Cranial Nerve VII

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7 Cranial Nerve VII

Facial

Clinical Vignette

A 62-year-old judge became aware of subtle weakness of his left lower face that he first noted while shaving. Two months later, he noted that he could no longer close his left eye lid fully and he was having increasing weakness of the remainder of his left face. He was referred to a neurologist, who reassured him that he had a “benign” Bell palsy. He sought a second opinion when his facial weakness continued to worsen over another month with an inability to close the eye and to form a symmetrical smile.

Neurologic examination demonstrated weakness in all divisions of the left CN-VII with total inability to close his eye or form a left-sided smile. Palpation of the cheek demonstrated some fullness in the left parotid gland, with the remainder of his head and neck examination being normal. Complete neurologic and otoscopic examinations were unremarkable. Audiologic test results were normal, including the left acoustic/stapedius reflex. A corneal reflex was sluggish on the left but present bilaterally.

A left parotid gland biopsy demonstrated a malignant adenocarcinoma with extension beyond the capsule at surgery. He died of metastatic cancer 20 months later.

Comment: Fortunately, this case represents a relatively rare occurrence. However, it emphasizes that what may initially look routine and benign indeed may have a much more serious pathophysiologic mechanism. The issue in this case is to appreciate the history of a gradual evolution of the neurologic deficits in contrast to the relatively acute onset of idiopathic Bell palsy. Furthermore, Bell palsy is typically preceded by retroauricular pain and often associated with hyperacusis and loss of taste on the anterior two thirds of the tongue. When these symptoms are lacking, as in this instance, the pathoanatomic site is distal to the styloid foramen and potentially within the parotid gland as the facial nerve passes through its body. In addition, the gradual progression of this patient’s symptoms provided a strong suspicion of a neoplasm.

Facial nerve (CN-VII) lesions are the most common cranial mononeuropathy. This is one of the most complex cranial nerves having multiple functions (Fig. 7-1). It has a long and somewhat circuitous course with four primary components. (1) Motor fibers, which constitute the major division and serve the primary function of CN-VII: innervating the muscles of facial expression (unilateral, complete facial weakness is the hallmark of almost all facial neuropathies); (2) autonomic fibers, which are responsible for lacrimal, salivary, and mucous secretions; (3) special sensory fibers, which provide taste from the anterior two thirds of the tongue; and (4) general sensory fibers, which innervate the external auditory canal and a small area behind the ear.

When a patient presents with facial weakness, differentiation should be made between peripheral facial nerve lesions and CNS processes. With the latter, when the patient is relaxed, subtle suggestions of a facial nerve lesion may be appreciated by nasolabial fold flattening on the affected side. Brain lesions such as cerebral infarction, tumor, inflammation, or demyelination are often associated with other findings that can help with localization. For example, a small lesion near the Broca area may result in motor aphasia and facial weakness. Larger lesions affecting a significant portion of a hemisphere, as with large hemispheric strokes, cause a constellation of symptoms, including face, arm, and leg weakness and sensory loss; gaze deviation; and neglect or aphasia. Posterior limb lesions of the internal capsule result in face, arm, and leg weakness without sensory, visual, or cognitive changes. While peripheral facial weakness involves the upper and lower part of the face to the same degree, upper motor neuron lesions typically present with a gradient of weakness (Fig. 7-2), with relative preservation of movement in the brow and forehead (orbicularis oculi and frontalis muscles). This is due to presumed dual hemispheric innervation of the forehead muscles. In addition, corticobulbar tract involvement, as in various suprabulbar palsies, leads to absence of voluntary facial movement but retained reflexive movements such as in response to emotional stimuli.

Anatomy

Intrapontine Portion

CN-VII consists of two primary roots (Fig. 7-1). The larger division carries somatic motor fibers and has its origin within the facial nucleus in the caudal pons, where it lies adjacent to the spinal tract of the trigeminal nerve (CN-V). It then passes dorsally and rostrally to curve around the abducens nerve (CN-VI) nucleus (internal genu) and exits the brainstem at the bulbopontine angle between CN-VI and CN-VIII. Its smaller component, the nervus intermedius (intermediate nerve of Wrisberg), contains a combination of autonomic, special sensory (taste), and general sensory fibers. Its preganglionic parasympathetic fibers arise from the superior salivatory nucleus, relay through the pterygopalatine and submandibular ganglions, and eventually provide efferent function for lacrimation and salivation. The remaining intermediate nerve fibers carry taste and general somatic sensation and have their primary cell bodies in the geniculate ganglion and ultimately terminate within the nucleus solitarius and the spinal tract of CN-V, respectively.

