Vernet syndrome resulting from varicella zoster virus infection-a very rare clinical presentation of a common viral infection.

Vernet syndrome is a unilateral palsy of glossopharyngeal, vagus, and accessory nerves. Varicella zoster virus (VZV) infection has rarely been described as a possible cause. A 76-year-old man presented with 1-week-long symptoms of dysphonia, dysphagia, and weakness of the right shoulder elevation, accompanied by a mild right temporal parietal headache with radiation to the ipsilateral ear. Physical examination showed signs compatible with a right XI, X, and XI cranial nerves involvement and also several vesicular lesions in the right ear's concha. He had a personal history of poliomyelitis and chickenpox. Laringoscopy demonstrated right vocal cord palsy. Brain MRI showed thickening and enhancement of right lower cranial nerves and an enhancing nodular lesion in the ipsilateral jugular foramen, in T1 weighted images with gadolinium. Cerebrospinal fluid (CSF) analysis disclosed a mild lymphocytic pleocytosis and absence of VZV-DNA by PCR analysis. Serum VZV IgM and IgG antibodies were positive. The patient had a noticeable clinical improvement after initiation of acyclovir and prednisolone therapy. The presentation of a VZV infection with isolated IX, X, and XI cranial nerves palsy is extremely rare. In our case, the diagnosis of Vernet syndrome as a result of VZV infection was made essentially from clinical findings and supported by analytical and imaging data.

Bilateral vocal cord immobility resulting from cytomegalovirus pharyngitis: A case report.

Human cytomegalovirus (CMV) is an infectious herpes virus present in approximately 50% of the world's population. Pharyngitis is an uncommon manifestation of CMV infection, and vocal cord immobility (VCI) following CMV pharyngitis is quite rare. An 83-year-old man with well-controlled diabetes mellitus and hypertension was admitted due to dyspnea, odynophagia, and dysphagia. Laryngeal fiberscopy revealed bilateral vocal cords almost fixed at the median position, with mucosal redness, swelling, and edema at the hypopharyngeal area. The airway was so narrowed that an emergency tracheostomy was performed to secure an airway. VCI resulting from a malignant tumor was suspected at first, but repeated pathological examinations revealed CMV infection in the pharyngeal mucosa. Despite intravenous ganciclovir treatment (5 mg/kg), the patient's bilateral VCI improved only slightly. Laryngeal electromyography was used to investigate the causes of VCI, and revealed vocal fold paralysis on the left side and cricoarytenoid joint fixation on the right side. This case highlights the importance of considering CMV infection in the differential diagnosis of patients with pharyngitis and VCI. To the best of our knowledge, this is the first case report describing the etiology of VCI following CMV pharyngitis using laryngeal electromyography.

Postviral vagal neuropathy.

OBJECTIVES: Postviral vagal neuropathy (PVVN) is a clinical diagnosis characterized by laryngeal complaints initiated by an upper respiratory tract infection (URI). Little is known about the natural history of this disease, and only small case series have been reported. We describe the clinical presentation, symptoms, patient demographics, and natural history of PVVN. METHODS: A cross-sectional survey of all patients with a diagnosis of PVVN from January 1, 2006, to December 31, 2006, was prospectively administered, detailing disease onset, type and duration of symptoms, demographics, and previous treatment. The Reflux Symptom Index, Voice Handicap Index, and laryngoscopic findings were collected for each patient. RESULTS: Forty-four patients with PVVN were identified. The mean age (+/-SD) was 48 +/- 13 years, and 73% of the patients were female. The most common initial URI symptoms were cough (89%), nasal congestion (75%), and rhinorrhea (64%). Fifty-nine percent of the patients took antibiotics, and the mean time between symptom onset and presentation to the laryngologist was 83 +/- 127 weeks. The most common persistent symptoms were cough (52%), throat clearing (48%), dysphonia (41.5%), and vocal fatigue (43%). Fifty-seven percent of the patients consulted 3 or more physicians for their symptoms. The mean Voice Handicap Index was 13.4 +/- 10.3, and the mean Reflux Symptom Index was 17.7 +/- 11. Forty-nine percent of the patients had evidence of vocal fold paresis on strobovideolaryngoscopy. CONCLUSIONS: PVVN is a clinical entity characterized by a complex of laryngeal symptoms that begin after a URI. The symptoms include chronic cough, excessive throat clearing, dysphonia, and vocal fatigue. Affected individuals are typically in their fifth decade of life and appear more likely to be women. Most patients have seen multiple physicians, and the time to laryngologist referral is often delayed.

