Facial Nerve Paralysis Examination
The facial nerve provides motor, sensory, and parasympathic innervation to the head and neck. The functional and aesthetic consequences of facial nerve paralysis can potentially be physically and psychologically devastating. Facial palsy is almost invariably accompanied by severe emotional distress. A complete history and thorough examination should be the primary focus of the treating physician. The goal of this chapter is to simplify the clinical evaluation of patients with facial nerve pathology. There are distinct aspects of the history, evaluation, and treatment strategy that differ between patients with acute and chronic paralysis. We separate patients with chronic facial paralysis into the following four categories: facial paresis without synkinesis, facial paresis with mild synkinesis, facial paresis with moderate to severe synkinesis, and complete, flaccid facial paralysis.
History
The history for patients presenting with facial palsy serves to narrow the differential diagnosis ( Table 4.1 ). In the evaluation of an acute event, the onset and grade of the facial palsy are key determining factors for the etiology, prognosis, and additional laboratory and diagnostic testing. The priority during the evaluation of new onset facial paralysis without a clear cause (e.g., acoustic neuroma surgery, parotidectomy, trauma, etc.) centers on identifying the etiology of the paralysis and preventing ocular complications. All patients presenting with facial nerve paralysis should have the following documented:
Duration of paralysis
Onset: immediate versus progressive
Inciting factors: pregnancy, stress, etc.
History of previous facial nerve paralysis
Family history of facial nerve paralysis
Systemic medical conditions (autoimmune diseases, diabetes)
Skin changes or rashes around ear, face, neck, chest, or back
Prodromal symptoms such as nasal congestion, sore throat, fever, or arthralgias
History of perioral herpes simplex virus infection
Travel history
Otologic symptoms including ear drainage, hearing loss, vertigo, otalgia, or aural fullness
Recent tick bite or camping
Full oncologic history including cutaneous neoplasms of the face
Recent trauma
Past surgeries including surgeries to the ear and central nervous system
Neurological symptoms including cranial neuropathies, weakness, or tingling
In patients with long-standing facial nerve paralysis, it is equally important to obtain the history of initial paralysis as detailed previously. In addition, the functional and aesthetic concerns associated with chronic facial nerve paralysis need to be addressed. As aesthetic concerns are common in this population, it is important to document such information in the patient′s own words. The possible sequelae of chronic facial nerve paralysis include:
Nasal airway obstruction
Oral incompetence
Aberrant facial nerve regeneration leading to involuntary or uncoordinated facial movements (synkinesis)
Buccal mucosa irritation
Visual changes, ocular irritation, lagopthalmous, dry eye syndrome, epiphora, corneal ulceration, or blindness
Facial asymmetry due to flaccid atrophic muscles, loss of tone, synkinesis, or volumetric loss
Loss of dynamic furrows
Brow ptosis and asymmetry
Effacement or deepening of the nasolabial folds
Drooping or elevation of the oral commissure
Dimpling of the chin (peau d′orange)
It is imperative that an underlying neoplasm is ruled out in all patients with facial nerve pathology, both acute and chronic. The clinical features that raise our suspicion for a neoplastic entity include:
Slowly progressive facial paralysis
Additional cranial neuropathies
History or presence of suspicious skin lesion or cutaneous malignancy
Parotid mass
Facial twitching
Absence of facial nerve recovery 4 months after onset of symptoms
Concurrent sensorineural hearing loss, aural fullness, or tinnitus
Concurrent vestibular symptoms
Ipsilateral recurrence of facial paralysis
History of neoplasm
Any patient with these features requires additional radiological imaging (magnetic resonance imaging, computed tomography) to rule out underlying malignancy.
Physical Examination
Head and Neck Examination
In patients presenting with facial nerve paralysis, a complete head and neck physical examination is warranted. Particular focus is placed on the ear, mastoid, parotid gland, facial skin, and cranial nerves.
The external ear is examined for evidence of an erythematous or vesicular rash suggestive of Ramsay-Hunt syndrome, a condition caused by varicella zoster virus. The skin and scalp should also be inspected for scars that could indicate previous cutaneous neoplasm or traumatic injury.
The temporal bone and ear contents should be examined in a comprehensive fashion. The mastoid is palpated for tenderness that can be associated with fractures of the temporal bone or mastoiditis. Ecchymosis over the mastoid process following a traumatic event (Battle sign) is suggestive of a basilar skull fracture. Multiple middle ear processes such as acute or chronic otitis media, middle ear effusion, hemotympanum, tympanic membrane perforation, neoplasm, and cholesteatoma can cause facial nerve paralysis. In patients suspected of having middle ear pathology, it is imperative to perform a complete microscopic examination of the region or refer the patient to a neuro-otologist. If any abnormalities of the middle ear are appreciated or the patient subjectively complains of hearing loss, an audiogram is obtained.
