Palsy 7 James M. Gilchrist

Abstract Facial neuropathy is the most common cranial neuropathy, due to its extensive course and multiple sites of potential . The causes of facial neuropathy are many, but 70% are diagnosed as Bell’s palsy, an idiopathic syndrome but increasingly being associated with virus infection as the cause of the majority of cases. Ramsay Hunt syndrome (herpes zoster oticus) is the second most common cause. Facial neuropa- thy causes weakness of the muscles of facial expression on the ipsilateral side, and can be distinguished from a central, or upper motor neuron, caused by the involvement of forehead muscles. Taste, hearing, salivation, lacrimation, and sensation over the ipsilateral ear and the face may also be disturbed. Diagnosis can be confi rmed by electrodiagnostic testing or MRI but is often not necessary. Treatment is directed at the underlying cause. In cases of Bell’s palsy a short course of steroids has been shown effective, if started within 72 h of onset. Treatment with antiviral agents against herpes virus is probably best reserved for patients with severe or complete facial neuropathy or those with Ramsay Hunt syndrome.

Keywords Antiviral agents • Bell’s palsy • Herpes simplex • Herpes zoster • Lyme • Ramsay Hunt syndrome • Seventh cranial neuropathy • Steroids

J. M. Gilchrist , MD () , Warren Alpert Medical School of Brown University, Rhode Island Hospital , Providence , RI , USA e-mail: [email protected]

K.L. Roos (ed.), Emergency Neurology, DOI 10.1007/978-0-387-88585-8_7, 133 © Springer Science+Business Media, LLC 2012 134 J.M. Gilchrist

Introduction Pathophysiology and Pathogenesis

The facial nerve, also known as the seventh cra- Facial nerve palsy cannot truly be understood nial nerve, is the most commonly diagnosed without at least some knowledge of the anatomy cranial neuropathy. The reasons for this lie in its of the seventh cranial nerve (Fig. 7.1 ). The motor anatomy and its obviousness. The facial nerve has root of the facial nerve arises in the facial nucleus both an intracranial and an extracranial course, in the lateral pons. Fibers leaving the nucleus taking three signifi cant bends along the way and execute a loop (the internal genu of the facial traversing several potential points of diffi culty nerve) around the nucleus of the , (lateral pons, cerebellopontine cistern, the bony traveling medially from below to above the sixth facial canal which it shares for part of the way nerve nucleus before exiting at the pontomedul- with the acoustic nerve, the inner ear, the parotid lary junction. The motor root then traverses the g land). And facial nerve palsy is the absolute cerebellopontine cistern to enter the internal manifestation of being “in your face.” The facial acoustic canal. The sensory root of the facial nerve provides innervation for muscles of facial nerve is separate from the motor root between the expression, which is a primary mode of express- brainstem and the internal acoustic canal and is ing emotion in humans and an important aspect of often called the nervus intermedius. Within the nonverbal communication, as well as a major aes- nervus intermedius are sensory fi bers which end thetic component of beauty. As such, we are espe- in the spinal nucleus of cranial nerve V, and para- cially attuned to facial movement and any sympathetic fi bers. asymmetry is immediately evident and upsetting. In the internal acoustic canal, the now-whole Patients do not sit at home and wait out a new facial nerve is accompanied by the eighth cranial facial palsy. They set out for the emergency room nerve. The nerves travel to the meatal foramen soon after onset and with considerable anxiety. (“porous acusticus”), which is divided into bony compartments, to then enter the facial canal, also called the fallopian canal. The meatus is the nar- Epidemiology rowest portion of the entire facial canal, less than 0.7 mm [8 ] . The facial nerve then enters the laby- Facial neuropathy is a common neurologic syn- rinthine portion of the facial canal, so called drome, and 70% will be diagnosed as Bell’s palsy because it is close to the superior semicircular [1 ] . The annual incidence of Bell’s palsy is 25 per canal. The labyrinthine canal ends at the genicu- 100,000 [ 2] with a lifetime risk of 1 in 60–70 [ 3 ] . late ganglion, where the cell bodies of the sensory Males and females are affected equally and the and parasympathetic neurons are located. The frequency per decade of life is remarkably simi- greater petrosal nerve branches off at the genicu- lar between age 10 and over 70 years of age [ 2 ] . late ganglion to head to the sphenopalatine and There is no preference between right and left pterygopalatine ganglia, from whence it supplies sides, though bilateral involvement is rare, at the lacrimal gland with parasympathetic innerva- 0.3–2% [4 ] . tion. From the , the facial Ramsay Hunt syndrome is the second most canal takes its fi rst external genu, and is called the common cause of facial neuropathy and can occur tympanic segment. The nerve to the stapedius in children (16.7% of unilateral facial palsies) muscle branches off within the tympanic canal. and adults (18.1% of facial palsies) with nearly The tympanic segment ends as the facial canal equal frequency, though less so in children under makes its second external bend, this time at a 90° the age of 6 [ 5 ] . Zoster sine herpete looks to be angle. The fi nal intracranial part of the facial especially common in children between 6 and canal is called the mastoid segment and proceeds 15 years of age and may account for over a third in a vertical descent to the stylomastoid foramen of all facial neuropathies in that age group [ 6, 7] . where the facial nerve becomes extracranial. 7 Facial Nerve Palsy 135

