eMedicine Specialties > Neurology > Neurological Infections

Ramsay Hunt Syndrome

Augusto A Miravalle, MD, Fellow, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School

Updated: Aug 20, 2009

Introduction

Background

Ramsay Hunt syndrome is defined as an acute peripheral facial neuropathy associated with erythematous vesicular rash of the skin of the ear canal, auricle (also termed herpes zoster oticus), and/or mucous membrane of the oropharynx.

Herpes zoster oticus, day 6. Image courtesy of Manolette Roque, MD, Ophthalmic Consultants Philippines Co, EYE REPUBLIC Ophthalmology Clinic.

• VZV auricularis
• VZV in any of the zoster zones of the head and neck (herpes auricularis, herpes facialis, and herpes occipito-collairs) with facial palsy
• VZV in any of the zoster zones with facial palsy and auditory symptoms (eg, tinnitus, deafness, vertigo, nystagmus, ataxia)

Pathophysiology

Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) might be also involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy.  

VZV infection causes 2 distinct clinical syndromes. Primary infection, also known as varicella or chickenpox, is a common pediatric erythematous disease characterized by a highly contagious generalized vesicular rash. The annual incidence of varicella infection has significantly declined after the introduction of mass vaccination programs in most countries of the world.² After chickenpox, VZV remain latent in neurons of cranial nerve and dorsal root ganglia. Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome.

Frequency

United States

Ramsay Hunt syndrome is a rare complication of latent VZV infection.³ As stated above, Ramsay Hunt syndrome might occur in the absence of cutaneous rash (zoster sine herpete). Interestingly, VZV has been detected by polymerase chain reaction (PCR) in the tear fluid of patients diagnosed with Bell palsy.⁴  Ramsay Hunt syndrome is estimated to account for 16% of all causes of unilateral facial palsies in children, and 18% of facial palsies in adults. Ramsay Hunt syndrome is rare in children younger than 6 years.³

Ramsay Hunt syndrome is thought to be the cause of as many as 20% of clinically diagnosed cases of Bell palsy.⁴

The incidence of Ramsay Hunt syndrome among patients with HIV infection is unknown. However, it may occur at a higher rate than in the general population because individuals with HIV infection have a higher risk of VZV infection.¹

International

Similar frequency has been reported in other countries.

Mortality/Morbidity

Ramsay Hunt syndrome is not usually associated with mortality. It is a self-limiting disease; the primary morbidity results from facial weakness. Unlike Bell palsy, this syndrome has a complete recovery rate of less than 50%.

Clinical

History

A careful history must be obtained in patients with suspected Ramsay Hunt syndrome.

• Patients usually present with paroxysmal pain deep within the ear. The pain often radiates outward into the pinna of the ear and may be associated with a more constant, diffuse, and dull background pain.
• The onset of pain usually precedes the rash by several hours and even days.
• Classic Ramsay Hunt syndrome can be associated with the following:
  • Vesicular rash of the ear or mouth (as many as 80% of cases)
  • The rash might precede the onset of facial paresis/palsy (involvement of the seventh cranial nerve [CN VII])
  • Ipsilateral lower motor neuron facial paresis/palsy (CN VII)  
  • Vertigo and ipsilateral hearing loss (CN VII)
  • Tinnitus
  • Otalgia
  • Headaches
  • Dysarthria
  • Gait ataxia
  • Fever
  • Cervical adenopathy
• Facial weakness usually reaches maximum severity by 1 week after the onset of symptoms.
• Other cranial neuropathies might be present and may involve cranial nerves (CNs) VIII, IX, X, V, and VI.
• Ipsilateral hearing loss has been reported in as many as 50% of cases.
• Blisters of the skin of the ear canal, auricle, or both may become secondarily infected, causing cellulitis.
• Poor prognostic factors for good functional recovery include the following:
  • Age older than 50 years
  • Complete facial paralysis
  • Lack of CN VII nerve excitability

Physical

• The primary physical findings in classic Ramsay Hunt syndrome include peripheral facial nerve paresis with associated rash or herpetic blisters in the distribution of the nervus intermedius.
• The location of the accompanying rash varies from patient to patient, as does the area innervated by the nervus intermedius. It may include the following:
  • Anterior two thirds of the tongue
  • Soft palate
  • External auditory canal
  • Pinna
• The patient may have associated ipsilateral hearing loss and balance problems.
• A thorough physical examination must be performed, including neuro-otologic and audiometric assessment.