Peripheral CN-VII

Both roots of CN-VII leave the brainstem to enter the temporal bone via the internal auditory meatus, where they accompany the auditory nerve (CN-VIII) passing through the internal auditory canal (Fig. 7-1, bottom). CN-VII continues to the periphery through the facial canal; this segment has five parts, based on their relation to surrounding anatomic structures. (1) The labyrinthine segment passes above the labyrinth and leads anterolaterally to the geniculate ganglions that contain the cell bodies of CN-VII afferents. (2) At this site, the canal abruptly turns posteriorly and forms the external genu of CN-VII. (3) The greater petrosal nerve originates here; it carries preganglionic parasympathetic fibers to the pterygopalatine ganglion, where they synapse and subsequently direct postganglionic fibers to the lacrimal gland. (4) The tympanic segment of CN-VII travels posteriorly and laterally along the medial wall of the middle ear. At the posterior wall of the middle ear, the facial canal changes its course and travels inferiorly toward its exit at the stylomastoid foramen. (5) The vertical portion is named the mastoid segment and has two important branches: proximally, the stapedius nerve arises to innervate the stapedius muscle; more distally, the chorda tympani branches and exits the facial canal and, after traversing the middle ear, joins the lingual nerve belonging to the third division of CN-V. The chorda tympani contains preganglionic parasympathetic fibers that synapse within the submandibular ganglion to innervate the submandibular and sublingual glands. The chorda tympani also carries taste fibers. Their cell bodies originate within the geniculate ganglion, mediating taste sensation from the anterior two thirds of the tongue.

Soon after leaving the skull at the stylomastoid foramen, the distal CN-VII gives rise to several small motor branches innervating the posterior auricular, occipital, digastric, and stylohyoid muscles (Fig. 7-1, top). The main motor trunk of CN-VII then passes through the parotid gland to terminate as the temporal, zygomatic, buccal, mandibular, and cervical branches. The first two innervate the muscles involved in moving the forehead, closing the eyes, and wrinkling the nose. Muscles of the lower face and neck are primarily innervated by the latter two branches. CN-VII subserves all muscles of facial expression except the levator palpebrae superioris and, therefore, CN-VII impairment, with a resultant asymmetric facies, is a major social and cosmetic impediment.

Clinical Correlations and Entities

The facial nerve can be damaged at any level along its complex course. Paralysis of the facial musculature is the hallmark of seventh cranial nerve lesions no matter what the lesion’s anatomic site. The clinical presence or absence of symptoms related to the various other components of the facial nerve is very important in identifying the lesion site.

The patient with a peripheral seventh (facial) nerve palsy in most instances, with the exception of an early very distal branch lesion within the parotid gland, loses function of the entire ipsilateral side of their face and cannot smile, close their eyelid (orbicularis oculi), or wrinkle (frontalis) their forehead.

When intrapontine (Fig. 7-3, #1) lesions affect the facial motor nucleus per se, as well as its exiting fibers, involvement of neighboring brainstem structures is typically seen. The association of peripheral facial paralysis with ipsilateral conjugate gaze palsy (paramedian pontine reticular formation lesion), ipsilateral lateral rectus palsy (sixth cranial nerve lesion), or paresis of the opposite arm and leg (corticospinal tract lesion) usually indicates a pontine localization.

Extramedullary lesions (Fig. 7-3, #2) affecting the seventh nerve as it enters its intracranial course primarily occur within the cerebellopontine (CP) angle. Most commonly these are benign, relatively large acoustic neuromas that initially involve the eighth nerve and later extend to produce a seventh-nerve lesion. Thus, diminished hearing, sometimes initially presenting with tinnitus, usually precedes the onset of this type of peripheral facial paresis (see Fig. 7-4). Occasionally, with very large CP angle tumors there is concomitant involvement of the ipsilateral fifth cranial nerve (trigeminal nerve V) with unilateral facial numbness or initially only loss of the corneal reflex.

A relatively proximal pregeniculate, intracanicular facial nerve lesion (Fig. 7-3, #3) characteristically leads to diminished lacrimation from greater petrosal nerve involvement as well as hyperacusis (an increased sensitivity to sound that is particularly noticeable while using a telephone), due to associated stapedius muscle paresis. These lesions also lead to diminished salivation, absent or altered taste sensation for the anterior two thirds of the tongue, and affected somatic sensation for the external auditory canal.