Fig. 7.1 Anatomy of the seventh cranial nerve

The chorda tympani branches off in the mastoid the geniculate ganglion [ 10 ] . Increased rates of segment and then enters the tympanic cavity HSV genome fragments by PCR were seen in the before joining the lingual nerve. It sends pregan- saliva of patients with Bell’s palsy [11 ] , and PCR glionic parasympathetic fi bers to the sublingual also identifi ed such fragments in human genicu- and submaxillary glands. The chorda tympani late ganglia at autopsy [12, 13 ] . Murakami found also conveys taste from the anterior two-thirds of active HSV sequences in the endoneurial fl uid of the tongue. Once the facial nerve is extracranial, the facial nerve in patients with Bell’s palsy [14 ] , it divides into the posterior auricular branch and facial neuropathy was induced in animals by which supplies sensation to the auricle and pinna reactivating HSV [15– 18 ] . Reactivation of the of the ear, although it also has motor fi bers. Other HSV virus presumably causes infl ammation of terminal branches control muscles of facial the facial nerve in the facial canal, initially caus- expression, as well as branches to the digastric ing demyelination, but if severe, causing axonal and stylohyoid muscles. damage and Wallerian degeneration distal to the The potential causes of facial neuropathy are lesion [19 ] . protean (Table 7.1 ), as are the related pathophysi- Ramsay Hunt fi rst described the condition ologies. There is mounting evidence that Bell’s which bears his name in 1907 [ 20 ] . Ramsay Hunt palsy is associated with herpes simplex (HSV) syndrome is defi ned as a peripheral facial neu- infection. McCormick fi rst postulated a connec- ropathy accompanied by an erythematous vesicu- tion with HSV infection in 1972 [9 ] , and several lar rash of the ear (herpes zoster oticus) or mouth lines of evidence support that up to 79% of Bell’s [ 20] . The infection involves the contiguous facial palsy is caused by reactivated HSV infection in nerve in the tympanic segment, leading, as in 136 J.M. Gilchrist

Table 7.1 Causes of unilateral seventh cranial neuropathy Relatively common Parasitic (trichinosis, Bell’s palsy (idiopathic) neurocystercercosis) Herpes simplex virus Infl ammatory Ramsay-Hunt syndrome (herpes zoster) Leukemia (children) Lyme Infections Zoster sine herpete HIV seroconversion Trauma Osteomyelitis of skull base mellitus Otogenic infections Pregnancy Parotitis/abscess Guillain–Barré syndrome Sarcoid Leprosy Neoplastic meningitis Poliomyelitis Pontine infarct Mycoplasma Pontine hemorrhage Infl uenza Multiple sclerosis Miscellaneous Brainstem tumor Benign intracranial hypertension Facial neuropathy from forceps/birth trauma Melkersson–Rosenthal Acoustic neuroma Amyloidosis Relatively less common Wegener’s granulomatosis Pontine Polyarteritis Encephalitis Sjogren’s syndrome Abscess HTLV-1 Congenital/postnatal Hereditary neuropathy with Mobius syndrome pressure palsies (HNPP) Hemicranial microsomia Familial Bell’s Congenital lower lip CIDP Charcot-Marie-Tooth Albers-Schoenberg () Histiocytosis X Infantile hypercalcemia Interferon therapy Cardiofacial syndrome Sclerosteosis Tumor Ethylene glycol intoxication Meningioma Wernicke–Korsakov syndrome Stevens-Johnson syndrome Metastatic Neurinoma Parotid tumor Meningitis Infectious Bacterial Fungal Tuberculous Syphilis

