Imaging manifestations on sequential magnetic resonance imaging in pharyngolaryngeal involvement by varicella zoster virus.

Clarifying temporal changes in magnetic resonance imaging (MRI) offers a good chance to understand the pathology of neural lesions; however, such information is scarce in varicella zoster virus (VZV) neuropathies for the glossopharyngeal and vagus nerves. Here, we present the changes in sequential MR images of such a pathology over a period of 12 months from symptom onset.A 27-year-old woman with difficulty in swallowing and hoarseness due to a palatal palsy and arytenoid fixation on the left presented 2 days after onset. MRI revealed a lesion which largely filled the left jugular foramen on T2-weighted images (T2-WI) with high diffusion-weighted imaging (DWI) signals, which has never been previously described, on the 3rd day after onset. The DWI signals were highest on day 3, then deteriorated over 2 months until the signal was only detectable at the intracranial level, but not in the jugular foramen. The glossopharyngeal nerve had returned to normal by 2 months.The time course of the glossopharyngeal and vagus nerve swelling detected on T2-WI suggests that nerve swelling reduces over several months, even though the paralytic symptoms persist. Furthermore, the high DWI signal suggests that nerve swelling was caused by edematous swelling of the nerve fibers, rather than fiber disruption with water displacement in the extracellular space. These findings may provide good clues to speculate on the dynamically changing pathology of VZV neuropathies of the glossopharyngeal and vagus nerves.

Postviral Vagal Neuropathy: What Is the Role of Laryngeal Electromyography in Improving Diagnostic Accuracy?

OBJECTIVES: To investigate the convenience of laryngeal electromyography (EMG) findings in patients with chronic cough thought to be postviral vagal neuropathy (PVVN) with the clinical symptoms. STUDY DESIGN: Prospective cohort study. METHODS: We applied PVVN questionnaire and chronic cough quality of life (QoL) questionnaire, which is for determining the effect of chronic cough on the QoL, to 20 chronic cough applicants who has no explanatory cause in differential diagnosis. We also carried out videolaryngostroboscopy (VLS) and laryngeal needle EMG in these patients. RESULTS: The mean duration of persisting cough was 1.875 months (SD ±0.825). The overall mean symptom score of chronic cough questionnaire was 58.80 (SD ±9.89). There was a significant positive correlation between total EMG score and chronic cough score (Spearman r, 0.489, P < 0.05). The correlation between VLS findings and either chronic cough scores or EMG scores did not reach statistical significance. CONCLUSIONS: Cranial nerves might be affected by inflammatory processes as occur in the PVVN, which must be considered in the etiology of chronic cough. We showed that the laryngeal EMG can be used as an appropriate diagnostic tool for these patients.

Cough after laryngeal herpes zoster: a new aspect of post-herpetic sensory disturbance.

OBJECTIVE: Although neurogenic cough is increasingly recognised, its pathophysiology remains obscure. We describe two cases of chronic cough following laryngeal herpes zoster, a rarely described manifestation of varicella-zoster virus reactivation, and suggest that this may be analogous to post-herpetic neuralgia. The same mechanisms may cause both phenomena. CASE REPORTS: We describe two cases of chronic cough persisting for more than three months following an acute attack of laryngeal herpes zoster. CONCLUSION: Neuronal damage by varicella-zoster virus results in irritable nociceptors and deafferentation, mechanisms known to cause post-herpetic neuralgia. When the vagus nerve is affected, as in laryngeal herpes zoster, the result may be a chronic cough. Similar damage may underlie chronic neurogenic cough in other contexts.

Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis.

Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found. In this speculative article, I describe a new hypothesis for the etiology of CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release proinflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized proinflammatory cytokines, and send a signal to the brain to initiate sickness behavior. Sickness behavior is an involuntary response that includes fatigue, fever, myalgia, depression, and other symptoms that overlap with CFS. The vagus nerve infection hypothesis of CFS contends that CFS symptoms are a pathologically exaggerated version of normal sickness behavior that can occur when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria. Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal. According to this hypothesis, any pathogenic infection of the vagus nerve can cause CFS, which resolves the ongoing controversy about finding a single pathogen. The vagus nerve infection hypothesis offers testable hypotheses for researchers, animal models, and specific treatment strategies.

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.

A case of Vernet syndrome with varicella zoster virus infection.

