Teaching Case

66-year-old male patient presented with 5-minutes lasting paroxysmal pain (electric discharge type) on the right V3 region triggered by speaking or mouth opening. Carbamazepine improved the symptoms but was not well tolerated by the patient. Neurological examination: Mild horizontal rotatory nistagmus with extreme sight. No mastication weakness or alterations in sensibility.

Brain MRI was performed demonstrating multiple vascular structures of small calibre around the intracisternal segment of the V cranial nerve (Fig. 1a). On the angiographic sequence (Fig. 1b) these vascular structures show high flow, extending to the right transverse and sigmoid sinuses, suggesting cerebellar AVM.

Angiography was performed and a small nidus located in the cerebellopontine angle was demonstrated, it showed mixed feeding from pial branches (Fig. 2a, from the right superior cerebellar artery) and dural branches (Fig. 2b, from the inferolateral trunk of the right internal carotid artery).

Trigeminal neuralgia (TGN) is a transient, recurrent and intense pain in the area of the face where the trigeminal nerve is distributed. Vascular compression at the root entry zone (REZ, 2-6 mm from emergence of the brainstem, [1]) is the causative of around 80-90% of trigeminal neuralgias [2]. Other TGN aetiologies include lesion of the nuclei of V, lesions of the root within the cisterns and Meckel's cave, lesions of the cavernous sinus or distal branches lesions [1].
Patients with unruptured bAVMs have a 3.3% (men) and 1.3% (women) risk of rupture and bleeding each year [3].

Pre-operative MRI is helpful to confirm neurovascular contact, tailored to delineate the trigeminal nerve and adjacent vessels [4], including angiographic sequences that can help determine the arterial or venous supply of the AVM [1]. Brain angiography should also be performed to confirm the diagnosis and help to characterise the lesion.

Treatment of TGN caused by bAVMs includes medical treatment (carbamazepine), but most of the patients seek non-drug treatments that include surgical resection of bAVMs, microvascular decompression, stereotactic radiosurgery, destructive neurosurgical manipulation of the TG nerve or interventional embolisation [5].

Because the patient did not tolerate the medical treatment, the case was presented in a MDT where it was decided to perform an embolisation of the right cerebellar AVM. The procedure passed without early complications.
Brain MRI two months after treatment showed absence of flow in the embolised vessels and the patient remains asymptomatic.