Bell’s palsy, to infl ammation, edema, demyelina- Only 11 had CSF pleocytosis, and nine had ele- tion, and potentially, axonal damage. Ramsay vated protein concentration, and he suggested Hunt syndrome can be seen in the absence of a that meningitis might occur concomitantly with rash (zoster sine herpete) when accompanied by facial neuropathy but not as a cause of facial neu- either a fourfold rise in varicella zoster virus ropathy [22 ] . (VZV) antibody or detection of VZV DNA [ 20 ] . This may occur in anywhere from 2.4% to 19% [5, 21 ] of patients who otherwise might have Clinical Features been thought to have Bell’s palsy. The cause of Lyme facial neuropathy is likely Facial neuropathies can affect either sex and not from meningitis. Halperin examined the CSF occur at any age [2 ] . Facial neuropathies are of 31 patients with Lyme facial neuropathy [ 22 ] . nearly always unilateral [ 4 ] , with only 1–2% 7 Facial Nerve Palsy 137 being bilateral. The most obvious fi nding on severe to complete paralysis in 52% of adults and examination is facial paresis or paralysis ipsilat- 44% of children [5 ] . Age over 50 years, complete eral to the neuropathy, involving all muscles of paralysis and lack of nerve excitability are poor facial expression, although to potentially varying prognostic factors [ 24] . Between 80% and 85% degrees. This is in contradistinction to facial will have a good recovery [ 5 ] . Unlike Bell’s weakness from a lesion above the level of the palsy, other cranial neuropathies (VIII, IX, or X) pontine facial nucleus (such as from a ), are frequent, with up to 53% of adults suffering which will cause weakness of contralateral lower hearing loss, which did not improve in 38% [ 5 ] . only, sparing the frontalis muscle. Tinnitus and vertigo are also common [5 ] . The facial nucleus receives cortical innervation Cranial neuropathies occur in 5–10% of for muscles of the upper face from both cerebral patients with and 80% are facial hemispheres, but only from the contralateral neuropathies [25 ] . Lyme disease is a relatively cerebral hemispheres for lower facial muscles. frequent cause of bilateral facial neuropathy. Facial neuropathies proximal to or at the level Unilateral or bilateral facial palsies are the most of the geniculate ganglion will also cause hypera- frequent neuropathic manifestation, accounting cusis due to paralysis of the stapedius muscle, but for 50% of patients with neurologic involvement there will not be any hearing loss from an isolated [26 ] . Residual symptoms of Lyme-associated facial neuropathy. In addition, salivation and lac- facial neuropathy are uncommon, with complete rimation will be hindered or lost altogether due to or near-complete recovery in over 90%, even damage to parasympathetic fi bers. Lesions at or without treatment [ 22, 27 ] . Peripheral Lyme sero- proximal to the second external genu (i.e., in the logic testing is abnormal in 90% of patients at the tympanic segment of the facial canal) will result time of facial neuropathy but can also become in dysgeusia and from damage to the positive subsequently [ 22 ] . Western blots are usu- chorda tympani. Sensation over the ipsilateral ear ally negative, consistent with facial neuropathy lobe will be affected in any facial neuropathy being a very early manifestation of Lyme disease, proximal to the stylomastoid foramen. Subjective and is also uncommon [ 22 ] . and/or objective numbness over the paretic por- The time course of recovery from facial palsy tions of the face is also not uncommon [ 2 ] . This is is dependent on the type and degree of pathophys- presumed due to connections between the maxil- iologic lesion. A neurapraxic, or purely demyeli- lary branch of the and the sphe- native, lesion will recover within days to weeks nopalatine ganglion [23 ] . Pain early in the course as the Schwann cell remyelinates the affected is present in a signifi cant minority of patients with segment. More severe lesions resulting in axonal Bell’s palsy [2 ] and a high proportion of patients damage and distal Wallerian degeneration will with Ramsay-Hunt disease [20 ] . As the orbicu- take longer to recover function as nerve regenera- laris oculi will be weak, inhibiting complete eye tion will be required. The regeneration may well closure, protection of the cornea is important, be incomplete, resulting in the major sequelae of especially at night when the patient is asleep. Eye facial palsy, which are persistent paresis or paral- lubrication and taping the eye shut should be ysis, corneal injury secondary to incomplete eye- instituted immediately in any patient with incom- lid closure, facial muscle contracture, and plete eye closure. Patching the eye