Neurovascular compression in cranial nerve and systemic disease

Abstract

As we age, our arteries elongate and our brains "sag." As a consequence of these processes, redundant arterial loops and bridging or intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebellopontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. Symptoms of trigeminal or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory) and some cases of "essential" hypertension are caused by these vessels compressing cranial nerves V, IX--X, VII, VIII, and left X and medulla oblongata. Using microsurgical techniques, the symptoms may be relieved by vascular decompression, findings and results in 695 paients are briefly reviewed and correlated. A chronic primate model of "essential" hypertension is briefly described.