6 Cranial Nerve VII: Facial Nerve Disorders

10.1055/b-0040-174405

6 Cranial Nerve VII: Facial Nerve Disorders

Matthew Kircher, Abigail Thomas, and John Leonetti

Abstract

A cost-effective approach to facial nerve disorders starts with a complete history and physical examination. The routine use of imaging, laboratory, and/or electrophysiologic studies is typically not warranted in the most common case of facial paralysis, Bell’s palsy. The cost of addressing Bell’s palsy can be significant, and the routine use of ancillary testing in a situation where the result is unlikely to alter diagnosis or treatment is not cost-effective. However, other causes of facial paralysis need consideration, and this analysis begins once again with the history and physical examination. Selective testing is therefore warranted on an individual basis with sufficient clinical suspicion.

6.1 Introduction

The facial nerve is responsible for a myriad of head and neck functions: innervating motor fibers to the muscles of facial expression and middle ear, taste receptors from the anterior two-thirds of the tongue, parasympathetic fibers to salivary glands, and somatic afferents from the external auditory canal and pinna. This nerve takes a long anatomic course through the cerebellopontine angle, temporal bone, and parotid gland, and may be at risk of injury due to inflammatory, infectious, neoplastic, traumatic, and congenital disorders. Facial nerve disorders result in life-changing functional and social deficits for many patients. About one-half of 22,594 patients surveyed at the Edinburgh facial palsy clinic demonstrated a considerable degree of psychological distress and restriction in social activities as a consequence of their facial palsy. ¹ The workup of this disorder requires an in-depth understanding of anatomy and pathophysiology in order to provide efficient, cost-effective diagnoses and treatment.

6.2 Anatomy

The facial nerve exits the pontomedullary junction as a motor root and a mixed visceral root known as the nervus intermedius. The nerve traverses the cerebellopontine angle and enters the internal auditory canal along with the branches of the vestibulocochlear nerve before traversing the meatal foramen. The fallopian canal extends from the meatal foramen down to the stylomastoid foramen and consists of the labyrinthine segment, geniculate ganglion, horizontal tympanic segment, second genu, and vertical mastoid segment of the facial nerve. The meatal foramen is the narrowest segment of the fallopian canal with an average diameter of 0.68 mm, and it is in this region that the nerve can become compressed and dysfunction as a result of inflammation and/or trauma.

The greater petrosal nerve branches off the facial nerve at the geniculate ganglion and travels along the middle cranial fossa floor before exiting through the foramen lacerum toward the pterygopalatine ganglion to supply lacrimal and palatine glands. The nerve to the stapedius muscle branches at a point just distal to the second genu. The chorda tympani, carrying secretomotor fibers to salivary glands and taste fibers from the tongue, branches from the mastoid segment, passes under the tympanic membrane, and continues anterior to join the lingual nerve. The remaining facial nerve fibers emerge at the stylomastoid foramen to supply motor function to the muscles of facial expression (▶Fig. 6.1). ²

**Fig. 6.1** Facial nerve anatomy (Adapted from Carter HV, Gray H. Anatomy of the Human Body; 1918. Bartleby.com: Gray’s Anatomy, Plate 788.)

6.3 Clinical Assessment

History and physical examination are the most important step in evaluating facial paralysis. Timing of onset, degree of weakness (partial vs. complete), duration, and associated signs and symptoms should dictate the diagnostic workup. Patients will commonly present to an emergency department (ED) or primary care physician. The cost-effective evaluation of these patients begins with these front-line care providers to assess the patient and exclude identifiable causes of facial paresis or paralysis.

Comprehensive history and physical examination are the most readily available, informative, and cost-effective method of determining etiology of facial nerve disorder. This includes a complete head and neck examination with special attention to regional facial movement, facial resting tone, and parotid palpation. The patient may complain of dry eye secondary to incomplete eye closure (lagophthalmos) and decreased tearing ability due to loss of parasympathetic innervation of lacrimal gland by the greater superficial petrosal nerve. The efferent aspect of the corneal reflex may be absent or reduced if the motor branches to the orbicularis oculi are involved. Associated facial or auricular congenital or traumatic defects should also be noted. Sensation in the posterior auricular region can be painful or diminished, and patients may complain of hyperacusis due to stapedius muscle involvement and taste disturbance due to chorda tympani involvement. An otologic examination should document any periauricular vesicle eruption or middle ear lesions, and a neurologic examination should also be performed. The House–Brackmann (HB) scale (▶Table 6.1) may be used to classify and communicate the degree of facial paralysis.