alone is not synkinesis [ 28 ] . Synkinesis is the phenomenon appropriate, especially with gauze, as that will whereby the intended activation of one muscle wick away lacrimation, and hasten corneal injury. will result in contraction of other muscles as well. Other cranial nerve abnormalities, such as hear- This cocontraction may be due to either aberrant ing loss, tinnitus, dysphagia, dysarthria, and nerve fi ber regeneration or to ephaptic transmis- diplopia, often accompany secondary causes of sion. Facial synkinesis can involve motor nerve facial neuropathy and require further evaluation. fi bers as well as fi bers to the lacrimal and saliva- In Ramsay Hunt syndrome, tory glands, resulting in the so-called crocodile reaches maximum by 1 week after onset with tears phenomenon, in which gustatory salivation 138 J.M. Gilchrist causes tearing as well. Facial synkinesis is seen of normal, full-complete recovery can be expected in the majority of patients with Bell’s palsy who at 2 months after onset [33 ] . have evidence of axonopathy [28 ] . Latency of the direct facial motor nerve stimu- lation is not as useful as amplitude measurement [ 34] . When done 5–7 days after onset, three types Diagnosis of evoked responses are found: normal, which virtually assures patients of a complete recovery The diagnosis of facial palsy does not require without aberrant recovery; prolonged latency sophisticated testing and should be possible using compared with the opposite side, with frequent bedside acumen. The most common diagnostic good recovery but some chance of synkinesis; question for acute unilateral facial weakness is and no response, with high incidence of synkine- between facial neuropathy and a stroke, and this sis and some patients with no recovery. should not be clinically diffi cult. Upper motor The blink refl ex is the electrical correlate of neuron, or “central,” facial weakness spares the the bedside corneal refl ex [32 ] . The blink refl ex forehead, does not cause , dysgeusia differs from direct facial nerve study in that it or pain, and usually involves symptoms and signs examines the trigeminal nerve and the pons in beyond the face. Examination of the ear, tym- addition to the facial nerve, and assesses proxi- panic membrane, and mouth for vesicles is mal segments of the facial nerve inaccessible to important and an ELISA screen for Lyme disease the direct stimulation technique. Facial motor is essential in any area endemic for the Borrelia synkinesis can be assessed by expanding the set burgdorferi -bearing deer tick, Ixodes scapularis . up for the blink refl ex to also include recording Lumbar puncture is not routinely indicated unless electrodes over the orbicularis oris or other facial there are complicating factors, such as multiple muscles [ 32 ] . The blink refl ex as a prognostic cranial neuropathies, signifi cant meningismus, or method has not been particularly helpful in that it other neurologic signs or symptoms implying offers little beyond direct facial nerve studies and involvement beyond the facial nerve. is limited by the same time constraints. The electrodiagnostic methods most com- At this time there is no electrodiagnostic tech- monly used to study the facial nerve are direct nique which reliably predicts prognosis in Bell’s facial motor nerve conduction studies (elec- palsy within the fi rst 24–48 h after onset. CMAP troneurography). Most patients referred to the amplitude comparing side-to-side difference at EMG laboratory because of a facial paresis are day 5–7 after onset appears to be the most reli- sent for a prognosis, which is directly related to able parameter for ultimate prognosis [30, 32 ] . whether the facial nerve lesion is demyelinative MRI with gadolinium enhancement allows or axonopathic. Electrodiagnostic studies are imaging of the abnormal facial nerve but is not quite useful for making that determination but usually indicated in isolated, unilateral facial are limited because Wallerian degeneration of neuropathy. A very high percentage of Bell’s motor nerve fi bers takes 5–8 days after axonal palsy patients will show enhancement, as will injury and NCSs will be of little prognostic value 50% of Ramsay Hunt disease patients [ 35 ] . before that time [29 ] . Enhancement can also be seen in Lyme-related Amplitude of the direct motor nerve evoked facial palsy. The only diagnostically reliable response 5–7 days after onset is probably the best abnormality is enhancement in the distal intrac- available method [30– 32 ] . When the CMAP analicular and labyrinthine segments [ 36 ] , but amplitude is less than 10% of that on the healthy other than confi rming the diagnosis, enhance- side, maximum recovery will