Cranial Nerves Compression Syndromes

Objective: To highlight some uncertainties we still face in neurovascular syndromes.

Definition: Vascular compression of cranial nerves has been related to disorders such as trigeminal neuralgia, glossopharyngeal neuralgia, hemifacial spasm, disabling positional vertigo, geniculate neuralgia, spasmodic torticollis, cyclic oculomotor spasm, superior oblique myokymia, and arterial hypertension.

Recent Clinical and Research Developments: Jannetta suggested that vascular compression develops when blood vessels elongate, thus causing a risk for vascular compression of cranial nerves. He assumed that the mechanical effect of a pulsating blood vessel was the cause of the disease. Vessel contact with a cranial nerve is commonly seen at autopsies; symptoms of vascular compression are rare. This leads to an assumption that a second factor, such as previous minor injury, is necessary for creating symptoms. Damage of the central inhibitory mechanisms seems to play an important role in the clinical symptoms' development. It has also been suggested that habitually small posterior fossa may be a predisposing factor for the development of neurovascular conflict. A studied group of patients with trigeminal neuralgia had statistically significant smaller posterior fossa than the control group.

Questions: What is the mechanism and basis of the “second event”? Why do sixth, twelfth, and right tenth nerves not cause clinical neurovascular compression syndrome? Is small posterior fossa really a predisposing factor?

Conclusion: We have a procedure that could be used in many conditions, but paradoxically we lack the pathophysiological understanding and sufficiently sensitive diagnostic tools to use the procedure more frequently.