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 fold palsy caused by chronic motor axonal neuropathy.

The authors report a first case of chronic motor axonal neuropathy involving ENT manifestations, in a 64-year-old male presenting with gait difficulties, effort dyspnoea and dysphonia. Eleven months after the first symptoms, he developed severe hypoventilation, limb weakness and bilateral vocal fold palsy and had to be intubated for respiratory failure. The diagnosis of chronic motor axonal neuropathy was suspected on clinical and electrophysiological grounds. The patient improved dramatically after a five-day course of 0.4 g/kg intravenous immunoglobulin. He is still being treated with methylprednisolone 0.5 mg/kg every other day and remains stable. We conclude the bilateral vocal fold palsy may be associated with chronic motor axonal neuropathy and that the immunosuppressive treatment may be effective in such cases.

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.

Association of arytenoid chondritis with equine lymphocyte antigens but no association with laryngeal hemiplegia, umbilical hernias and cryptorchidism.

Associations were sought between ELA A1-A10 and W11 antigens and the presence of laryngeal hemiplegia, arytenoid chondritis, umbilical hernias and cryptorchidism in Thoroughbreds and/or Quarter Horses. No significant associations were detected between laryngeal hemiplegia and any ELA antigen in Thoroughbreds. The association between arytenoid chondritis and A9 was significant with a relative risk (RR) of 15.6 and aetiologic fraction (EF) of 0.80 in Thoroughbreds. There were apparent associations based on RR between A4 and A5 in Quarter Horses with umbilical hernias (RR = 7.5 and 6.1 respectively); however, these were not statistically significant. No significant associations were detected with cryptorchidism in Quarter Horses when the control population included both sexes. When only unaffected males were used as the control group, there was an apparent increase in relative risk with A6 (from RR = 1.7 to 4.3); however this was not statistically significant. Cryptorchidism in Thoroughbreds showed an increased relative risk with A5 regardless of whether the control population included males and females (RR = 4.1) or only males (RR = 4.7) but the increases were not statistically significant.

Herpes simplex virus and recurrent laryngeal nerve paralysis. Report of a case and review of the literature.

A 61-year-old man experienced the abrupt onset of a nonspecific febrile illness followed by the acute development of bilateral vocal cord paralysis. There was no evidence for Guillain-Barré syndrome, multiple sclerosis, brainstem encephalitis, myasthenia gravis, metabolic encephalopathy, poliomyelitis, diphtheria, botulism, tumor, vasculitis, or extrinsic nerve compression. No cause for the fever was ascertained, and the vocal cord paralysis improved sponaneously. Acute and convalescent viral serological studies demonstrated a diagnostic complement-fixation antibody titer rise to herpes simplex virus (HSV) and no rise in titer to influenza A and B, cytomegalovirus, poliomyelitis, or Mycoplasma. This case is similar to several others reported in the literature that suggest a viral neuritis in tenth nerve paralyses in children. The difficulties involved in diagnosing HSV CNS disease before death are discussed, and the medical literature is reviewed for evidence that HSV is the etiological agent in selected cranial neuropathies.