Electrical Testing for Facial Nerve Paralysis

Educational Objectives

The goal of this program is to improve management of facial nerve paralysis. After hearing and assimilating this program, the clinician will be better able to:

1. Use electrical diagnostic testing to predict outcomes in patients with facial nerve paralysis.

2. Develop management strategies for patients with facial nerve paralysis based on results of electrical testing.

3. Predict the degree of nerve injury and likelihood of full recovery based on the rate of Wallerian degeneration.

Summary

Sunderland classification of nerve injury: class I — neurapraxia; structures are intact, but signal is unable to travel through the nerve; class II — axonotmesis; axons are disrupted and Wallerian degeneration occurs; endoneurial tube is intact; full recovery is expected; class III — neurotmesis; neural tube is disrupted; risk for synkinesis is increased; class IV — epineurium is intact, but perineurium, endoneurium, and axons are disrupted; class V — complete disruption

Testing of nerve function: primary purpose — predict the likelihood of recovery; topographic test — each branch of the facial nerve is tested to determine the site of injury; does not predict recovery of function; not widely used; electrical diagnostic test — primary test used for prognostication; not required for patients with movement in the face (likely to have full regeneration) or those with single-branch weakness in the absence of surgery or trauma (should be worked up as possible cancer)

Nerve excitability test: compares the amount of current required to elicit minimal muscle contraction in healthy vs paralyzed sides (a difference of ≥3.5 mA between sides is considered significant); standardizing the test is difficult because results vary widely based on obesity status and sex

Maximal stimulation test: similar to the nerve excitability test but uses maximal muscle contraction; equal or slightly decreased responses are favorable for complete recovery; markedly decreased and absent responses indicate advanced degeneration with poor prognosis; however, the test is subjective and operator-dependent; used infrequently

Blink reflex test: electromyography (EMG) of the orbicularis oculi is obtained; the supraorbital nerve is stimulated and responses through the brainstem connection that causes blink reflex are measured; early (ipsilateral) response (R1) and late (bilateral) response (R2) are recorded; in facial nerve lesions, R1 is hypoexcitable and R2 is hyperexcitable; primarily used by neurologists to test brainstem reflexes

Evoked EMG (electroneuronography [ENOG]): most accurate for determination of prognosis; most useful when performed 3 to 21 days after onset (nonevoked EMG is more accurate for prognosis >21 days after onset); heights of compound action potential are compared between affected and unaffected sides; the amplitude of the compound action potential is proportional to the number of intact axons; degeneration of <90% in the first 3 wk indicates a high rate of spontaneous recovery, whereas degeneration >90% predicts poor prognosis

Limitations: uncomfortable; moderate test-retest variability, which can be overcome by stimulating multiple times to promote synchronization; performing multiple measurements in the same session allows for averaging values, which provides a more accurate number; however, relevance of test-retest variability is low if the compound action potential is decreased

Pitfalls: for chronic conditions (eg, facial schwannomas) that involve degeneration and regeneration of nerve fibers, there is variation in the pace at which axons in a nerve bundle regenerate, causing action potentials to travel at different rates; the action potentials do not stack, which creates the appearance of a flat line on ENOG (ie, dyssynchrony causes overestimation of the degree of degeneration)

Voluntary EMG: the patient is asked to move muscles in the face enervated by various branches during testing with needle electrodes; responses are recorded using surface electrodes; a couple of action potentials of the motor unit indicate good prognosis and no need for further therapy

Contraindications for ENOG: patients with facial movement or bilateral paralysis or who are <3 days or >21 days from the onset of paralysis

Electrodes: needle electrodes are usually used (surface electrodes are only used in children) and are placed in orbicularis oculi, orbicularis oris, frontalis, mentalis, and nasalis muscles

Prognosis: specificity is higher in the first 21 days, and sensitivity for poor prognosis is higher after 21 days; action potential of the motor unit with voluntary contraction during the first 14 days indicates early deblocking of conduction and high likelihood of recovery

