Modified hypoglossal-facial nerve anastomosis for peripheral-type facial palsy caused by pontine infarction: A case report and literature review

Abstract

Background: Peripheral-type facial palsy could be caused by a lesion in the tegmentum of the pons, such as infarction, with a rare occurrence. We herein described a case of unilateral peripheral-type facial palsy induced by dorsolateral pontine infarction and treated this patient using modified hypoglossal-facial nerve anastomosis.

Case presentation: A 60-year-old female presented with dizziness, hearing drop, diplopia, and peripheral-type facial palsy. Brain Magnetic Resonance Imaging showed a dorsolateral pontine infarction on the right side which exactly refers to the location of the ipsilateral facial nucleus or facial nerve fascicles at the pons. Subsequent electrophysiological examinations confirmed poor facial nerve function of this patient and modified hypoglossal-facial nerve anastomosis was then performed.

Conclusions: This case reminded medical practitioners not to ignore the possibility of involvement of a central cause in peripheral-type facial palsy patients. In addition, modified hypoglossal-facial nerve anastomosis served as a useful skill improvement that may help reduce hemiglossal dysfunction while restoring facial muscle function.

Keywords: Case report; Nerve anastomosis; Peripheral-type facial palsy; Pontine infarction.

Fig. 1

Representative photographs depicting the patient with right peripheral-type facial palsy. (A, B). Preoperative photographs demonstrating severe facial palsy. (C). The patient showed no movement of the right forehead and eyebrow (red arrowhead) compared to the contralateral healthy side while wrinkling with maximal effort.

Fig. 2

The brain MRI images showed a subacute infarction located in the dorsolateral to the right pons. (A, B). A lesion with hypo-intense signal or moderated-intense signal (red arrowhead) located in the dorsolateral to the right pons was revealed by T1 (A) or T2-weighted MRI (B), respectively. (C). Brain diffusion-weighted image showing no signs of acute pontine infarction. (D). MRTA shows no vertebrobasilar artery main trunk occlusion or stenosis.

Fig. 3

Schematic drawing illustrated the possible damaged facial nerve tract due to pons infarction in the case. (A). Anterior view of the brainstem, roughly showing the course of the facial nerve. (B). Cross-section through the pons at the level of the internal genu of the facial nerve. The facial nerve tract damage caused by pons infarction was marked by a blue oval.

Fig. 4

Preoperative electrophysiological measurement results. (A). Electroneuronography showed that the amplitude of the right facial nerve compound muscular action potential was significantly decreased compared to the healthy contralateral side. (B). Electromyography revealed the presence of insertional activity in the right facial muscles, with greatly reduced voluntary activity.