OBJECTIVE: Brainstem compression caused by vascular abnormalities has rarely been reported in the literature. We describe five cases of large ectatic vertebral artery causing compression and distortion of the medulla oblongata with pyramidal tract signs and low cranial nerve dysfunction. Microvascular decompression by retracting the vertebral artery and anchoring it to the dura has been the treatment of choice. METHODS: Five patients, four male and one female, presented with progressive myelopathic features and lower cranial nerve dysfunction, especially dysphonia and dysphagia. Four patients were affected by systemic arterial hypertension. Magnetic resonance imaging showed impingement of the right vertebral artery in three patients and the left vertebral artery in two patients, on the right and left lateral medulla, respectively. In two patients, hypoplasia of the contralateral vertebral artery was documented. RESULTS: All patients underwent neurovascular decompression of the medulla oblongata. The ectatic and tortuous vertebral artery was detached from the medulla, shifted away, and repositioned by anchoring to the nearby dura mater using a Gore-Tex vascular slip. Postoperatively, all patients but one had improvement of their previous neurological symptoms. CONCLUSION: Brainstem dysfunction caused by a tortuous ectatic vertebral artery might be less uncommon than expected. It should be considered a new distinct clinical entity, the real incidence of which needs to be carefully evaluated by an appropriate diagnostic protocol, which includes primarily magnetic resonance imaging with specific three-dimensional sequences. Awareness of this condition is necessary to ensure the appropriate treatment. Surgical microvascular decompression seems very effective.
OBJECTIVE: Brainstem compression caused by vascular abnormalities has rarely been reported in the literature. We describe five cases of large ectatic vertebral artery causing compression and distortion of the medulla oblongata with pyramidal tract signs and low cranial nerve dysfunction. Microvascular decompression by retracting the vertebral artery and anchoring it to the dura has been the treatment of choice. METHODS: Five patients, four male and one female, presented with progressive myelopathic features and lower cranial nerve dysfunction, especially dysphonia and dysphagia. Four patients were affected by systemic arterial hypertension. Magnetic resonance imaging showed impingement of the right vertebral artery in three patients and the left vertebral artery in two patients, on the right and left lateral medulla, respectively. In two patients, hypoplasia of the contralateral vertebral artery was documented. RESULTS: All patients underwent neurovascular decompression of the medulla oblongata. The ectatic and tortuous vertebral artery was detached from the medulla, shifted away, and repositioned by anchoring to the nearby dura mater using a Gore-Tex vascular slip. Postoperatively, all patients but one had improvement of their previous neurological symptoms. CONCLUSION:Brainstem dysfunction caused by a tortuous ectatic vertebral artery might be less uncommon than expected. It should be considered a new distinct clinical entity, the real incidence of which needs to be carefully evaluated by an appropriate diagnostic protocol, which includes primarily magnetic resonance imaging with specific three-dimensional sequences. Awareness of this condition is necessary to ensure the appropriate treatment. Surgical microvascular decompression seems very effective.