Unilateral laryngeal paralysis in a newborn with congenital varicella syndrome.

We report a case of a newborn with unilateral laryngeal paralysis due to congenital varicella syndrome. The patient needed neonatal resuscitation with positive pressure ventilation for severe respiratory failure. Fiberoptic bronchoscopy showed left unilateral laryngeal paralysis. From the first week of life he presented left Horner's syndrome and difficult swallowing. He was hospitalised during the first 3 months of life for recurrent aspiration pneumonia and failure to thrive. At 11 months an ophthalmic evaluation with Ret-Cam showed a chorioretinal scar in the macular region that allowed the final diagnosis.

West Nile virus induced vocal fold paralysis.

OBJECTIVE: West Nile virus has recently become a public health concern in the United States, after an outbreak in New York City in 1999. It is a mosquito-borne virus that causes a spectrum of disease from flu-like symptoms to encephalopathy, muscle weakness, and, in some cases, death. STUDY DESIGN: Case Report. METHODS: A patient infected with West Nile virus presented with progressive muscle weakness, and later developed bilateral vocal fold paresis. His clinical presentation, physical and laboratory examination findings, and course of illness will be discussed. RESULTS: After a prolonged hospital stay, and presumptive treatment for Guillain-Barré, repeat CSF analysis revealed infection with the West Nile virus. The patient developed bilateral vocal fold paralysis during his hospital course. At long-term follow-up, the patient's left vocal fold paralysis persisted, while the right vocal fold paralysis had resolved. CONCLUSIONS: Although several viruses have been associated with recurrent laryngeal nerve injury, this is the first report of West Nile virus induced vocal fold paralysis.

[Paresis of the vagus and accessory nerve in the course of the herpes zoster]. / Porazenie nerwów X i XI w przebiegu pólpasca.

INTRODUCTION: The cephalic zoster is a cranial neuritis, with great tendency to diffusion along the nerves. The objective of this article is both to report a case of cranial polineuritis due to herpes zoster infection with laryngeal involvement and review of the relevant literature. MATERIAL AND METHODS: The case of 57-years-old man with unilateral laryngeal mucosal eruptions and complete left vocal paralysis is reported. Laryngeal symptoms, diagnostic criteria and therapeutic result are described. CONCLUSION: 1. In cases of head and neck herpes zoster, the investigations of all cranial nerves should be carried out, and the larynx must always be examinated; 2. Co-occurrence of the neuralgic pain (radiating especially to the ear or the occipital region) with unilateral laryngeal palsy should raise a suspicion that herpes zoster infection may by the causative factor; 3. The explanation of the etiologic cause of a vocal fold paralysis in idiopathic cases, may yield not only diagnostic, but also therapeutic value.

Atypical Presentation of a Common Disease: Shingles of the Larynx.

