Lateral spread response

In patients with hemifacial spasm (HFS), a lateral spread response (or abnormal muscle response) is recorded from facial muscles after facial nerve stimulation. The origin of this response is not completely understood.

During microvascular decompression for hemifacial spasm monitoring of the abnormal lateral spread response (LSR), an evoked response to facial nerve stimulation, has been traditionally used to monitor the adequacy of cranial nerve (CN) VII decompression.

Yamashita et al., studied the lateral spread responses elicited by double stimulation in 12 patients with HFS during microvascular decompression. The response was recorded from the mentalis muscle by Electrostimulation of the temporal branch of the facial nerve or from the orbicularis oculi muscles by stimulation of the marginal mandibular branch. The interstimulus intervals (ISIs) of double stimulation ranged from 0.5 to 7.0 ms. R1 was defined as the response elicited by the first stimulus, and R2 as the response elicited by the second stimulus. R1 had a constant latency and amplitude regardless of the ISI, whereas R2 appeared after a fixed refractory period without facilitation or depression in a recovery curve of latency and amplitude. From these findings, they considered that the lateral spread response is due to cross-transmission of facial nerve fibers at the site of vascular compression rather than arising from facial nerve motor neurons ¹⁾.

Intraoperative LSR monitoring has high specificity but modest sensitivity in predicting the spasm-free status following MVD. The persistence of LSR carries a high risk for immediate and long-term facial spasm persistence. Therefore, the adequacy of decompression should be thoroughly investigated before closing in cases where intraoperative LSR persists. ²⁾.

Chen et al., report a 34-year-old female with hemifacial spasm who was identified as a candidate for microvascular decompression. Lateral spread response (LSR) was not recorded at first because of anatomical shift of neurovascular relationship after drainage of cerebrospinal fluid, but they reappeared only after a piece of shredded gelatin sponge was placed near the posterior inferior cerebellar artery to expand surgical field. As they removed the gelatin sponge, the LSRs disappeared instantly. Subsequently, the authors put some soft shredded Teflon between the offending vessel and brainstem. Since then the authors did not find LSRs anymore. Clinical follow-up had been carried out with a questionnaire from 1 week to 3 months postoperatively, and the patient was cured with no complications. This report presented that the gelatin sponge placed in an inappropriate position resulting in compression potentially leading to the opposite effect of treatment. Such kind of excessive operation could be avoided by electrophysiological monitoring ³⁾.

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