Cranial nerve vascular compression syndromes

Hyperactive cranial nerve syndromes originate in a large number of cases from chronic neurovascular conflict. Classical trigeminal neuralgia is the most frequent syndrome, followed by primary hemifacial spasm. Vago-glossopharyngeal neuralgia is rare, but still underestimated. Vascular compression of the vestibulocochlear nerve may be at the origin of tinnitus and positional disabling vertigo. Vascular compression of the ventrolateral medulla can be a possible cause of neurogenic essential blood hypertension. Chronic pulsatile neurovascular compression would generate ectopic stimuli that are transmitted to neighbouring fibres through focal zones of demyelination, which provokes an ephaptic mechanism between fibres. Also, chronic pulsatile compression would induce hyperactivity of the corresponding cranial nerve nuclei. In trigeminal neuralgia this hyperactivity is expressed by epileptic-like clinical manifestations that respond to anticonvulsants. MRI imaging with high-resolution protocol, and the three following sequences—3D T2 high-resolution, TOF MR-angiography, and T1 with gadolinium—permit to depict the neurovascular conflict and predict the degree of compression. First option of the treatment is microvascular decompression.