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CC BY-NC-ND 4.0 · Asian J Neurosurg
DOI: 10.1055/s-0045-1811171
Original Article

Disappearance of Lateral Spread Response: Reliability as a Prognostic Marker in Hemifacial Spasm

Soumya Ranjan Rana 
1   Department of Neurosurgery, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Vikas Janu 
1   Department of Neurosurgery, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Raghavendra Kumar Sharma 
1   Department of Neurosurgery, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Mayank Garg 
1   Department of Neurosurgery, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Suryanarayanan Bhaskar 
1   Department of Neurosurgery, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Mahesh Arjundan Gadhvi 
2   Department of Physiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
› Author Affiliations

Funding None.
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Abstract

Objective

Intraoperative neuromonitoring (IONM) using lateral spread response (LSR) has been mostly studied as a tool in optimizing the benefits of microvascular decompression (MVD) in cases of hemifacial spasm (HFS). Although evidence suggests its utility as a prognostic marker, our experience with the same remains otherwise. The significance of the time of disappearance of LSR is also less studied as a factor determining the outcome. This is a pilot study involving a series of patients operated on for HFS using MVD. The prime objectives of the study are: (1) to review LSR in HFS as a prognosticator of outcome and (2) to study the significance of time of disappearance of LSR and its correlation with outcome.

Materials and Methods

Patients operated on for HFS with MVD under IONM guidance, between August 2022 and June 2024, were observed in the postoperative period in three phases—immediate, early, and late. The outcomes were divided into—complete, partial or no improvement, and recurrence. The results were studied against the corresponding findings of LSR in those cases.

Results

A total of six patients were studied. Of these, three were males and three were females. Intraoperatively, all the patients showed complete loss of LSR after separating the compressing vessel from affected facial nerve. In the immediate postoperative phase, two out of six patients had incomplete improvement in symptoms which later improved in one of the patients in early postoperative phase. The remaining one patient who had partial improvement of symptoms had increased symptoms within 3 months of follow-up.

Conclusion

Although LSR monitoring indicates adequate facial nerve decompression, in our experience, LSR disappearance was not congruent with the absence of symptoms in postoperative phase of HFS. The time of disappearance of the LSR waveform intraoperatively has a significant role in determining the outcome.


 

Keywords

lateral spread response - hemifacial spasm - microvascular decompression

Introduction

Hemifacial spasm (HFS) is defined as abnormal spasmodic contractions of the muscles supplied by the ipsilateral facial nerve.[1] The root cause for HFS has been described as vascular compression at the root entry zone of the seventh cranial nerve. Microvascular decompression (MVD) has been considered the gold standard treatment for HFS.[2] Intraoperative neuromonitoring plays an important role in guiding adequate decompression of the affected facial nerve. The concept of neuromonitoring is based on stimulating one branch of the facial nerve and eliciting the corresponding abnormal response on the related muscle innervated, called the lateral spread response (LSR). Mechanism for LSR has been considered to be an antidromic activity cross-transmission[3] from stimulation of the facial nerve to other branches due to hypersensitivity of the nerve.[4] Compression of the facial nerve by adjacent vessels results in injury to the myelin sheath of the nerve, causing ephaptic transmission of the facial nerve and ectopic stimulation. Literature suggests its disappearance intraoperatively as an indicator of satisfactory decompression of the facial nerve, but its value as a prognostic indicator is controversial.[2] [3] [5] [6] Also, the significance of the time of disappearance of LSR has not been highlighted in the available literature. Hence, the main objectives of the study were to review LSR in HFS as a prognosticator of outcome and to study the significance of time of disappearance of LSR and its correlation with the outcome.


 

Materials and Methods

Patients

Between August 2022 and June 2024, six patients were registered at the neurosurgery department. After being diagnosed with HFS, the patients had MVD. The exclusion criteria were preoperative injection of botulinum toxin and recurrent HFS. Prior to the procedure, written informed consent was obtained from each participant.