Causes

• Classic Ramsay Hunt syndrome is ascribed to infection of the geniculate ganglion by herpesvirus 3 (varicella-zoster virus [VZV]).

Differential Diagnoses

Bell Palsy
Persistent Idiopathic Facial Pain
Postherpetic Neuralgia
Temporomandibular Disorders
Trigeminal Neuralgia

Other Problems to Be Considered

Adenocystic carcinoma
Carcinoma of the nasopharynx
External otitis
Otitis media
Referred pain
Dental infection or abscess
Labyrinthitis
Vertigo

Workup

Laboratory Studies

• The diagnosis of Ramsay Hunt syndrome is usually made without difficulty when the clinical characteristics are present. If necessary, varicella zoster virus (VZV) may be isolated from vesicle fluid and inoculated into susceptible human or monkey cells for identification by serologic means.
• WBC count, erythrocyte sedimentation rate (ESR), and serum electrolytes are helpful in distinguishing the infectious and inflammatory nature of this syndrome.
• When CNS complications are suspected (eg, meningitis, meningoencephalitis, myelitis, arteritis [large and small vessel], and ventriculitis), spinal fluid analysis and CNS imaging studies are recommended.
• Viral studies include the following:
  • VZV isolation in conventional cell culture is considered the definite diagnostic test. However, growing VZV in cell culture can be difficult and is usually too slow to be clinically helpful.  
  • The sensitivity of conventional cell culture is 30-40%, with a specificity of 100%.
  • Other tests, including Tzanck test, electron microscopy, and polymerase chain reaction (PCR) are generally more rapid and sensitive. The sensitivity of conventional PCR technique is estimated to be 60%.
  • VZV has been detected by PCR in the tear fluid of patients with Bell palsy (prevalence, 25-35%).
  • VZV antigen detection by direct immunofluorescence assay (DFA) is also possible, with sensitivity of 90% and specificity close to 99%.⁵
  • Antibody determinations on paired sera may be helpful in establishing the diagnosis by comparing titers at time of presentation and a few weeks later.

Imaging Studies

• Structural lesions can be ruled out by CT scan, MRI, or magnetic resonance (MR) angiography.
• Gadolinium enhancement of the vestibular and facial nerves on MRI has been described in Ramsay Hunt syndrome.
• Recent advances in clinical MRI images (eg, 3-Tesla MRI, multichannel phased array coil, 3-dimensional fluid-attenuated inversion recovery [FLAIR]) allow the evaluation of subtle alterations at the level of the blood-labyrinthine barrier.⁶

Other Tests

• Audiometry usually reveals sensorineural hearing loss.
• Unilateral caloric weakness may be present on electronystagmography (ENG).
• Electrodiagnostic methods, such as facial motor nerve conductions studies (electroneurography), electromyography of facial innervated muscles, the blink reflex, and nerve excitability testing, could add information regarding the extent of seventh cranial nerve (CN VII) involvement, as well as prognostic factors.⁴

Procedures

• In the setting of a peripheral facial palsy, cerebrospinal fluid (CSF) rarely is analyzed. Although lumbar puncture is not recommended in the diagnosis of this disease, CSF findings can be helpful in confirming the diagnosis. In one study, CSF findings were abnormal in 11% of 239 patients with idiopathic peripheral facial palsy, in 60% of 17 patients with Ramsay Hunt syndrome (abnormal finding was pleocytosis), in 25% of 8 patients with Lyme disease, and in all 8 patients with HIV infection. Thus, if the CSF is abnormal, a specific cause should be sought.
• Temporary relief of otalgia in geniculate neuralgia may be achieved by applying a local anesthetic or cocaine to the trigger point, if in the external auditory canal.

Histologic Findings

• The affected ganglia of the cranial nerve roots are swollen and inflamed.
• The inflammatory reaction is chiefly of a lymphocytic nature, but a few polymorphonuclear leukocytes or plasma cells may also be present.
• Some of the cells of the ganglia are swollen and others degenerated.

