Reader response: Teaching NeuroImages: Amlodipine-responsive trigeminal neuralgia: An alibi for vascular compression theory.

Abstract

We read with interest the report by Uniyal et al.,1 which described a 55-year-old woman exhibiting hypertension with recurrent short-lasting episodes of left-sided trigeminal neuralgia. The patient noted pain relief after consumption of the antihypertensive drug amlodipine. Moreover, the pain recurred if the drug was discontinued. A brain MRI revealed tortuous blood vessels compressing the left rostral anterolateral medulla and the left trigeminal nerve root. This case reminded us of a patient with similar symptoms who we encountered years ago.2 A 59-year-old man with hypertension had a long history of left-sided refractory trigeminal neuralgia. The patient noted that the painful exacerbations occurred in parallel with hypertensive crises and was relieved only by clonidine administration. At the bedside, with continuous monitoring of systemic blood pressure, we demonstrated that the pain reliably resolved as soon as his systolic pressure dropped below 140 mm Hg. Continuous blood pressure monitoring also confirmed the temporal relationship between hypertensive crises often shortly preceding the pain. Catheter angiography demonstrated a dolichoectatic basilar artery compressing the left side of the posterior fossa with a loop compressing the root entry zone of the trigeminal nerve. We agree with Uniyal et al. that, in these cases, the continuous pulsatile compression against the trigeminal nerve root reinforced by hypertensive spikes could have triggered the pain attacks.1 These cases may lend further support to the vascular compression theory of trigeminal neuralgia popularized by Peter Jannetta and other authors,3–5 not necessarily representing a simple alibi for it.