When a facial nerve lesion is more distally situated, between the geniculate ganglion and the stapedius nerve all of the above findings occur, but lacrimation is spared as the greater petrosal nerve has already exited the geniculate ganglion. If damage occurs in the facial canal, involvement of the stapedius nerve and the chorda tympani (Fig. 7-3, #4) leads to hyperacusis and impaired salivation and taste but no change in lacrimation. When the seventh-nerve lesion is distal to the chorda tympani, it is characterized by a pure ipsilateral facial weakness (Fig. 7-3, # 5). Very rarely, a lesion of this type occurs after the facial nerve exits the skull through the stylomastoid foramen. On occasion, this can cause diagnostic difficulty early on as it may initially involve just individual motor branches, with limited weakness of individual facial muscles before a complete palsy develops. Facial trauma is the most common cause for acute pure motor CN-VII lesions; however, an insidious progressive course suggests that a parotid adenocarcinoma, as illustrated in the vignette on p. 98, is the most likely cause.

Clinical Vignette

A vigorous 18-year-old woman awakened with a mild dull ache behind her left ear. While washing her face she noted an inability to smile on that side and that her left eye lid could not close. As a grandparent had recently had a stroke presenting with facial weakness, she rushed to the local emergency room for immediate physician evaluation. Her clinical examination demonstrated that she was unable to smile, close her eyelid, or wrinkle the forehead on the left. Her left eye was slightly injected and dry secondary to diminished tearing. She had no taste sensation on the anterior of the left tongue. The remainder of her neurologic examination was normal. No imaging studies were indicated.

A diagnosis of idiopathic Bell palsy was made; this patient was most relieved to have not had a stroke. As she lived in an endemic area for Lyme disease, specific antibodies were obtained before discharge on oral prednisone treatment. Over the next 2 months, she experienced a gradual and total return of her facial muscle function.

Comment: This is a classic case of idiopathic Bell palsy with no associated neurologic dysfunction or any specific evidence of systemic disorders predisposing to a facial nerve lesion. However, when the patient lives in an endemic Lyme disease region it is reasonable to check Lyme-specific antibodies before corticosteroids are prescribed.

Differential Diagnosis

The examiner needs to first differentiate between an upper, central, or a lower motor neuron peripheral facial paralysis. Patients with upper motor neuron paralysis primarily have lower facial weakness with an asymmetric smile or unilateral drooling, while the upper face is relatively spared. In peripheral facial palsy, all musculature innervated by CN-VII is affected.

Lyme disease is the primary identifiable infectious etiology that may present with an acute facial palsy; later on, a contralateral lesion may develop. Typically, there are other neurological signs such as headache or radiculitis and cerebrospinal fluid pleocytosis. In the uncommon circumstance of a Bell palsy associated with herpes zoster infection (Ramsay–Hunt syndrome), facial paralysis often precedes the appearance of typical herpetic vesicles within the external auditory canal. Middle-ear infection can rarely damage the facial nerve as it travels through the petrous bone. In regions endemic to tuberculosis, facial nerve palsies in association with petrous bone or mastoid process infections have been described.

Bilateral sequential Bell palsies are the most common neurologic manifestation of sarcoidosis. Frequently, associated hypothalamic–pituitary axis dysfunction (particularly impotence in men) and other cranial neuropathies are also present. Simultaneous bilateral facial weakness is an initial presentation of Guillain–Barré syndrome that is soon followed by the more classic rapidly progressive polyradiculoneuropathy. Leprosy may lead to bilateral facial nerve lesions but with a unique patchy distribution.

A slowly progressive evolution of a unilateral facial palsy most typically suggests the presence of a neoplasm. Pontine lesions, especially brainstem gliomas (Chapter 52), are the most proximal cause for a peripheral facial weakness. These tumors usually present in conjunction with other signs such as a lateral rectus palsy. Extramedullary tumors originating near the brainstem are often associated with facial nerve lesions and other cranial neuropathies, as with eighth-nerve acoustic neuromas or other cerebellopontine angle tumors (Fig. 7-4). When there is diffuse leptomeningeal involvement, such as with metastatic carcinoma or lymphoma, the facial nerves may be part of the initial clinical profile of infiltration with these malignancies. Eventually other and often multiple cranial nerves become involved, particularly the trigeminal, oculomotor, and optic nerves. As noted in vignette on p. 98, evolving, progressive, and purely motor facial palsies presenting with varying degrees of individual facial muscle involvement are classic for a parotid malignancy (Fig. 7-5).

