Recognition and Diagnosis

Dysfunction of the facial nerve can result in several undesirable effects. Clinical consequences from injury may cause either a defect in facial expression or a functional deficit and/or may leave the patient with a cosmetic deformity all of which may lead to psychosocial issues. Studies have shown the incidence of facial nerve injury following TMJ surgery ranges from 12.5 to 32%. The majority of these injuries tend to be temporary with full return to function within 2-6 months [14].

The surgeon should evaluate all patients for facial nerve injury in the postoperative setting. A thorough clinical exam should be performed and any injury documented. Since weakness can be subtle, it helps to compare the operated side to the non-operated side when surgery is unilateral. There are specific clinical findings that will be associated depending on which terminal nerve branch is

Table 5.3 Terminal branches and the action on the corresponding facial muscle


Facial nerve branch


Corrugator supercilii Procerus


Pulls the eyebrow medially and downward Pulls the medial eyebrow downward

Orbicularis oculi

Temporal and

Closes the eyelid and contracts the skin

Zygomatic major

zygomatic Zygomatic and buccal

around the eye

Elevates corners of the mouth

Zygomaticus minor Levator labii superioris Risorius Buccinator Orbicularis oris Levator labii superioris alaeque nasi


Elevates the upper lip

Elevates the upper lip and midportion

nasolabial fold

Aids smile with lateral pull

Pulls corner of the mouth backward and

compresses the cheek

Closes and compresses the lips

Elevates the medial nasolabial fold and nasal


Depressor anguli oris

Buccal and marginal

Pulls corners of the mouth downward

Depressor labii inferioris


Pulls down the lower lip


Marginal mandibular

Pulls the skin of the chin upward



Pulls down corners of the mouth

injured and what muscle is innervated (Table 5.3). Observation of any difficulty or inability in the patient to raise their affected eyebrow, wrinkle their forehead, completely close their eyelids (lagophthalmos), and/or smile symmetrically could signify a facial nerve injury. There may also be limitations or dysfunction to special functions such as lacrimation, salivation, and taste. Particularly with lagophthalmos, lack of treatment can lead to exposure keratitis, corneal ulceration, and blindness.

If there is clinical injury, classifying the degree and type of nerve lesion becomes important, particularly for prognosis and planning treatment. There is no “gold standard” method of grading these injuries due to the subjectivity of assessment and reporting. Attempts have been made to develop a universal objective measurement, ranging from a simple diagnosis with handheld calipers to using complex processes with digital photographic and videographic computer systems. Several classification systems have been devised, but since the 1980s, the House-Brackmann system has been the most widely accepted system [12, 15-17]. There are six grades to this system, with grade I indicating normal function of the facial nerve and grade VI indicating total paralysis. The system is limited by ambiguity to distinguish accurately among the finer grades of dysfunction [12] (Table 5.4).

In addition to clinical classification of facial nerve injury with the House- Brackmann grading scale, understanding the use of electrical musculature testing is helpful in diagnosing and future treatment of the nerve injury. The goal of electrodiagnostic testing is to help evaluate the degree of facial nerve injury and the functionality of the facial musculature. Commonly used electrical tests are the nerve

Table 5.4 House-Brackmann facial nerve injury grading system






Normal facial function



At rest: Normal symmetry and tone

Forehead motion: Moderate to good

Eye motion: Compete closure with minimum effort

Mouth motion: Slight asymmetry



At rest: Normal symmetry and tone Forehead motion: Slight to moderate Eye motion: Compete closure with effort Mouth motion: Slightly weak with maximum effort


Moderately severe

At rest: Normal symmetry and tone

Forehead motion: None

Eye motion: Incomplete closure

Mouth motion: Asymmetric with maximum effort



At rest: Asymmetry Forehead motion: None Eye motion: Incomplete closure Mouth motion: Slight movement


Total paralysis

No movement

excitability test (NET), maximum stimulation test (MST), electroneurography (ENoG), and electromyography (EMG) [12, 18]:

  • 1. Nerve excitability threshold (NET): Requires a Hilger nerve stimulator, with the extratemporal portion of the nerve stimulated with a small, pulsed DC current. The face is observed for the lowest current to produce a visible twitch.
  • 2. Maximal stimulation test (MST): Is a modified version of the NET, with an attempt to determine the difference between the strength and amount of contraction. Allows for interobserver variation.
  • 3. Electroneurography (ENoG): This exam adds the ability to record facial muscle action potential with surface or needled electrodes to the stimulation tests. Percentages based on compound action potential (CAP) are used for interpretation. Excellent recovery of facial function occurs when the CAP in ENoG does not reach 90%.
  • 4. Electromyography (EMG): Measures muscle action potential generated by spontaneous and voluntary action. Researchers have found that EMG had 80% accuracy in predicting a poor outcome 10-14 days after onset of paralysis.

Currently, there is no standard of care when to use nonoperative vs. operative management with electrodiagnostic testing. Research has shown surgical exploration is warranted when ENoG tests produce an amplitude ratio > 90%; NET shows a difference of 3.5 mA or the MST shows no reaction when combined with EMG. Electromyography alone provides important information that can also help determine treatment options. Typically, resting muscle exhibits no spontaneous electrical activity. In the setting of denervation from nerve injury, electrical activity may be increased, and spontaneous fibrillation potentials develop. These fibrillation potentials are strong evidence that denervation has occurred and may encourage the surgeon to surgically explore.

In combination with electrodiagnostic testing, understanding the Sunderland classification is an additional helpful tool that uses a histopathological description of the nerve injury when deciding whether surgical exploration or management is necessary. There are five classes to this system that are listed as follows:

Class I: There is no physical disruption of axonal continuity with supportive tissue elements remain intact.

Class II: Generally caused by pressure, will have axonal disruption without injury to supporting structures. Wallerian degeneration occurs and propagates distally from site of injury.

Class III: Endoneurium disruption occurs and Wallerian degeneration occurs similar to Class II.

Class IV: Perineural disruption, implying a more severe injury and potential for incomplete or aberrant regeneration is common.

Class V: Complete transection of the facial nerve, including epineural sheath, carries almost no hope for useful regeneration.

5.5.1 There are important clinical findings to these classes in relation to electrodiagnostic testing. When a Class I injury has occurred, the facial muscles cannot be moved voluntarily, but a facial twitch can be elicited by electrodiagnostic testing of the nerve distal to the site of injury. This is helpful to understand the nerve may not need surgical exploration with this result. Class II to V injuries will involve some form of axonal discontinuity. In these injuries, electrodiagnostic testing will fail to produce a propagated action potential and muscle contraction within 1 week. In the case of facial nerve injury, the delay in Wallerian degeneration results in continued electrical stimulation of the distal segment for 3-5 days. It is important to note that during these first few days after an insult, electrodiagnostic testing of any form cannot distinguish between the various classes of injuries [12, 18].

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