**Table 6.1** House–Brackmann scale
Grade		Function
I	Normal	Normal facial function in all areas.
II	Mild dysfunction	Slight weakness noticeable on close inspection. At rest: normal symmetry of forehead; able to completely close eye with minimal effort. No to slight synkinesis.
III ^a	Moderate dysfunction	Obvious, but not disfiguring difference between sides; noticeable but not severe synkinesis, contracture, and/or hemifacial spasm. At rest: normal symmetry and tone. Motion: slight to no forehead movement, able to completely close eye with maximal effort and obvious asymmetry, and able to move corners of mouth with maximal effort and obvious asymmetry.
IV ^b	Moderately severe dysfunction	Obvious weakness and/or disfiguring asymmetry. At rest: normal symmetry and tone. Motion: no forehead movement; incomplete eye closure with maximal effort.
V	Severe dysfunction	Only barely perceptible motion. At rest: asymmetry. Motion: no forehead movement; incomplete eye closure and only slight lid movement with maximal effort; slight corner of mouth movement. Synkinesis, contracture, and hemifacial spasm usually absent.
VI	Total paralysis	Loss of tone; asymmetry; no motion; no synkinesis, contracture, or hemifacial spasm.
^aObvious but no disfiguring synkinesis, contracture, and/or hemifacial spasm are grade III regardless of motor ability. ^b Patients with synkinesis, mass action, and/or hemifacial spasm severe enough to interfere with function are grade IV regardless of motor ability.

6.4 Peripheral versus Central Lesions

An upper motor neuron lesion causing facial nerve weakness will spare the forehead muscles and leave the corneal reflex intact on the affected side because of bilateral innervation to this area. Patients presenting with isolated lower facial weakness with or without other focal neurologic findings require acute evaluation for an intracranial event. However, not all isolated lower facial weakness is due to an upper motor neuron lesion. An intraparotid lesion involving the lower division of the facial nerve and sparing the superior division can present in a similar manner. A peripheral or lower motor neuron lesion involves disruption of the nerve at any point from the facial nucleus to the parotid gland and will cause upper and lower face paresis or paralysis of the ipsilateral affected side with an impaired corneal reflex.

6.5 Diagnostic Studies

Diagnostic studies available to evaluate facial paralysis include computed tomography (CT), magnetic resonance imaging (MRI), electrophysiology, and lab studies. The fallopian canal is well defined on high-resolution CT, making this test useful in cases of suspected temporal bone pathology such as cholesteatoma, trauma, and neoplasm. MRI can be useful in patients with suspected retrocochlear pathology or parotid gland lesions. Electrophysiologic studies such as electroneuronography (ENoG) and electromyography (EMG) may have a role in selected cases of facial nerve injury offering prognostic information in patients with complete facial paralysis. Lab studies including Lyme titers and lumbar puncture can also be considered in cases of suspected infectious or inflammatory processes.

6.6 Differential Diagnosis

▶Table 6.2 provides a list of potential causes for facial paralysis. This chapter will focus on a cost-effective approach to some of the more common presenting facial nerve disorders.

**Table 6.2** Differential diagnosis of facial paralysis
Acute paralysis	Chronic or progressive paralysis
Polyneurities Bell’ s palsy Herpes zoster Guillain–Barre syndrome Autoimmune disease Lyme disease Human immunodeficiency virus infection Kawasaki’s disease	Malignancies Primary parotid tumor Metastatic tumor Benign tumor Schwannoma Glomus tumor Cholesteatoma
Trauma Temporal bone fracture Barotauma Birth trauma
Otitis media Acute bacterial Chronic bacterial Cholesteatoma
Sarcoidosis Melkersson-Rosenthal syndrome Neurologic disorders Human immunodeficiency virus infection Cerebrovascular disorder–central or peripheral
Source: Reproduced with permission from Mattox D. Clinical disorders of the facial nerve. In: Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology–Head and Neck Surgery. Philadelphia, PA: Elsevier; 2010:2391–2402.