 

Intraoperative Neurophysiological Monitoring and MVD

Intravenous fentanyl and propofol were used to achieve general anesthesia as infusion, while fentanyl, propofol, and an initial dose, short-acting muscle relaxant (cisatracurium; 0.15 mg/kg) were used to induce anesthesia. To elicit LSR, paired stimulation needle electrodes were positioned at 5 mm distance along the facial nerve's marginal mandibular branches.[5] The same side orbicularis oculi and mentalis muscles were each fitted with a pair of recording needle electrodes. The orbicularis oris muscle received the ground electrode. Single 0.2 milliseconds at 0.5 to 20 mA wave (rectangular) was the electrode stimulation parameter. Trigeminal and facial nerves were monitored by electromyography using respective innervated muscles.[5] Software used was NIM Eclipse by Medtronic (version 3.5.350, Medtronic Sofamor, Danek, United States). The neuromuscular blockade degree was evaluated using the train-of-four ratio. The following times were used to record the LSR waves and amplitudes[5]: (1) postanesthesia induction, (2) following bone flap removal, (3) at arachnoid incision and release of cerebrospinal fluid, (4) during Teflon patch placement, and (5) after MVD. Patients were observed in immediate (48 hours), early (1 week), and late (6 months) follow-up period. Responses were then recorded and analyzed.


 

 

Observations and Results

The patients enrolled in our study had the following demographic variables, as shown in [Table 1]. Of the six patients, the average age was 43 years, with an average duration of symptoms being 18 months. Two patients had preoperative ipsilateral facial nerve palsy. Patients with facial palsy also had prolonged duration of symptoms as compared with other patients, suggesting severity of symptoms corresponding to long-standing anatomical cause for the disease. None of our patients had any known comorbidities prior to surgery, suggesting there were no confounding factors contributing to their postoperative complications.

Table 1

Shows demographic distribution along with clinical presentation of the included patients

Sl. no.

Demographic variables

Value

1

Age

> 50 yr—4

< 50 y—2

2

Sex

Male—3

Female—3

3

Comorbidities

None

4

Duration

> 1 y—4

> 1 y—2

5

Symptoms

Ipsilateral facial nerve palsy—2 with hemifacial spasm

Intraoperatively, four patients had shown complete disappearance of electromyographic response in neuromonitoring (LSR), after separation of the offending vessel from the facial nerve. Disappearance was present in both mentalis and orbicularis oculi muscles, as shown in [Fig. 1].

Zoom
Fig. 1 Intraoperative neuromonitoring graph of the mentalis and orbicularis oris muscle in a case of hemifacial spasm undergoing microvascular decompression. Here, there is a disappearance of lateral spread response as soon as the Teflon patch is placed, thereby achieving adequate decompression of the facial nerve.

We observed the disappearance of LSR in two patients, in an earlier stage, when dissection of the facial nerve was started. This is shown in [Fig. 2] below.

Zoom
Fig. 2 A neuromonitoring graph showing the early disappearance of lateral spread response in the mentalis muscle, before adequate microvascular decompression was achieved.

In the immediate postoperative period, four patients had complete recovery of spasms, while two patients had partial recovery of symptoms, with decreased frequency and intensity. One of the partially recovered patients became symptom-free at 3 weeks postdecompression, while one patient had persistent symptoms even on late follow-up after 6 months with decreased frequency and severity. This patient had a recurrence of symptoms to baseline after 1 year.

Patients with complete disappearance of LSR had complete improvement in HFS with no recurrence. Two patients having persistent HFS in the immediate postoperative period had an early disappearance of the LSR wave even before separating offending vessels. The results are summarized in [Table 2].

Table 2

Summarizes data showing intra-operative neuro monitoring changes and the corresponding outcomes in the operated patients

Patient sl. no.

LSR disappearance

Result

Follow-up

1

Complete—at MVD

No residual symptoms

No recurrence

2

Complete—before MVD

Persistent symptoms

No recurrence

3

Complete—at MVD

No residual symptoms

No recurrence

4

Complete—at MVD

No residual symptoms

No recurrence

5

Complete—before MVD

Persistent symptoms

Recurrence

6

Complete—at MVD

No residual symptoms

No recurrence

Abbreviations: LSR, lateral spread response; MVD, microvascular decompression.


Note: Of the two patients with persistent symptoms after surgery, one improved completely (sl. no. 2), while the other patient had partial improvement (sl. no. 5) after 3 weeks.