be delayed 6–12 ment provides no indication of severity or prog- months and function will be moderately or severely nosis [35, 37 ] . Enhancement can persist for weeks limited. If the amplitude is 10–30% of the healthy or months after resolution of the facial palsy. For side, recovery may take 2–8 months with mild to patients suspected of secondary causes of facial moderate residua. If the CMAP amplitude is >30% neuropathy, MRI may be indicated to assess for 7 Facial Nerve Palsy 139 pontine lesions, cerebellopontine cistern and Bell’s palsy was hindered by few randomized internal acoustic canal masses, and meningitis. trials with limited number of patients. In the lat- est Cochrane review of steroids in Bell’s palsy, published in 2004, there were only four trials Differential Diagnosis with a total of 179 patients [38 ] . No signifi cant difference between steroids and nontreatment As discussed above, the primary initial differen- was found. Nearly the same conclusion was tial is between facial neuropathy and a stroke. reached by the authors of a Cochrane review of Once this has been clarifi ed in favor of facial antiviral agents in Bell’s palsy [ 39 ] . They found neuropathy, the differential is between Bell’s only three randomized trials which met inclusion palsy, an idiopathic facial neuropathy, and sec- criteria, with a total of 246 patients. Benefi t was ondary causes of facial neuropathy (see Table 7.1 ). again uncertain, as was harm. Bell’s palsy accounts for up to 70% of facial neu- Three recent studies and a meta-analysis have ropathy [1 ] . As mentioned above, clues to sec- helped to clarify the picture, although contro- ondary causes include involvement of other versy remains. In 2007, Hato et al. [ 40 ] published (with the exception of mild subjec- a prospective, randomized, multicenter, placebo- tive or objective sensory loss over the cheek), controlled trial of valacyclovir and prednisone and signs or symptoms of other neurologic versus placebo and prednisone. The valacyclovir involvement. Concomitant medical conditions dosage was 1,000 mg/day for 5 days, and predni- associated with facial neuropathy (see Table 7.1 ) sone was 60 mg/day for 5 days, 30 mg/day for 3 would also be reasons to look beyond Bell’s days, and 10 mg/day for 2 days. The overall palsy. The most common secondary cause is results indicated 96.5% of patients treated with Ramsay Hunt syndrome from herpes zoster oti- both valacyclovir and prednisone recovered ver- cus, which may account for up to 18% of facial sus 89.7% for those treated with placebo and neuropathies [5 ] , and will be mistaken for Bell’s prednisone, which was signifi cant at p < 0.05. But palsy if the external auditory canal, mouth, and the largest difference was in those patients with tongue are not examined for vesicles [20 ] . complete palsy, and if complete and severe palsy The presence of bilateral facial neuropathy, were grouped together, the absolute rate of while uncommon, provides a further clue to etiol- improvement increased to 9.1% (as versus 6.8% ogy. Bell’s palsy remains the most common cause in the entire group) [40 ] . [4 ] , but Guillain-Barré and Miller Fisher syn- Also in 2007, Sullivan et al. [ 41 ] published a dromes need to be considered, as do HIV infec- prospective, randomized, placebo-controlled trial tion, meningitis, a variety of pontine pathologies, of Bell’s palsy within 3 days of onset. There were and Lyme disease [4 ] . four groups, receiving either 10 days of predniso- lone, acyclovir, both, or placebo. The predniso- lone was dosed at 25 mg twice daily, and the Treatment acyclovir was 400 mg fi ve times daily. They ana- lyzed the fi nal outcome of 496 patients. In patients The pathophysiologic theory that Bell’s palsy is receiving placebo, 64.7% recovered by 3 months caused by infl ammation in the facial canal, pre- and 85.2% by 9 months. For steroid versus no sumably secondary to HSV reactivation, which steroid, 83% improved at 3 months versus 63.6%, leads to demyelination and, if severe, to axonal for an odds ratio of 2.44, and 94.4% improved loss, has led to the hypothesis that steroids and/or versus 81.6% at 9 months, an odds ratio of 3.32. antiviral agents will assist in the recovery from The antiviral outcome was different, with no per- Bell’s palsy and lead to lower long-term sequelae ceived benefi t: at 3 months, 71.2% on acyclovir such as paralysis, paresis, and synkinesis. and 75.7% not on acyclovir recovered, an odds Until recently, the assessment of whether ste- ratio of 0.86; and at 9 months, 85.4% on acyclo- roids or antivirals, or both, were benefi cial in vir and 90.8% not on acyclovir recovered, an 140 J.M. Gilchrist odds ratio of 0.61. They concluded