OBJECTIVE: Herpes zoster is a neurocutaneous disease resulting from the reactivation of endogenous varicella-zoster virus (VZV) in dorsal sensory or cranial nerve ganglia. Rarely, this infection manifests without the characteristic dermatomal rash, a condition termed zoster sine herpete. Viral spreading of herpes zoster in the head and neck may manifest as various signs and symptoms because of the multiple possible combinations of cranial neuropathies. With only six cases reported in the English literature up to now, isolated neuropathies of the vagus nerve in the absence of cutaneous lesions tend to be misdiagnosed as idiopathic laryngeal paralysis. METHODS: We report a case of herpes zoster of the larynx in an 80-year-old man presenting with sore throat, dysphagia, and hoarseness. RESULTS: Endoscopic examination revealed unilateral vocal fold paralysis, pooling of secretions, and mucosal vesicles of the hemilarynx. After the diagnosis of VZV infection with polymerase chain reaction (PCR) testing, the patient was treated with valacyclovir and corticosteroids, leading to complete recovery after 2 months. CONCLUSIONS: Herpes zoster of the larynx is an uncommon condition that should be included in the differential diagnosis of laryngeal paralysis of idiopathic cause. We recommend performing a thorough examination of the pharyngolaryngeal structures and ordering PCR testing as the diagnostic method of choice.

Herpes zoster laryngis with prelaryngeal skin erythema.

A 74-year-old man came to our hospital with complete left vocal cord paralysis and erythema of the prelaryngeal skin. The patient also had mucosal swelling and erosions in the left arytenoid cartilage, aryepiglottic fold, and pyriform sinus. Herpetic vesicles developed over the prelaryngeal erythema 4 days after admission. An increase in the varicella-zoster immunoglobulin G level to 3,294 IU/mL confirmed varicella-zoster virus infection of the larynx and prelaryngeal skin. The patient was treated with acyclovir without marked effect. Nevertheless, in cases of unilateral vocal cord paralysis and erythema of the ipsilateral prelaryngeal skin, we advise that herpes zoster laryngis must be considered and treatment with early intravenous acyclovir started.

Cephalic zoster with laryngeal paralysis.

Herpes zoster reactivaction in the head and neck region is often associated with multiple cranial neuropathies, the most common one being facial paralysis. Laryngeal paralysis has also been occasionally reported with zoster infection. We present two such cases, and discuss the relevant literature on the pathophysiology, evaluation and management of this disease. Recent advances in antiviral therapy have allowed for specific medical treatment, thus making it all the more imperative to suspect zoster, even in clinically atypical cases. We suggest aggressive treatment with intravenous acyclovir for cephalic zoster complicated by vocal cord paralysis.

Vocal cord paralysis associated with Ramsay Hunt syndrome: looking back 50 years.

Ramsay Hunt syndrome is defined by herpes zoster oticus and peripheral facial nerve palsy which is often associated with otalgia. The syndrome is, in rare cases, associated with other cranial nerve paralyses including the vagal nerve causing unilateral vocal cord paralysis. Vocal cord paralysis is more often seen as a symptom of various other diseases, that is, malignant tumours, neurodegenerative illness, cerebrovascular assaults, inflammatory processes or as a result of intubation or surgical procedures. The symptoms of unilateral vocal cord paralysis are mainly hoarseness, dyspnoea and dysphagia. We present a case of Ramsay Hunt syndrome combined with unilateral hearing loss and left vocal cord paralysis. The patient underwent MRI, CT and a lumbar puncture causing anxiety in the patient and delaying the initiation of antiviral and anti-inflammatory treatment, which is only efficient when initiated within 72 h. We hope to raise the awareness of this disease.

Bilateral vocal cord abductor paralysis associated with primary herpes simplex infection: a case report.

