Idiopathic trigeminal neuralgia (ITN) is increasingly regarded as being due to microvascular compression of the trigeminal sensory root, either by an artery or a vein close to the brainstem.1 Yet vascular contacts are found in entirely asymptomatic cases, no vascular contacts are found in some asymptomatic patients, and, most importantly, ITN suddenly switches off, even for years, only to return later, in the face of continuing vascular compression.2 Despite this, microvascular decompression produces immediate virtually complete (98–100%) relief in 82% of the cases and 64% after 10 years.3 Adams has suggested that, ITN being a hyperfunctional disorder of the brainstem, microvascular decompression “produces chronic trauma to a sensitive zone of the cranial nerve... by the dissection necessary and by the manipulation required microvascular decompression produces sufficient trauma to achieve interference of normal functioning of that nerve”, thus dampening the abnormal brainstem activity responsible for ITN.2 Failure to achieve an initial result or early recurrence would imply insufficient surgical trauma.2 We evaluated this hypothesis in our patients submitted to microvascular decompression. Forty one out of 410 patients with …