental data that can only be obtained from patients with trigeminal neuralgia.
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Extradural cortical stimulation is a recent addition to the armamentarium of functional neurosurgery. This article reviews results of treatment of chronic central and neuropathic pain. ⋯ It is concluded that extradural cortical stimulation may be effective in several refractory cases.
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Review
Peripheral and gasserian ganglion-level procedures for the treatment of trigeminal neuralgia.
This review discusses the various peripheral and ganglion-level procedures available for treating trigeminal neuralgia and summarizes specific success and complication rates for each technique. ⋯ Each patient should receive an informed and impartial account of the available surgical options. There is a need for prospective randomized controlled studies in procedure-naïve subjects to determine the optimal surgical management of trigeminal neuralgia.