A 40-year-old man was admitted to our department, because of sudden onset of dysphagia, hoarseness, left neck pain and headache. There were no skin lesions. On neurological examination, there were paralysis of the left soft palate and constrictor muscles of the pharynx, weakness of the left sternocleidomastoid and left upper trapezius. In cerebrospinal fluid (CSF) examination, cell count and protein concentration were elevated. Antibody titer to varicella zoster virus (VZV) was elevated in both the serum and CSF. And VZV-DNA was detected by PCR from CSF. Gd enhanced MRI showed the nodular lesion at the left jugular foramen. The diagnosis of Vernet's syndrome (VS) associated with VZV infection was made. The patient's symptoms were immediately improved with 30 mg of prednisone and 3 g of varaciclovir daily for 14 days. Only a few cases of VS due to VZV have been reported previously. Our case is the first case that detected VZV-DNA in CSF by PCR.

Effectiveness of amitriptyline versus cough suppressants in the treatment of chronic cough resulting from postviral vagal neuropathy.

OBJECTIVE: The objective of this prospective, randomized, controlled study (N = 28) was to evaluate the effectiveness of amitriptyline versus cough suppressants in the treatment of chronic cough resulting from postviral vagal neuropathy. METHODS: Patients were selected based on a clinical history consistent with postviral vagal neuropathy and a history of an antecedent upper respiratory tract infection. All patients had been tried on antireflux medication (proton pump inhibitors) and had a negative chest x-ray before presentation. All were nonsmokers without a history of asthma. Patients on angiotensin-converting enzyme inhibitors were excluded from the study. All patients completed a pretreatment, validated cough-specific quality-of-life (QOL) survey. Patients were randomized by chart numbers to either 10 mg amitriptyline at bedtime or 10 to 100 mg/5 mL, 10 mL codeine/guaifenesin every 6 hours standing dose while awake. Both groups were instructed to complete 10 days of therapy and then asked to subjectively rate the reduction in the frequency and severity of their cough by 100%, 75%, 50%, 25%, or 0% as well as completing the posttreatment cough QOL questionnaire. Those patients experiencing a 75% to 100% reduction were recorded as having a complete response, 25% to 50% a partial response, and 0% as having no response. Final results and the cough QOL survey were recorded and used for statistical analysis. RESULTS: A majority of patients in the amitriptyline group achieved a complete response on the initial dose of 10 mg. None of the codeine/guaifenesin group achieved a complete response. The data were analyzed using a logistic regression model, and amitriptyline was found to be a highly significant predictor of a greater than 50% response when compared with codeine/guaifenesin (P = .0007). The same data were analyzed using a proportional odds model and similar results were noted. CONCLUSIONS: Chronic cough can have a profound impact on the psychosocial function of patients. The most common causes of a persisting cough in the absence of infection or chronic smoking are laryngopharyngeal reflux, asthma, particularly the cough variant, allergy, rhinosinusitis, bronchitis, and medications, in particular angiotensin-converting enzyme inhibitors. Currently, there are few effective treatments for cough with an acceptable therapeutic ratio and more selective drugs with a more favorable side effect profile are needed. This is this first prospective, randomized, controlled study comparing the effectiveness of amitriptyline versus codeine/guaifenesin for select cases of chronic cough resulting from suspected postviral vagal neuropathy.

Isolated velopalatine paralysis associated with parvovirus B19 infection.

A case of isolated velopalatine paralysis in an 8-year-old boy is presented. The symptoms were sudden-onset of nasal speech, regurgitation of liquids into the nose and dysphagia. Brain MRI and cerebrospinal fluid examination were normal. Infectious serologies disclosed an antibody arrangement towards parvovirus B19 that was typical of recent infection. In the absence of other positive data, the possibility of a correlation between the tenth nerve palsy and parvovirus infection is discussed.

Isolated velopalatine paralysis associated with parvovirus B19 infection / Paralisia velopalatina isolada associada a infecção por parvovírus B 19

A case of isolated velopalatine paralysis in an 8-year-old boy is presented. The symptoms were sudden-onset of nasal speech, regurgitation of liquids into the nose and dysphagia. Brain MRI and cerebrospinal fluid examination were normal. Infectious serologies disclosed an antibody arrangement towards parvovirus B19 that was typical of recent infection. In the absence of other positive data, the possibility of a correlation between the tenth nerve palsy and parvovirus infection is discussed.

Apresentamos um caso de paralisia velopalatina isolada, num menino de 8 anos, que se manifestou por voz nasalada, regurgitação de líquidos pelo nariz e disfagia, de início súbito. A ressonância magnética encefálica e o estudo do líquido cefalo-raquidiano foram normais. O perfil serológico dos anticorpos anti-parvovírus B19 era típico de infecção recente. Na ausência de outros dados positivos, discute-se a possibilidade de uma correlação entre a parésia do X nervo e a infecção por parvovírus.