Nerve Compression Syndromes in the Posterior Cranial Fossa

Abstract

Background: Nerve compression syndromes in the posterior cranial fossa can severely impair patients' quality of life. There is often uncertainty about the best treatment. In this article, we provide an overview of these conditions and the corresponding treatment strategies.

Methods: This review is based on pertinent publications retrieved by a selective search in PubMed and on a scientific analysis of the authors' patient collective.

Results: These syndromes are caused by compression of a cranial nerve by an artery or vein at the zone of the nerve's entry to or exit from the brainstem. The best-known neurovascular compression syndrome is trigeminal neuralgia, followed by hemifacial spasm. Less well known are glossopharyngeal neuralgia, nervus intermedius neuralgia, and vestibular paroxysmia. The initial treatment of trigeminal neuralgia is medical: the first line of treatment is with sodium-blocking anticon- vulsants, such as carbamazepine. For patients with hemifacial spasm, botulinum toxin injection is the recommended initial treatment and often leads to a satisfactory regression of the spasms. If these treatments fail, a microvascular decompression operation is indicated. The aim of the procedure is to separate the irritating vessel from the nerve and to keep these structures apart permanently. There is hardly any available evidence on these treatment strategies from randomized controlled trials.

Conclusion: Nerve compression syndromes in the posterior cranial fossa can generally be treated nonsurgically at first. Over the course of the condition, however, treatment failure or intolerable side effects may arise. In such cases, a microvascu- lar decompression operation is indicated. This is a causally directed form of treat- ment that generally yields very good results.

Figure 1

Magnetic resonance imaging in hemifacial spasm. a) The TOF (time of flight) and b) CISS (constructive interference in steady-state) sequences in the axial plane clearly reveal vascular compression of the facial nerve (arrow, F) by the posterior inferior cerebellar artery (arrowhead, P)

Figure 2

Babinski-2 sign in hemifacial spasm. During the spasms, the eyebrow rises while the eye simultaneously closes

Figure 3

Endoscopically assisted microvascular decompression for hemifacial spasm. a) Inspection through the endoscope reveals vascular compression of the facial nerve (F) by a loop of the posterior inferior cerebellar artery (P), while the anterior inferior cerebellar artery (A) courses parallel to the nerve. b) Inspection through the operating microscope reveals the posterior inferior cerebellar artery (P) but does not directly reveal the site of compression, which is hidden behind the lower cranial nerve group (cranial nerve IX, the glossopharyngeal nerve, and cranial nerve X, the vagus nerve). c) After mobilization of the artery (P), inspection through the endoscope reveals that the facial nerve (F) is paper-thin after years of compression (14 years of symptoms) (arrow). The brainstem vessels are visible through the flattened, translucent nerve. d) Two Teflon pledgets have been interposed between the posterior inferior cerebellar artery (P) and the facial nerve (F) to hold these two structures apart without touching the nerve at the site of its previous compression. The hemifacial spasm finally regressed 13 months after surgery; the long delay may be due to the severe structural change of the facial nerve as a result of its longstanding compression. The anterior inferior cerebellar artery (A) is marked as well.

Figure 4

Endoscopically assisted microvascular decompression for trigeminal neuralgia. a) View of the trigeminal nerve (T) and the superior cerebellar artery (S) through the operating microscope. b) Inspection through the endoscope (0° optics), revealing the entire cisternal course of the trigeminal nerve (T) and the superior cerebellar artery (S). c) Inspection through the endoscope with 30° optics reveals severe vascular compression of the trigeminal nerve (T) by the elongated loop of the superior cerebellar artery (S). d) The superior cerebellar artery (S) has been transposed and sewn upward toward the tentorium with a loop of Teflon. Ideally, the trigeminal nerve (T) should be entirely free after the decompression, without any contact either with the vessel or with the Teflon pledget. The abducens nerve (arrow A) and the vestibulocochlear nerve (V) can be seen in the vicinity.