Prognosis

The severity of the underlying facial nerve injury determines how quickly and completely recovery from Bell palsy occurs. The degree of injury ranges from mild, with pure demyelinating conduction block, to severe, with axon loss and resulting wallerian degeneration. Up to 90% of Bell palsy cases are caused by a demyelinating conduction block with little or no associated axon loss, and therefore, recovery is prompt, complete, and without synkinesis. The remaining patients have axonal damage with wallerian degeneration, and improvement requires regenerating axons to reinnervate paralyzed muscles, resulting in slow and incomplete recovery.

The recovery rate from Bell palsy follows two patterns: most patients begin to regain facial strength within 3 weeks after onset, but in some, the initiation of recovery is delayed for at least 3–6 months. The overall prognosis is good; most patients (80–85%) recover completely, but the rest may have various residual effects. These include synkinesis, residual weakness, tearing, or contracture. Synkinesis, the most frequent permanent sequel, clinically manifests as synchronized movement of different muscles that normally do not contract together. Typically, there is subtle eye closure with smiling, or a lip or chin twitch with blinking. Synkinesis occurs when there is a misdirection of regenerating axons into muscles that they originally did not innervate. This is rarely disabling but can be disfiguring and cause involuntary eye closure at inopportune times. Botulinum toxin injections have emerged as a symptomatic treatment of these abnormal movements. Another rare phenomenon following recovery of facial nerve injury is excessive lacrimation when eating (“crocodile tears”) and results from aberrant regeneration of salivatory fibers to the lacrimal glands.

An EMG provides valuable prognostic information, especially in those individuals not beginning to demonstrate improvement within the first few months after onset of Bell palsy. It should never be performed until approximately 3 weeks after onset. By then, it is possible to distinguish between nerve fibers that have undergone wallerian degeneration and those that are only temporarily blocked. A significantly reduced amplitude of the facial nerve compound muscle action potential and abundant fibrillation potentials in facial muscles indicates severe axonal damage, whereas a demyelinating conduction block is typically partially resolved by that time, evidenced by absent or scarce fibrillation potentials.

Infectious Facial Palsies

Lyme Disease

Clinical Vignette

Five weeks after returning from her family’s summer home in Old Lyme, Connecticut, this 32-year-old woman presented with left facial drooping and arm pain. Three days prior, she had woken up with severe pain behind the neck shooting down her right arm to the thumb. She noted difficulty holding a coffee mug to her lips.

Her temperature was 38°C (100.6°F). There was a 10-cm circular rash on the medial aspect of her right thigh. Her neck was slightly rigid; no intra-auricular vesicles were noted. Neurologic examination results demonstrated severe left facial weakness associated with loss of taste. On attempted eye closure, her left eyelids remained 6 mm apart. Her right biceps, brachioradialis, and pronator teres were weak. Right brachioradialis reflex was absent.

Brain computed tomography (CT) results were unremarkable. Lumbar puncture revealed a white blood cell count of 23/mm3, primarily lymphocytes, with a normal protein level and a slightly decreased glucose level. CSF and serum Lyme antibody test results were positive.

Comment: This vignette is typical of facial palsy secondary to Lyme disease (neuroborreliosis). At times, as in this case, facial weakness occurs with concomitant, often very painful, nerve root lesions. Although relatively uncommon, this classic syndrome of Lyme meningoradiculitis should always be considered, particularly in endemic areas.

Facial paralysis is the most common focal manifestation of neuroborreliosis; 40% of these patients have cranial neuropathies, and approximately 80% have CN-VII involvement. Multiple cranial nerves are affected in one fifth of those with a cranial neuropathy; two thirds with multiple cranial neuropathies primarily have bilateral facial palsy. Patients with an acute facial palsy in the presence of systemic signs, such as erythema migrans, or a history of possible exposure to disease-transmitting ticks warrant further studies for neuroborreliosis.

