Bilateral Vocal Fold Paralysis After Epidural Anesthesia.

Cranial neuropathies are known potential complications of spinal anesthesia, with most reports describing upper cranial nerve involvement. Intrathecal hypotension resulting in traction injury of the cranial nerves is the likely mechanism of injury. Unilateral vagal neuropathy was first described recently. The patient discussed in this case presented with hoarseness and dysphagia after receiving epidural anesthesia for childbirth. Following videostroboscopy and laryngeal electromyogram, she was diagnosed with bilateral vocal fold paralysis. The patient was managed conservatively with expectant management. She exhibited complete spontaneous recovery, as has been the natural history previously described for similar injuries. The proposed mechanism for this patient, and in others described in the literature, is puncture of the dura with subsequent egress of cerebrospinal fluid, leading to intracranial hypotension and traction on cranial nerves. Unilateral vocal fold paralysis following spinal anesthesia has been reported in one case series consisting of three patients, but this represents the first case of bilateral paralysis. Spontaneous resolution has been observed in all patients. Patients presenting with idiopathic vocal fold paralysis, in summary, should be questioned about recent history of epidural or spinal anesthesia, as a positive history may point to transient intrathecal hypotension as a potential etiology of the paralysis.

Vocal fold paralysis secondary to phonotrauma.

A unique case of acute onset vocal fold paralysis secondary to phonotrauma is presented. The cause was forceful vocalization by a drill instructor on a firearm range. Imaging studies revealed extensive intralaryngeal and retropharyngeal hemorrhage. Laryngoscopy showed a complete left vocal fold paralysis. Relative voice rest was recommended, and the patient regained normal vocal fold mobility and function after approximately 12 weeks.

An old flame reignites: vagal neuropathy secondary to neurosyphilis.

OBJECTIVE: This report describes neurosyphilis presenting as vocal fold paresis and velopharyngeal incompetence. This represents the first reported case of neurosyphilis presenting as a vagal neuropathy since 1963. STUDY DESIGN: Case report. METHODS: Review of medical records and literature search. RESULTS: The patient presented with voice changes and nasopharyngeal reflux of liquids. Examination showed a left vocal fold paresis and moderate velopharyngeal incompetence. Laryngeal electromyography revealed evidence of denervation, and neurologic evaluation showed bilateral Adie's pupils and a positive CSF VDRL. A remote history of syphilis treated with one intramuscular injection was obtained. The patient was treated with 6 weeks of penicillin and regained normal vocal function with minimal residual intermittent hypernasality. CONCLUSIONS: Given the recent increase in the incidence of syphilis in the United States, this case serves as a reminder of the importance of including syphilis in the differential diagnosis of cranial neuropathies and the increasing likelihood of syphilis presenting to otolaryngology and speech pathology practices. Syphilis, a disease whose incidence had declined progressively for 60 years in the United States, is now resurgent and must be considered in the evaluation of patients presenting with unexplained cranial neuropathies.