Staging

Several scales have been developed to quantify the degree of facial muscle weakness. Of those, the House-Brackmann scale is most commonly used.⁴

The House-Brackmann facial neuropathy scale is as follows:

• 1- Normal
• 2 - Mild dysfunction (slight weakness only noticeable on close inspection)
• 3 - Moderate dysfunction (obvious weakness, but not disfiguring differences between both sides)
• 4 - Moderately severe dysfunction (obvious weakness and disfigurement)
• 5 - Only barely perceptive motor function
• 6 - Complete paralysis

Treatment

Medical Care

• Corticosteroids and oral acyclovir are commonly used in the treatment of Ramsay Hunt syndrome.
• In a recent review, combined therapy using corticosteroids plus intravenous acyclovir did not show benefit over corticosteroids alone in promoting facial nerve recovery after 6 months. However, randomized clinical trials evaluating both therapies are required.⁷
• A recent study concluded that controlled-release oxycodone was safe and generally well tolerated in patients experiencing acute pain due to herpes zoster.⁸
• Vestibular suppressants may be helpful if vestibular symptoms are severe.
• As with Bell palsy, care must be taken to prevent corneal irritation and injury.
• Temporary relief of otalgia may be achieved by applying a local anesthetic or cocaine to the trigger point, if in the external auditory canal.
• Carbamazepine may be helpful, especially in cases of idiopathic geniculate neuralgia.

Surgical Care

• Surgical decompression of the facial nerve has no role in this syndrome.

Consultations

• Consultation with an infectious disease specialist is recommended.
• If a structural lesion is discovered on imaging, consultation with a neurosurgeon or otolaryngologist is recommended.
• Consultation with an ophthalmologist to assist with eye care, especially pertaining to the cornea, may be appropriate.

Medication

Corticosteroids and oral acyclovir are frequently prescribed in patients with Ramsay Hunt syndrome. Vestibular suppressants may be helpful if vestibular symptoms are severe. Carbamazepine may be helpful, especially in cases of idiopathic geniculate neuralgia.

Corticosteroids

These agents reduce the inflammation of the cranial nerves and help alleviate the pain and neurologic symptoms.

Prednisone (Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. May be taken during acute inflammatory period (1-2 wk) and then tapered slowly. As an alternative, Dosepaks (ie, several prepackaged tablets with decreasing doses) can be taken. Individualize dose based on response.

Dosing

Adult

10 mg PO bid

Pediatric

Not established

Interactions

Coadministration with estrogens may decrease prednisone clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; fungal, viral, tubercular skin, and connective tissue infections; peptic ulcer disease; hepatic dysfunction

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Patients on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chickenpox and measles; drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dose; use cautiously in patients with ocular herpes simplex because of possible corneal perforation; use with caution in nonspecific ulcerative colitis, active or latent peptic ulcer disease, renal insufficiency, hypertension, osteoporosis and myasthenia gravis

Antivirals

Acyclovir can be used to combat infection caused by herpesviruses such as VZV.

Acyclovir (Zovirax)

Patients experience less pain and faster resolution of symptoms when used within 48 h from onset of symptoms. May prevent recurrent outbreaks.

Dosing

Adult

Acute treatment: 800 mg PO q4h (5 times/d) for 7-10 d
Chronic suppressive therapy for recurrent disease: 400 mg PO bid for 12 mo

Pediatric

Not established

Interactions

Concomitant probenecid or zidovudine prolongs half-life and increases CNS toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or when using nephrotoxic drugs; possibility of appearance of less sensitive viruses in humans must be kept in mind

Anticonvulsants

Mechanism of action of antiepileptics in this syndrome is still unknown. Carbamazepine has been shown to help the neuralgic pain associated with this syndrome, especially in cases of idiopathic geniculate neuralgia.

Carbamazepine (Tegretol)

DOC that may reduce polysynaptic responses and block posttetanic potentiation. Adjust dose depending on response to treatment and blood levels.

Dosing

Adult

400-800 mg PO qd in divided doses (usually tid)

Pediatric

Not established

Interactions

Serum levels may increase significantly within 30 days of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)

Contraindications

Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain baseline CBC count and serum iron prior to treatment, during first 2 months, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness

Antihistamines

These agents prevent histamine responses in sensory nerve endings and blood vessels. They are effective in treating vertigo.

Meclizine (Antivert, Antrizine, Meni-D)

Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. Associated with therapeutic effects in relief of nausea and vomiting.

Dosing

Adult

25 mg PO q4-6h

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

May increase toxicity of CNS depressants, neuroleptics, and anticholinergics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in angle-closure glaucoma, prostatic hypertrophy, pyloric or duodenal obstruction, and bladder neck obstruction; drowsiness, dry mouth, and blurred vision can occur

Dimenhydrinate (Dimetabs, Dramamine)

A 1:1 salt of 8-chlorotheophylline and diphenhydramine thought to be useful in treatment of vertigo. Through central anticholinergic activity, diminishes vestibular stimulation and depresses labyrinthine function.

