Cases reported "Vocal Cord Paralysis"

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1/85. Idiopathic bilateral vocal fold weakness.

    OBJECTIVE: To describe an unrecognized clinical entity, idiopathic bilateral vocal fold weakness, and propose recommendations regarding the diagnosis and management of these cases. STUDY DESIGN: Retrospective, nonrandomized case study. methods: All cases of bilateral vocal fold weakness evaluated at the University of washington voice disorders Clinic between 1991 to 1998 were reviewed. RESULTS: Four patients with bilateral laryngeal weakness were determined to have idiopathic bilateral vocal fold paresis following exhaustive workups, including videostroboscopy, bilateral laryngeal electromyography (EMG), neurological consultation, and other pertinent studies. CONCLUSIONS: Performing bilateral laryngeal EMG is an essential aspect of the workup of any laryngeal weakness case, particularly if the etiology is unknown on presentation. Idiopathic bilateral vocal fold weakness is an underrecognized but real clinical diagnosis that will become more familiar with the increasing utilization of laryngeal EMG in clinical situations.
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keywords = paresis
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2/85. Vocal fold paresis.

    Vocal fold paresis (VFP) is a relatively common and often overlooked condition that can be difficult to diagnose based on the laryngeal examination alone. A retrospective review of the records of 50 consecutive adult patients with VFP was performed. In each case, the diagnosis of VFP was confirmed by laryngeal electromyography. The presenting symptoms were dysphonia (100%), vocal fatigue (76%), diplophonia (40%), and odynophonia (12%), and the findings were unilateral vocal fold hypomobility (50%), unilateral bowing (36%), and bilateral bowing (22%). laryngoplasty and/or lipoinjection was performed in 54% of the subjects, and significant vocal improvement was achieved in 85%. VFP appears to be underdiagnosed because many VFP patients have compensatory hyperkinetic disorders at presentation. Although the diagnosis of VFP may be suspected based on the patient's symptoms and findings, the diagnostic sine qua non is laryngeal electromyography. In addition, surgical treatment for VFP appears to be safe and effective.
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ranking = 5
keywords = paresis
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3/85. Bilateral vocal cord paralysis after anterior cervical discoidectomy and fusion in a case of whiplash cervical spine injury: a case report.

    BACKGROUND: Bilateral vocal cord paralysis is a risk of anterior cervical discoidectomy and fusion. We discuss the mechanism of vocal cord paralysis and the precautions necessary to avoid this catastrophic complication. A rare case of bilateral vocal cord paralysis after anterior cervical discoidectomy and fusion (ACD/F) is reported. CASE DESCRIPTION: The patient, a 37-year-old male, was paraplegic, had bilateral intrinsic hand muscle weakness and sphincter involvement following a whiplash cervical spinal injury. A C5-C6 ACD/F for traumatic C5-C6 disc prolapse was performed. On the third postoperative day, he developed difficulty in coughing and a husky voice. Otolaryngological evaluation revealed bilateral vocal cord paralysis. He later required a tracheostomy that partially alleviated his major symptoms. CONCLUSION: In patients undergoing ACD/F, a mandatory preoperative evaluation of the vocal cords should be performed. An appropriate modification in surgical planning should be made if vocal cord palsy is diagnosed preoperatively to prevent bilateral vocal cord paralysis. Proper and judicious use of Cloward retractors is advocated.
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ranking = 0.0024346187098484
keywords = muscle
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4/85. Morphometric study of nucleus ambiguus in multiple system atrophy presenting with vocal cord abductor paralysis.

    AIM: To identify lesions responsible for vocal cord abductor paralysis (VCAP) in multiple system atrophy (MSA), we performed a morphometric study of the nucleus ambiguus which innervates the intrinsic laryngeal muscles. methods: Two autopsied cases of MSA presenting with VCAP and one control were examined. Both cases of MSA showed selective neurogenic atrophy of the posterior cricoarytenoid muscles among the intrinsic laryngeal muscles, while no abnormalities were seen in the control. From a block of the medulla oblongata, sections 10 microm thickness were cut serially without spacing and stained with cresyl violet. The ambiguus neurons were counted in all the sections to make a histogram. RESULTS: In the control case, ambiguus neurons showed densely populated areas and sparsely populated areas alternately with significant difference in the mean neuronal density between two areas. In MSA, ambiguus neurons were significantly decreased in number at all levels. It indicates that the neurogenic atrophy of the posterior cricoarytenoid muscle is derived from the neuronal loss of the nucleus ambiguus. CONCLUSION: Though it has still been controversial whether or not the ambiguus neurons are decreased in number in MSA with VCAP, we speculated possible reasons for the disagreement on the involvement of the nucleus ambiguus as follows: different mechanism of VCAP are playing role, and histometric data have been disturbed by factors such as split-cell counting error and marked variation in the distribution of the ambiguus neurons.
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ranking = 0.0097384748393937
keywords = muscle
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5/85. Simultaneous vocal fold and tongue paresis secondary to Epstein-Barr virus infection.

