Neurology Central

Toward an etiology-based management of trigeminal neuralgia

Despite its relative rarity, trigeminal neuralgia (TN) is well known by the medical community, not the least because of the location and stereotypic presentation of the pain. As first described in detail over 200 years ago [1], the key features difficult to miss are short-lived pain intense paroxysms, set off by innocuous mechanical stimuli, their abrupt onset and cessation, and the presence of trigger zones within the central mask [2]. Among chronic pain conditions, TN stands out as one of the very few whose treatment outcome is measured by the proportion of patients in complete or nearly complete remission. Moreover, there is an abundance of treatment options available, which range from medication to percutaneous neuroablative procedures to intracranial surgery [3–5]. While patients are usually commenced on medication, the lack of effect or poor tolerability is not disastrous, because a suitable intervention can usually be found, irrespective of the patient’s age, comorbidity or acceptance of risk. For someone undergoing microvascular decompression (MVD) for their TN, the likelihood of their neuralgia still being controlled in 10 years of time is over 70%, and for many of those in whom the pain recurs, a repeat posterior fossa exploration or a percutaneous neuroablative procedure (PNAP) – that is, balloon compression, glycerolysis and radiofrequency lesioning of the trigeminal ganglion – is likely to guarantee many more years of freedom from their neuralgia [4,6–8]. For those not suitable for general anesthesia or who cannot tolerate the long sitting position after a glycerol injection, less demanding options such as stereotactic radiosurgery (SRS) of the trigeminal nerve root and intracutaneous botulinum toxin A injections are available [8,9]. In this commentary, I will focus on the choice of surgical treatment in an unoperated patient with clinically established TN [2].
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