Electromyography: biphasic or triphasic potential; fibrillation potential is observed with denervation of muscle; action potentials are observed 6 to 12 wk prior to clinical return of facial function and indicate functional return with recovery (degree of recovery is unpredictable); conduction block or neuropraxia — neural discharge occurs with electrical stimulation distal to the disruption; axonotmesis and neurotmesis — the segment distal to the injury has degenerated; regeneration of entire axon is needed; the segment distal to disruption cannot be stimulated; synkinesis occurs only with neurotmesis

Rate of Wallerian degeneration: duration after injury — <6 days likely indicates neurotmesis, and 14 to 21 days likely indicates axonotmesis; 6 to 14 days is associated with equal rates of neurotmesis and axonotmesis and a ≈50% chance of synkinesis; studies from the 70s and 80s — showed degeneration ≥95% associated with a low likelihood of return of facial function; patients with ≥10% of fibers that were stimulable had good outcomes and did not require intervention; full transection of nerve — occurs within 1 to 2 days and is followed by total loss of function; compression of nerve due to conduction blockage — occurs 14 to 21 days after injury; patients have good outcomes

Surgical decompression: 1999 study — surgical decompression of the middle cranial fossa was offered to patients with complete paralysis of the facial nerve and degeneration >90%; 58% of patients who received steroids only (ie, opted not to undergo surgery) had poor facial function (grade III or higher); 91% of patients who underwent surgical decompression within 14 days of onset had good outcomes; prompt testing is important to determine need for surgery

Iatrogenic injury to the facial nerve: may occur during surgery of the ear or parotid gland; if transection of the nerve occurs during surgery, exploration of the facial nerve for ≈5 mm on each side (or as much as possible) is recommended; testing — stimulation proximal to the injury is recommended at low level (≈0.5 mA); if no response occurs at low level, stimulation is increased to ≤1.0 mA and performed superior to cochleariform process; if loss of function is observed immediately after surgery, re-evaluate a few hours later to allow effects of lidocaine to wear off; long-lasting anesthetics — not recommended near the ear; the area in front of the mastoid tip or anterior to the ear below the tragus are the most common sources of paralysis of the facial nerve from injection of anesthetic

Management: administration of steroids and testing with ENOG after 72 hr is recommended; the speaker obtains voluntary EMG to identify whether the nerve is intact; if action potentials are not obtained from the face, ENOG is performed; degeneration >90% warrants exploration (monitoring is recommended for degeneration <90%); if symptoms worsen, exploration to reduce edema around the nerve may be considered

Blunt trauma leading to paralysis of the facial nerve: usually caused by extratemporal trauma around the mastoid tip or to the face; may occur with forceps delivery during birth; surgical exploration is usually not warranted because most cases result from conduction blockage, and recovery (normal or near-normal) occurs in >90% of patients; electrical testing is recommended when determining need for surgical management in patients with complete facial paralysis after temporal bone fracture; evoked and nonevoked needle EMG can be performed to determine whether the nerve is intact; ≥1 action potentials in the face is associated with full recovery; for partial loss of function or delayed paralysis, steroids are given and patients generally recover without issues

Penetrating trauma: the chance of transection is high and exploration may be warranted; for extratemporal injuries, exploration is not recommended if the injury is distal to the lateral canthus because nerve endings are difficult to find and the area has a rich anastomotic network; exploration should be performed within 3 days of injury because distal branches can be stimulated and distal segments are difficult to find; delayed exploration — may be warranted with gunshot wounds, depending on the type of gunshot and velocity of the bullet; waiting to perform electrical testing prior to surgery may be beneficial

