Approach to the Patient with Facial Weakness

John Leonetti

Sam J. Marzo

All human emotions and expressions are conveyed via the complex interactions of facial muscle groups innervated by the seventh cranial nerve (CN VII). Facial weakness or paralysis can, therefore, lead to both physical and psychological distress. The deficits are both cosmetic and functional. A logical assessment algorithm must be utilized in order to implement timely and effective diagnostic studies and treatment protocols.

I. ANATOMY

A. Central pathway.

The somatomotor cortex in the precentral gyrus provides facial nerve projection fibers, and the cell bodies in this area are primarily pyramidal nerve cells. Fascicles of the corticobulbar tract project through the internal capsule, through the basal part of the pons within the pyramidal tracts. Most of the nerve fibers decussate to reach the facial nucleus on the opposite side. Some fibers innervate the ipsilateral facial nucleus accounting for emotional control of facial expression.

The facial motor nucleus (7,000 neurons) is within the reticular formation beneath the fourth ventricle. The superior (ventral) facial nucleus receives bilateral cortical input, whereas the inferior (dorsal) portion of the facial nucleus receives only contralateral cortical input for lower facial musculature innervation; hence, the “forehead sparing” clinical finding in patients with a unilateral cortical (upper motor) versus a peripheral (lower motor) lesion.

In addition to the motor fibers of the facial nerve responsible for facial expression, there are sensory fibers for taste to the anterior two-thirds of the tongue (chorda tympanii), external auditory canal cutaneous sensation, along with parasympathetic fibers to the lacrimal, submandibular, and sublingual glands.

The facial nerve enters the internal auditory canal with the cochleo-vestibular nerve (CN VIII) and the nervus intermedius after leaving the pons and traversing the cerebellopontine angle.

B. Transtemporal.

The facial nerve is located in the antero-superior portion of the internal auditory canal. Upon entering its own fallopian canal, the dural covering is replaced with epineurium. The three intratemporal segments of the facial nerve are the labyrinthine, tympanic, and mastoid segments. The facial nerve exits the skull at the stylomastoid foramen.

C. Extratemporal.

The facial nerve exits the stylomastoid foramen and divides into the upper (temporofacial) and lower (cervicofacial) segments. A variety of anastomotic branching occurs between the commonly identified temporal, zygomatic, buccal, man dibular, and cervical branches of the facial nerve.

II. CLINICAL ASSESSMENT

A. History.

The single most important information obtained in the clinical history of a patient with facial paralysis is the rate of onset of the facial weakness. Acute onset of facial weakness, if nontraumatic, may be vascular or viral in origin. Subacute onset of facial
weakness is usually idiopathic (Bell’s palsy), whereas delayed, gradual, and progressive facial weakness may be caused by intracranial, intratemporal, or extracranial neoplasms.

Other important factors in the history of facial weakness include whether the deficit is unilateral or bilateral, any past history of similar facial weakness, a history of ipsilateral hearing loss, associated ear or facial pain, trismus, or temporal trauma.

A general medical history can also assist in the evaluation of facial weakness. Predisposing factors include patient’s age, hypertension, diabetes mellitus, cigarette smoking, and a prior history of facial weakness. Lyme’s disease, Sjogren’s syndrome, and a history of facial skin cancer may also be associated with facial paralysis.

B. Physical examination.

Upper motor neuron (UMN) facial weakness caused by a contralateral brainstem lesion above the level of the upper medulla oblongata affects only the lower facial muscles. The forehead movement and eye closure are normal. The corneal reflex and emotional facial movements are intact.

Lower motor neuron (LMN) lesions from the facial nucleus to the parotid gland cause weakness of all branches of the facial nerve. Complete paralysis is apparent with voluntary and emotional (involuntary) attempts to animate the face, and the corneal reflex is impaired (Table 15.1—House-Brackmann Scale).

TABLE 15.1 House-Brackmann Classification of Facial Function

Grade	Characteristics
I, normal	Normal facial function
II, mild dysfunction	Gross Slight weakness noticeable on close inspection May have slight synkinesis At rest, normal symmetry and tone Motion Forehead—moderate to good Eye—complete closure Mouth—slight asymmetry
III, moderate dysfunction	Gross Obvious, not disfiguring Noticeable synkinesis, contracture, spasm At rest, normal symmetry and tone Motion Forehead—slight to moderate movement Eye—complete closure with effort Mouth—slightly weak with maximal effort
IV, moderately severe dysfunction	Gross Obvious weakness and/or disfiguring asymmetry At rest, normal symmetry and tone Motion Forehead—none Eye—incomplete closure Mouth—asymmetric with maximum effort
V, severe dysfunction	Gross Barely perceptible motion At rest, asymmetry Motion Forehead—none Eye—incomplete closure Mouth—slight movement
VI, total paralysis	No movement

A complete neurologic examination may identify other focal findings such as other cranial nerve deficits, hemiparesis, hemisensory loss, sensorineural hearing loss (SNHL), or gaze palsy. Facial skin inspection may demonstrate a malignant lesion causing perineural invasion and facial weakness, whereas bimanual parotid palpation, especially in the patient with trismus, can identify a parotid gland malignancy as a cause for facial paralysis. Microscopic otoscopy will help disclose an infectious (acute otitis media) or neoplastic source of facial weakness within the middle ear of mastoid bone.

C. Diagnostic studies.

1. CT of the temporal bones is useful in patients with acute otitis media, temporal bone fractures, or suspected primary temporal bone tumors (facial neuroma, glomus tumor, and minor salivary gland neoplasm).

2. MRI with contrast is useful in patients with suspected brainstem, cerebellopontine angle, or parotid gland lesions.

Only gold members can continue reading. Log In or Register to continue