 

Discussion

Two of the accepted theories that make the basis for HFS are central and peripheral origination theories.[5] According to the theory of “central origination,” the motor facial nerve nucleus becomes hyperexcitable, which in turn causes the hyperexcitability of the facial nerve,[5] [7] while the notion of peripheral origination posits that myelin damage and ephaptic transmission result from facial nerve compression at the REZ.[5] [8] For HFS, MVD has been regarded as the most effective and preferred treatment.

On stimulating one branch of facial nerve, an aberrant response known as the “lateral spread response” is recorded electromyographically.[6] The mechanism has been considered to be antidromic activity cross-transmission[3] from stimulation of facial nerve to other branches due to hypersensitivity of nerve.[4] A disappearance of LSR is an indication of satisfactory decompression of facial nerve, with a decrease in amplitude by 80% ensuring complete relief of symptoms.[3]

In a study conducted by Song et al, on 73 patients, complete LSR disappearance was noted in 61 patients, while 9 patients had partial, and 3 patients had no disappearance.[5] There were 55 individuals who had short-lasting clinical cures, 49 of whom had the LSR completely disappear and 6 of whom had it partially disappear. The LSR completely disappeared in 53 of the 61 patients who had long-term clinical cures, partially disappeared in 7, and did not change in 1. The LSR vanished in 11 individuals before Teflon pledgets were inserted (7 had short-lasting and 9 long-lasting clinical improvement), and in the remaining 50 patients following Teflon pledget insertion (42 had short-lasting and 44 had long-lasting clinical improvement).[5] The duration of total LSR disappearance did not correlate with the results of surgery.[5]

To sum up, intraoperative LSR monitoring can verify proper facial nerve decompression and assist in identifying the problematic arteries in HFS patients. The surgical results of MVD are intimately linked to the LSR's disappearance throughout the procedure. Although the period at which LSR completely disappears is not considered a valid prognostic sign, intraoperative LSR monitoring is seen as a useful strategy for forecasting the prognosis of HFS after MVD.[5] [6]

Kim et al[9] found that patients whose LSR vanished before proper decompression fared worse than those whose LSR vanished after adequate decompression. The finding of our study is consistent with the above finding. Patients who showed early disappearance of LSR were found to have either incomplete relief or recurrence of symptoms, in contrast to those with complete absence of LSR at the end of facial nerve decompression.[9]

A meta-analysis conducted by Thirumala et al (2020)[10] inferred that the disappearance of LSR had a high specificity but a lower sensitivity in predicting postdecompression HFS free period. The same study also underlined the causes of early disappearance of LSR, having significance, but failed to establish a direct link with the resolution of HFS. As stated in the above study, there can be various factors leading to the early disappearance of LSR such as a change in cerebrospinal fluid dynamics attributed to dural or arachnoid opening and cerebellar retraction.[10]

A similar study with 523 patients was performed by Chai et al in 2023 to look into the possible causes of early LSR disappearance and its additional role in affecting the outcomes in HFS. They concluded that there is no significant effect of early LSR disappearance. Despite having a larger sample size, the heterogeneous distribution of patients as per the intraoperative factors for likely early LSR disappearance can be looked at as a limiting factor to the said conclusion.[11]


 

Conclusion

Previously, many articles have touched upon the findings of disappearance and persistence of LSR after MVD to assess its significance as a prognostic factor for improvement in HFS. However, there is limited available evidence discussing the significance of the early disappearance of LSR in these cases. This study was performed on six patients, which is a small number to find out any statistically significant difference. Long-term follow-up needs to be done to find out long-term prognostic value of early LSR disappearance in HFS. Further research is needed to explore this aspect and better understand its potential as a predictor of long-term clinical outcome following MVD.


 

 

Conflict of Interest

None declared.


Address for correspondence

Soumya Ranjan Rana, MCh
Department of Neurosurgery, All India Institute of Medical Sciences
Jodhpur 342005, Rajasthan
India   

Publication History

Article published online:
20 August 2025

© 2025. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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Zoom
Fig. 1 Intraoperative neuromonitoring graph of the mentalis and orbicularis oris muscle in a case of hemifacial spasm undergoing microvascular decompression. Here, there is a disappearance of lateral spread response as soon as the Teflon patch is placed, thereby achieving adequate decompression of the facial nerve.
Zoom
Fig. 2 A neuromonitoring graph showing the early disappearance of lateral spread response in the mentalis muscle, before adequate microvascular decompression was achieved.