that early Bell’s palsy with moderate paresis with steroids treatment with prednisolone in Bell’s palsy sig- alone, while reserving antiviral treatment for those nifi cantly improved the chance of recovery, but patients with severe to complete palsies [ 10 ] . for acyclovir “there is no evidence of a benefi t of Other treatments have been considered but acyclovir given alone or an additional benefi t of remain controversial. A Cochrane review of acu- acyclovir in combination with prednisolone” puncture in Bell’s palsy found six studies with 537 [41 ] . The benefi t of prednisone was present in patients but was unable to reach any conclusion patients with moderate facial weakness as well as due to poor study quality [ 45 ] . Surgical treatment severe palsy [42 ] . of Bell’s palsy has followed a changeable course, In 2008, Engstrom et al. [ 43 ] published another with the preferred site of decompression and tim- prospective, double-blind, randomized, placebo- ing changing over time [46, 47] . May, once an controlled trial of Bell’s palsy within 72 h of ardent advocate of surgical decompression, onset. Patients were assigned to either placebo changed his opinion to the belief it was of no ben- and placebo, prednisone 60 mg for 5 days plus efi t [ 48 ] . A more recent multicenter, prospective placebo, valacyclovir 1,000 mg three times a day trial of surgical decompression via a middle cranial for 7 days plus placebo, or prednisone and vala- fossa exposure utilized electroneurography and cyclovir. Eight hundred and thirty nine patients needle electromyography to select patients [ 46 ] . were assigned with 829 included in the intention- Patients seen within 3 days were placed on ste- to-treat analysis. The primary endpoint was the roids. At 14 days, those patients with total facial time to complete recovery. There was a signifi - paralysis and >90% decrease in motor amplitude cant decrease in the time to completely recover in compared to the unaffected side, and no voluntary the patients who took prednisone compared to MUPs on needle electromyography, were offered those that did not (hazard ratio of 1.40). However, . Nineteen patients who met the criteria had there was no difference in time to complete surgical decompression within 14 days, and 18 had recovery between those patients who took vala- good recovery. Eleven patients declined surgery cyclovir and those that did not (hazard ratio 1.01). and four recovered to a satisfactory degree and At 12 months, 72% of patients given prednisone seven had some recovery. Another seven patients recovered versus 57% for those who did not, and had decompression surgery after 14 days, and fared 58% for those given just valacyclovir. Synkinesis similar to those who had declined surgery. The was seen in 14% of the prednisone-treated group study was not randomized or blinded in any way, but was present in 29% of the nonprednisone- and the numbers are small. But it does bring back treated patients. into consideration early surgical decompression in Finally, in 2009, de Almeida et al. [44 ] pub- those patients with the worst prognosis [ 46 ] . lished a meta-analysis of 18 studies, containing There is a lack of prospective, randomized con- 2,786 patients, concerning and/or trolled trials in Ramsay Hunt disease. The largest antiviral agents in Bell’s palsy. Steroids were retrospective trial used oral prednisone and intra- found to signifi cantly reduce the risk of an unsat- venous acyclovir in 80 patients, divided by onset isfactory outcome (relative risk reduction of 0.69) of treatment [ 49 ] . 75% of those treated within 3 with a number needed to treat to benefi t one per- days recovered completely, down to 48% when son of 11. Antiviral agents alone did not reduce treatment was not started until days four through the risk of poor outcome, but when combined seven, and only 30% had complete recovery when with steroids, provided marginal benefi t than ste- treatment was delayed until after 7 days [ 20, 49 ] . roids alone. Oral antiviral dosages differ from what is effective These studies have confi rmed the benefi t of for HSV, requiring 3,000 mg/day of valacyclovir corticosteroids in the acute treatment of Bell’s or 4,000 mg/day of acyclovir for 7 days for VZV, palsy, if initiated by 72 h after onset. However, versus 1,000 mg/day of either for 5 days for HSV they have engendered further debate about the [10 ] and as they inhibit viral replication but do not role of antiviral agents. A reasonable course of destroy viruses, treatment must be initiated within action based on these studies would be to treat 3 days to be effective [ 10 ] . 7 Facial Nerve Palsy 141

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