Standard CSF analysis usually demonstrates a pleocytosis with lymphocytic predominance. Confirmatory studies include titers of anti–Borrelia burgdorferi antibodies, and polymerase chain reaction detection of bacterial DNA in blood and CSF. Western blot improves sensitivity of serologic studies by identifying the specific antigens against which the patient generates antibodies. Facial paralysis may also occur before seroconversion, e.g., early in the disease before antibody testing results become positive. When clinical suspicion of Lyme disease is high, follow-up serologic tests are indicated.

Optimal treatment is still debated; the use of IV antibiotics is probably appropriate in severe cases with other manifestations such as headache or radiculitis, in the presence of CSF pleocytosis, or when parenchymal brain or cord involvement is suspected. Typical regimen consists of ceftriaxone (2 g daily) or cefotaxime (6 g daily) for 2 weeks. In mild cases with an isolated facial neuropathy, oral doxycycline (200 mg daily) for 2 weeks is felt to be an acceptable option. Once treated, the prognosis of facial palsy in Lyme disease is excellent, with most patients recovering completely.

Traumatic Facial Palsy

Clinical Vignette

A 40-year-old man was brought to emergency room after being hit by a motorcycle while crossing a busy street. He received a blow to the forehead as he fell on the pavement, and was knocked unconscious for 2 minutes. In the emergency room, he complained of headache and decreased hearing on the right side. Urgent ENT evaluation found fresh blood in the right meatus and a ruptured tympanic membrane. Neurologic exam demonstrated incomplete right peripheral facial weakness and loss of taste over the right anterior two thirds of the tongue. A high-resolution CT of the skull base revealed a transversely oriented fracture through the petrous bone, as well as right hemotympanum, pneumocephalus, and occipital soft tissue swelling. The patient was treated conservatively with complete resolution of the hearing loss and facial weakness within 3 months.

Comment: This is a rather typical case of traumatic incomplete facial paralysis and thus has a good prognosis in contrast to those who present with complete loss of facial nerve function.

Nearly all patients with facial palsy after blunt head trauma have a temporal bone fracture. Concomitant damage to CN-VIII, cochlea, labyrinth, or middle ear structures may produce hearing loss and vestibular dysfunction. Contusion, compression, and edema of the CN-VII have all been proposed as possible mechanisms of traumatic facial paralysis. Some of these processes can evolve gradually and lead to delayed facial palsy after several days. Immediate and complete facial palsy often indicates that the nerve has been transected, and portends a poor prognosis for functional recovery. In such cases, surgical exploration should be considered. Conversely, patients with incomplete weakness and with early signs of improvement, similar to the one in this vignette, usually achieve good recovery within months with conservative management alone.

Neuromuscular Disorders with Facial Weakness

The motor portion of the CN-VII nucleus as well as the respective brainstem nuclei of CN-V, -IX, -X, -XI, and -XII may be involved in various motor neuron diseases, particularly amyotrophic lateral sclerosis and bulbospinal muscular atrophy (Kennedy disease).

CN-VII is affected in 33–50% of Guillain–Barré syndrome cases and often bilaterally. Although usually evident when limb weakness is severe, CN-VII lesions may develop at any stage, including as the presenting sign. The Miller–Fisher syndrome, a variant of Guillain–Barré syndrome, is characterized by ophthalmoplegia, ataxia, and areflexia. However, involvement of cranial nerves other than CN-III, -IV, and -VI occurs in many cases. Facial weakness has been reported in nearly half of the Miller–Fisher syndrome cases, underscoring the important clinical overlap between classic ascending Guillain–Barré syndrome and Miller–Fisher syndrome.

Neuromuscular junction disorders (NMJDs), particularly myasthenia gravis (MG), often lead to bifacial weakness. This is a common finding in the majority of MG patients where there is associated ptosis and extraocular muscle involvement. Interestingly, although some patients with the less common Lambert–Eaton myasthenic syndrome have diplopia, ptosis, dysphagia, and dysarthria, facial nerve weakness is not found in this presynaptic NMJD.

Some primary myopathies may cause bilateral facial weakness, typically accompanied by wasting. In adult-onset myotonic dystrophy, muscles innervated by CN-III and CN-V, such as the levator palpebrae superioris and the temporalis, are also involved. Therefore, ptosis and jaw weakness often also occur. Congenital myotonic dystrophy may present with bilateral facial diplegia and is sometimes associated with severe neonatal hypotonia. Facial weakness occurs in 95% of patients with facioscapulohumeral (FSH) dystrophy who are younger than 30 years. It affects predominantly the orbicularis oris and is often asymmetric. Although facial weakness is rarely the presenting problem, most patients with FSH dystrophy reveal long histories of difficulties whistling or blowing balloons. Therefore, facial involvement is likely to be an early, slowly progressing sign.