The parotid gland should be palpated for masses or lesions that may impinge on the facial nerve. Sparing of individual branches of the facial nerve increases suspicion for a parotid neoplasm; however, this finding may also be observed with iatrogenic injury. The neck is palpated for masses such as metastatic nodes or parapharyngeal tumors.
A complete neurological examination including vestibular and cranial nerve testing is essential. Additional neuropathies raise suspicion for tumors of the temporal bone, skull base, nasopharynx, or central nervous system.1 Concurrent vestibulopathy in the setting of facial nerve paralysis is a poor prognostic sign. If clinical suspicion for a nasopharyngeal mass arises, fiberoptic examination of the nasopharynx is undertaken.
Facial Nerve Examination
The majority of patients with a peripheral facial nerve paralysis will demonstrate ipsilateral weakness of all muscles of facial expression, with only 2% of patients having bilateral involvement.1 Central etiologies of facial paralysis spare the frontalis muscle and are relatively rare.
During the facial nerve examination, all patients are asked to perform a variety of movements including forehead elevation, eye closure, nasal wrinkling, whistling, pursing of lips, soft smile, full smile, and showing of all dentition ( Fig. 4.1 ). The muscles of the forehead including frontalis, procerus, corrugator supercilli, and depressor supercilli are assessed. The frontalis, a brow elevator, is innervated by the frontal branch of the facial nerve, while the brow depressors such as the procerus, corrugator supercilli, and depressor supercilli have dual innervation from the frontal and zygomatic branches. Position of the eyebrows should be assessed for symmetry as well as location in relation to the supraorbital rim.
Periocular examination emphasizes the shape and function of the eye. Bell phenomenon, or upward rotation of the eye on attempted eye closure, should be confirmed in all patients. Patients with facial paralysis that demonstrate poor Bell phenomenon are at an exceedingly high risk of developing corneal ulceration and blindness if proper eye protection measures are not instituted ( Fig. 4.2 ). The height of the lateral canthus should be 2 mm superior to the medial canthal angle. The orbicularis oculi and the levator palpebrae are responsible for eyelid opening, closure, shape, support, and tear pumping. The orbicularis oculi receives dual innervation from the frontal and zygomatic branches. The levator palpebrae, an upper eyelid elevator, is innervated by the oculomotor cranial nerve and therefore not affected by facial nerve palsy. Normal palpebral fissure and ocular width is ∼12 mm and 29 mm, respectively. Patients with total facial paralysis have poor eye closure leading to lagophthalmos. On the other hand, patients with synkinesis often have narrowing of their palpebral fissure leading to asymmetric eyes.
The lower lid lash line should be positioned at the lower border of the lower limbus ( Fig. 4.3 ). If it is inferiorly displaced, then the patient has lower lid malposition. Marginal reflex distance–2 (MRD2) is the distance measured between the light reflex and central portion of the lower lid when a patient′s eye is in the neutral position. Lower lid malposition is present if the MRD2 is significantly > 5.5 mm. Lower eyelid tone and support should be verified by the snap and lid retraction test ( Fig. 4.4 ). If the lid does not snap back into its anatomical position within 1 second, the puncta displaces > 3 mm, or the lid distracts > 7 mm, lid laxity is diagnosed.
The midface region has significant arborization of the buccal and zygomaticus branches of the facial nerve and as a result, all muscles in this region likely have dual innervation. The buccal nerve is the dominant branch to the buccinators and supplies part of the dual innervation to the orbicularis oris and the depressor angulii oris. The zygomatic nerve is the dominant branch to the orbicularis oris, zygomaticus major, zygomaticus minor, levator angulii oris, levator labii superiorus, and levator labii superiorus alaeque nasi (all lip elevators). The mentalis, depressor angulii oris, depressor labii inferioris, and platysma are innervated by the marginal mandibular branch. The cervical branch of the facial nerve innervates the platysma muscle ( Table 4.2 ; Fig. 4.5 ). The marginal mandibular nerve is a terminal branch and as a result is less likely to recover from injury.
There are three types of smiles that can be appreciated: zygomatic, canine, and full denture ( Fig. 4.6 ). Zygomatic smile is dominated by the zygomaticus major and is present in 67% or the population. The canine teeth and lower teeth are typically not visible. Canine smile usually involves the activation of zygomaticus muscles as well as levator labii alequae nasi and is present in 31% of the population. Two percent of the population has a full denture smile where all upper and lower teeth are appreciated due to the activation of both elevators and depressors.2 Knowing the characteristics of the smile will allow the physician to better understand what procedures are necessary to create a natural appearing smile.