Dosing

Adult

50 mg PO/IM q4-6h; 100 mg supp q8h

Pediatric

<2 years: Not established
2-6 years: Up to 12.5-25 mg PO q6-8h; not to exceed 75 mg/24h
6-12 years: 25-50 mg PO q6-8h; not to exceed 150 mg/24h
>12 years: Administer as in adults

Interactions

Alcohol or other CNS depressants may have additive effect on dimenhydrinate; may mask ototoxic symptoms caused by certain antibiotics, resulting in irreversible damage (use cautiously with these antibiotics)

Contraindications

Documented hypersensitivity; neonates (IV products may contain benzyl alcohol, which has been associated with fatal "gasping syndrome" in premature infants and low-birth-weight infants)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Do not treat severe emesis with antiemetic drugs alone; may contain either sulfites or tartrazine, which may cause allergic-type reactions in susceptible persons; may impede diagnosis of conditions such as brain tumors, intestinal obstruction, and appendicitis; may obscure signs of toxicity from overdosage of other drugs

Anticholinergics

These agents are thought to work centrally by suppressing conduction in the vestibular-cerebellar pathways.

Scopolamine (Isopto)

Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS. Antagonizes histamine and serotonin action.
Transdermal scopolamine may be most effective agent for motion sickness. Its use in vestibular neuronitis limited by its slow onset of action.

Dosing

Adult

0.6 mg PO q4-6h or 0.5 mg TD q3d

Pediatric

6 mcg/kg/dose IV/IM/SC q6-8h, not to exceed 0.3 mg/dose; alternative, 0.2 mg/m² q6-8h

Interactions

Antipsychotic medication effectiveness may be decreased by anticholinergic coadministration; anticholinergic side effects may be increased by concurrent phenothiazine therapy (adjust phenothiazine dose prn); may increase anticholinergic side effects of tricyclic antidepressants such as dry mouth, constipation, and urinary retention due to additive effect; a TCA with less anticholinergic activity may be beneficial

Contraindications

Documented hypersensitivity; primary glaucoma (including initial stages); pyloric obstruction; toxic megacolon; hepatic disease; paralytic ileus; severe ulcerative colitis; renal disease; obstructive uropathy; myasthenia gravis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use caution in elderly because of increased incidence of glaucoma; large doses may suppress intestinal motility and precipitate or aggravate toxic megacolon; may aggravate hiatal hernia associated with reflux esophagitis; patients with prostatism can have dysuria and may require catheterization; use cautiously in patients with asthma or allergies; a reduction in bronchial secretions can lead to inspissation and formation of bronchial plugs

Follow-up

Further Outpatient Care

After initiation of medical therapy, the patient with Ramsay Hunt syndrome should be seen in follow-up at 2 weeks, 6 weeks, and 3 months.

Prognosis

In general, prognosis is good for the resolution of symptoms. However, fewer than 50% of patients have complete recovery of facial function.

Patient Education

The patient should be educated concerning care of the eyes to prevent corneal irritation or injury.

Multimedia

Media file 1: Herpes zoster oticus, day 6. Image courtesy of Manolette Roque, MD, Ophthalmic Consultants Philippines Co, EYE REPUBLIC Ophthalmology Clinic.

References

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Keywords

Ramsay Hunt syndrome, geniculate neuralgia, herpes zoster oticus, nervus intermedius neuralgia, herpesvirus 3, varicella-zoster virus, VZV, varicella zoster, tinnitus, deafness, vertigo, nystagmus, ataxia, ipsilateral facial neuropathy, radiculoneuropathy, geniculate ganglionopathy, chickenpox, treatment, diagnosis

Contributor Information and Disclosures

Author

Augusto A Miravalle, MD, Fellow, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School
Augusto A Miravalle, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Medical Editor

Marion Priscilla Short, MD, Assistant Professor, Departments of Neurology, Pediatrics, and Pathology, University of Chicago Hospitals and Clinics
Marion Priscilla Short, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuropathologists, American College of Medical Genetics, American Medical Association, and American Society of Human Genetics
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

,, Kathy Roarty Placeholder
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Deepak Awasthi, MD, to the development and writing of this article.

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