CN-VII Hyperactivity

Several positive symptoms occur from excessive reactivity of CN-VII; synkinesis, facial myokymia, and hemifacial spasm are the most frequent.

Synkinesis is frequently observed subsequent to aberrant reinnervation in patients with antecedent severe Bell palsy; an inappropriate facial movement results, for example, concomitant blinking while smiling. Ephaptic transmission, or “artificial synapse,” may arise at a lesion site where depolarization of the injured fibers acts as a stimulus to the intact portion of the nerve.

Facial myokymia is characterized by subtle, continuous, undulating movement of facial muscles. The movements are usually unilateral, subtle, often confined to one to two facial muscles, and sometimes accompanied by facial contracture or weakness. Observed mainly in multiple sclerosis, it much less commonly reflects an intrinsic brainstem tumor, particularly pontine gliomas. In the former, it is usually self-limited and abates after several weeks. Some cases of facial myokymia are thought to be caused by antibody to a specific subtype of voltage-gated potassium channels. The specific antibody identified in some patients with facial myokymia also occurs with Isaac syndrome.

Hemifacial spasm consists of intermittent paroxysms of rapid, irregular, clonic twitching facial movements. The attack typically starts around the eyes and spreads to other ipsilateral facial muscles, especially in the perioral region. It is strictly confined to muscles innervated by CN-VII; preceding CN-VII lesions are rare. Paroxysms are often induced by voluntary or reflex facial movements, stress, and fatigue and may persist during sleep. The most common pathogenic mechanism for hemifacial spasm seems to be vascular compression of CN-VII by an aberrant arterial loop near the brainstem. Therefore, detailed imaging studies including MR angiography are essential for diagnosis of hemifacial spasm. Less frequent pathophysiologic mechanisms include tumors and localized infectious processes. Botox injections are an effective symptomatic treatment. Surgical decompression is an alternative sometimes leading to remission.

Diagnostic Modalities

Diagnostic modalities include imaging studies that may define direct involvement of CN VII or the presence of contiguous lesions. Other specialized testing modalities are used to study the various functions of CN-VII. Cerebrospinal fluid analysis is important in infections, Guillain–Barré syndrome, and if meningeal infiltration (usually cancerous) is suspected. The use of EMG in Bell palsy is discussed earlier in this chapter.

Intrinsic CN-VII Topognostic Testing Studies

Intrinsic CN-VII topognostic testing studies are based on the presence or absence of specific anatomic branch-point functions. With modern imaging studies, these are used less often but are occasionally valuable.

The Schirmer test of lacrimal flow depends on an intact geniculate ganglion, the site of the most proximal anatomic branch point along the course of CN-VII, giving rise to the greater superficial petrosal nerve. The greater superficial petrosal nerve carries autonomic fibers to the lacrimal gland. Decreased lacrimation based on Schirmer testing suggests involvement of the greater superficial petrosal nerve, or CN-VII proximal to the ganglion. An associated facial palsy eliminates the former two possibilities.

Evidence

Allen D, Dunn L. Aciclovir or valacyclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004;(3):CD001869. Review of data from three randomized studies including 246 patients found inconclusive evidence in regard to antiviral use in Bell palsy.

Engström M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valacyclovir in Bell’s palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol 2008 Nov; 976-977, 993-1000. A randomized, double-blind, placebo-controlled, multicenter trial of patients aged 18–75 years who sought care directly or were referred from emergency departments or general practitioners within 72 hours of onset of acute Bell palsy. Prednisone was effective but acyclovir was of no value.

Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:830-836. This review summarizes available evidence for the treatment of Bell palsy.

Halperin JJ, Shapiro ED, Logigian E, et al. Practice Parameter: Treatment of nervous system Lyme disease (Evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2007;69:91-102. This review summarizes available evidence on treatment of neuroborreliosis and issues evidence-based recommendations. Some of the controversies are also discussed.

Sullivan FM, Swan IRC, Donnan PT, et al. Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med 2007;357:1598-1607. This well-conducted randomized, multicenter, placebo-controlled trial compares effectiveness of early treatment with corticosteroids, acyclovir, or both, on outcome of patients with Bell palsy.