Delayed Unilateral Soft Palate Palsy without Vocal Cord Involvement after Microvascular Decompression for Hemifacial Spasm
A 33-year-old female was presented to our out-patient clinic with a history of left hemifacial spasm for 5 years. Her past medical history was unremarkable. The patient underwent microvascular decompression in 2010 at our medical center ().\nIntra-operatively, bilateral facial electromyography and brain stem auditory evoked potential was monitored. After the dura incision, gentle retraction of the cerebellum was applied using Greenburg retractor and we have exposed the lower cranial nerves. Dissection of the arachnoid was done from the rostral border of the lower cranial nerves. The arachnoid band was very tough and difficult to dissect, but no obvious injury occurred to the lower cranial nerve during the dissection. The left anterior inferior cerebellar artery was the offending vessel compressing the facial nerve from the caudal side and decompression was successfully completed without any adverse events and with no change in the intraoperative monitoring of brainstem auditory evoked potential. Patient recovered well from anesthesia with reduced facial spasm, compared to the pre-operative state. Postoperatively, neurologic exam revealed no abnormalities and also patient's swallowing and vocalization function was intact. Immediate postoperative brain CT scan performed on postoperative day showed no sign of hemorrhage.\nOn postoperative 5th day, the patient started to exhibit hoarsness with swallowing difficulty. Barium swallowing test was done to evaluate dysphagia, and minimal nasal regurgitation was demonstrated due to unilateral soft palate palsy. On endoscopic exam, performed by an otolaryngologist, the vocal cord was intact in both sides with unilateral left soft palate palsy, which suggested tensor and/or levator veli palatini muscle weakness (). Under the impression of possible lower cranial nerve palsy caused by postoperative edema of the nerve, steroid (prednisolone) was prescribed and we decided to observe the symptoms. Symptoms persisted with slight improvement with steroid therapy but repeatedly aggravated with steroid tapering. She received speech rehabilitation therapy for persistent difficulty of phonation and swallowing.\nOn postoperative 19th day, patient complained of difficulty breathing during sleep. Polysomnography was done to evaluate sleep apnea. Mild obstructive sleep apnea syndrome was observed secondary due to soft palate palsy. We encouraged her to sleep on her side; then her symptom improved.\nDespite persistent speech rehabilitation, symptoms still persisted. We performed cranial nerve MRI to evaluate for the possibility of any structural abnormalities, such as delayed hematoma or possible infection. However, MRI showed no abnormal structural lesions or abnormal enhancement, which may suggest infection (). The patient continued to receive speech rehabilitation with subjective improvement of swallowing and speech.\nOn postoperative 25th day, the patient developed grade II facial palsy by House-Brackmann grade on the left side. Patient's facial palsy improved with administration of acyclovir for 5 days, but hoarseness with swallowing difficulty showed little improvement.\nThe patient received prolonged speech and swallowing rehabilitation therapy, and follow up examination was done before discharge showed improvement of nasalization, but persistent hypernasality. Patient was discharged with recommendation for prolonged rehabilitation.\nPatient visited our out-patient for a follow up in postoperative 2 years. Endoscopic examination revealed normalized soft palate palsy and no abnormality in the vocal cord mobility (). However, patient's subjective difficulty of speech still persisted and we decided to observe her symptoms for any changes in the future.