Local botulinum-toxin injection is a safe and well-tolerated symptomatic treatment for hemifacial spasm. In the long term, however, lasting relief can only be achieved by microvascular decompression, a microsurgical intervention with a relatively low risk and a high success rate.

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Microvascular decompression represents an effective treatment for hemifacial spasm. The use of lateral spread response (LSR) monitoring remains a useful intraoperative tool to ensure adequate decompression of the facial nerve. The aim of this study was to assess the value of LSRs intraoperative monitoring as a prognostic indicator for the outcome of microvascular decompression in hemifacial spasm. Our study included 100 patients prospectively. The patients were classified into four groups whether LSRs were totally, partially, not relieved, or not detected from the start. According to clinical outcome, the patients were classified into four groups depending on the clinical course after surgery and the residual symptoms if any. Then, correlations were made between LSR events and treatment outcome to detect its reliability as a prognostic indicator. LSRs were relieved totally in 56 % of the patients, partially relieved in 14 %, not relieved in 10 %, and were not detected in 20 % of the patients from the start. HFS was relieved directly after operation in 62 % with clinical improvement of 90-100 %. Thirty-one percent described 50-90 % improvement over the next 3 months after surgery. Almost all of these 31 % (28 out of 31 patients) reported further clinical improvement of 90-100 % within 1 year after surgery. Three percent suffered from a relapse after a HFS-free period, and 4 % reported minimal or no improvement describing 0-50 % of the preoperative state. The percentage of the satisfied patients with the clinical outcome who reported after 1 year a clinical improvement of 90-100 % was 90 %. Statistical analysis did not find a significant correlation between the relief of LSRs and clinical outcome. LSRs may only represent an intraoperative tool to guide for an adequate decompression but failed to represent a reliable prognostic indicator for treatment outcome.

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 anticonvulsants, 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 microvascular decompression operation is indicated. This is a causally directed form of treatment that generally yields very good results.

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