Decompression of nerve in temporal bone: exposure of the area distal to the geniculate transmastoid muscle is usually possible; exposure of the pregeniculate segment may be possible in patients with good aeration of mastoid air cells; approach through the middle cranial fossa may be necessary if the geniculate transmastoid is inaccessible, although brain edema may be severe (not recommended in the early phase after injury); a translabyrinthine approach can be used for patients with no auditory or vestibular function; when working near the nerve, use of a diamond burr is recommended, ensuring ample irrigation for cooling; for hematoma or bruising of nerve, the speaker opens a small part of the nerve sheath if edema is present (more extensively if the nerve swells into the opening)

Case of 21-yr-old woman with bilateral paralysis: awakened with complete paralysis of the face 4 days after head trauma; computed tomography (CT) showed bilateral temporal bone fractures; evoked and voluntary EMG showed a single motor unit action potential around the eye on one side and one near the mouth on the other side, indicating that the nerve was intact; the patient was given steroids and had normal function 6 mo after injury

Case of child born after complex delivery with forceps: iatrogenic vs congenital causes — electrical silence on EMG indicates absence of neuromuscular junction and that paralysis is congenital; fibrillation potentials indicate injury and denervation, with significant disruption of the nerve; management of intact neuromuscular junction — wait and retest or perform imaging to identify the site of injury; intervention may be advised if a fracture is placing pressure on the stylomastoid foramen; if the site of injury cannot be identified on CT of the temporal bone, retesting after a waiting period is recommended; polyphasic potentials indicate return of function

Gradual onset of paralysis: gradual onset of paralysis or skin cancers on the face with partial paralysis of a single branch is suggestive of cancer; magnetic resonance imaging with contrast of the internal auditory canal and parotid gland is recommended

Case of patient with Bell palsy: reported complete paralysis 4 days after onset; primary care physician prescribed antiviral drugs and prednisone; management — perform ENOG and nonevoked EMG; consider decompression if degeneration is >90% and action potentials are not observed on EMG; if degeneration is <90%, testing should be repeated in 1 wk (or around day 12 of paralysis) and surgical decompression is considered if degeneration is >90%; if it has been ≈25 days since onset, the likelihood of improvement with surgery is low and steroids are recommended

Case of 38-yr-old physician: presented with marginal mandibular paralysis and weakness of the buccal branch after a subcision procedure performed on multiple areas of the face; the area with largest concentration of scars was medial to the lateral canthus; the patient reported return of normal nerve function 3 wk later

Readings

Ciorba A et al: Facial nerve paralysis in children. World J Clin Cases. 2015;3(12):973-979; Gantz BJ et al: Surgical management of Bell’s palsy. Laryngoscope. 1999;109(8):1177-1188; Grosheva M et al: Prognostic value of electroneurography and electromyography in facial palsy. Laryngoscope. 2008;118(3):394-397; Guntinas-Lichius O et al: Facial nerve electrodiagnostics for patients with facial palsy: a clinical practice guideline. Eur Arch Otorhinolaryngol. 2020;277(7):1855-1874; Kamble N et al: Peripheral nerve injuries: electrophysiology for the neurosurgeon. Neurol India. 2019;67(6):1419-1422; Ozgur A et al: Which electrophysiological measure is appropriate in predicting prognosis of facial paralysis?. Clin Neurol Neurosurg. 2010;112(10):844-848; Nash JJ et al: Management and outcomes of facial paralysis from intratemporal blunt trauma: a systematic review. Laryngoscope. 2010;120 Suppl 4:S214; Tolisano AM et al: Determining etiology of facial nerve paralysis with MRI: challenges in malignancy detection. Ann Otol Rhinol Laryngol. 2019;128(9):862-868.

Disclosures

For this program, the following has been disclosed: Dr. Djalilian is on the advisory board for Novus Therapeutics and is a cofounder of Beyond Tinnitus and Cactus Medical. The planning committee reported nothing to disclose.

Acknowledgements

Due to the COVID-19 pandemic, Dr. Djalilian was recorded using teleconference software, on June 2020. The Audio Digest Foundation thanks the speakers and sponsors for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

OT532001

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.