OBJECTIVE: To report a case of bilateral vocal cord abductor paralysis in the context of primary herpes simplex infection. CASE REPORT: A 63-year-old man was urgently admitted to hospital with laryngeal dyspnoea associated with dysphagia but without dysphonia. Physical examination demonstrated the vocal cords in a paramedian position with paralysis of abduction. The patient reported primary herpes simplex infection two weeks prior to this episode. HSV serology indicated recent infection and lumbar puncture demonstrated the presence of herpes simplex virus type 1 in the cerebrospinal fluid. Complete resolution of respiratory symptoms was observed after 21 days of treatment with intravenous aciclovir. DISCUSSION AND CONCLUSION: Gerhardt syndrome comprises inspiratory dyspnoea without dysphonia. It used to be mainly due to syphilis, but is now mostly observed in the setting of neurodegenerative disease. The authors report a case of Gerhardt syndrome occurring after an episode of primary herpes simplex infection with the presence of herpes simplex virus in the CSF. Treatment by intravenous antiviral drugs allowed rapid resolution of the symptoms. The pathophysiology of Gerhardt syndrome remains unexplained, but the possible role of herpes simplex infection should be considered in cases of laryngeal palsy.

Unilateral associated laryngeal paralysis due to varicella-zoster virus: virus antibody testing and videofluoroscopic findings.

The relationship between varicella-zoster virus and idiopathic associated laryngeal paralysis was examined in five patients, using complement fixation or enzyme immunoassay testing. In all cases, significant changes in serum levels of varicella-zoster virus antibody were observed. Videofluoroscopy was useful in assessing the severity of the dysphagia and in making an accurate diagnosis; both laryngeal elevation and weakness of pharyngeal wall contraction were also observed. In two cases in which antiviral therapy was delayed, the outcome was poor, with increased levels of varicella-zoster virus immunoglobulin M found on enzyme immunoassay. The outcome of the condition may thus depend both on the speed of antiviral therapy commencement following onset of symptoms, and on the levels of varicella-zoster virus immunoglobulin M antibody (measured by enzyme immunoassay). Our study suggests that varicella-zoster virus should be considered in the differential diagnosis of patients with idiopathic associated laryngeal paralysis, and rapid antiviral therapy should be initiated when necessary.

Laryngeal zoster with unilateral laryngeal paralysis.

The case of a 60-year-old man with a unilateral laryngeal mucosal lesion and complete left vocal cord paralysis is reported. The lesion localized to the left side of the larynx covered the laryngeal vestibule, arytenoid, false vocal cord and true vocal cord, but did not extend to the hypopharynx or oropharynx. Enzyme immunoassay for varicella-zoster virus (VZV) led to a diagnosis of VZV infection.

Acute palsy of the recurrent laryngeal nerve complicating Epstein-Barr virus infection.

We report an 11-year-old boy with active Epstein-Barr virus (EBV) infection who developed acute aphonia and had signs and symptoms of recurrent laryngeal nerve palsy. The association of isolated recurrent laryngeal nerve palsy and EBV infection has not previously been reported. This case report expands the spectrum of neurologic complications of EBV infection, and suggests that infectious mononucleosis should be considered in the differential diagnosis of acute aphonia in children.

Herpes simplex virus type I reactivation as a cause of a unilateral temporary paralysis of the vagus nerve.

Infection by neurotropic viruses, as exemplified by the herpes family, is universally accepted as a cause of palsies of the cochleo-vestibular and facial nerve. Palsies of the vagus nerve with a possible viral etiology have been described, although viruses have been identified in only a few selected cases. We report a 52-year-old man with unilateral otalgia, hoarseness and dysphagia. Examination revealed unilateral (left-sided) pharyngeal dysfunction, and paralysis of the left vocal cord fixed in the paramedian position. A barium swallow documented dysfunction of the left pharyngeal constrictor muscles. These findings suggested the lesion to be located either at the inferior ganglion of the vagus nerve or cranially. At direct laryngoscopy a smear was obtained from a 4-mm mucosal ulcer at the region of the left arytenoid cartilage. This smear demonstrated antibodies to herpes simplex virus (HSV) type I by immunofluorescence. On follow-up 19 months after the initial infection there was complete remission of the paralysis of the left vocal cord and normal pharyngeal function. The demonstration of HSV type 1 antibodies from a mucosal lesion in the distribution of the superior laryngeal nerve suggests that reactivation of HSV type I was the most likely explanation for the temporary nerve palsy seen.