    dysphonia is a common presenting symptom in cases referred for otolaryngologic evaluation. Similarly, primary care physicians frequently see adolescents or young adults with symptomatic Epstein-Barr virus infection. Some of the patients with active Epstein-Barr virus infection who have severe clinical manifestations of infectious mononucleosis will be referred for otolaryngologic evaluation. Voice abnormalities in these patients, though, are usually limited to altered resonance due to pharyngeal crowding by hyperplastic lymphoid tissue. We describe a patient with infectious mononucleosis who was referred for evaluation of dysphonia and was diagnosed with unilateral tongue and vocal fold paresis. We also discuss the patient's clinical course and review the related literature. Although uncommon, cranial nerve palsies must be considered in the patient with Epstein-Barr virus infection who presents with voice or speech disturbance. Arch Otolaryngol head neck Surg. 2000;126:1491-1494
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ranking = 5
keywords = paresis
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6/85. Unilateral or localized Reinke's edema (pseudocyst) as a manifestation of vocal fold paresis: the paresis podule.

    BACKGROUND: The nosology of free-edge vocal fold lesions remains imprecise. In particular, the lesion termed pseudocyst remains enigmatic, because its histology is poorly defined and because its etiology is unknown. We define pseudocyst as a discrete, unilateral, localized area of Reinke's edema (without a capsule), usually occurring at the midportion of the free-edge striking zone. OBJECTIVE: To report the demographic and clinical findings, as well as discuss our diagnostic and therapeutic strategies, in patients with unilateral Reinke's edema or pseudocyst. METHODOLOGY: All patients diagnosed with unilateral Reinke's edema or pseudocyst over a 2-year period (1998-1999) were identified from the clinical database of the Center for voice disorders of Wake Forest University, Winston-Salem, north carolina. The record of each patient was retrospectively reviewed. RESULTS: Thirteen patients were identified, 12 of whom were female. The mean age was 36 years. Sixty-nine percent (9 of 13) had unilateral pseudocyst and 31% (4 of 13) had unilateral Reinke's edema. All patients had documented vocal fold paresis on laryngeal electromyography. The 9 patients with pseudocyst underwent excision of their lesions; 7 had bilateral medialization laryngoplasties, 1 had lipoinjection, and 3 did not have surgical intervention. Significant improvement was noted postoperatively on a self-administered glottal insufficiency (symptom) index (P <.001). CONCLUSION: Unilateral Reinke's edema and localized Reinke's edema (pseudocyst) are distinct clinical entities, occurring most frequently in women in their fourth decade. The finding of unilateral Reinke's edema or pseudocyst should alert the clinician to the likelihood of vocal cord paresis. Surgical intervention with medialization laryngoplasty appears to be beneficial.
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ranking = 10
keywords = paresis
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7/85. Vagal neuropathy after upper respiratory infection: a viral etiology?

    PURPOSE: To describe a condition that occurs following an upper respiratory illness, which represents injury to various branches of the vagus nerve. patients with this condition may present with breathy dysphonia, vocal fatigue, effortful phonation, odynophonia, cough, globus, and/or dysphagia, lasting long after resolution of the acute viral illness. The patterns of symptoms and findings in this condition are consistent with the hypothesis that viral infection causes or triggers vagal dysfunction. This so-called postviral vagal neuropathy (PVVN) appears to have similarities with other postviral neuropathic disorders, such as glossopharyngeal neuralgia and Bell's palsy. MATERIALS AND methods: Five patients were identified with PVVN. Each patient's chart was reviewed, and elements of the history were recorded. RESULTS: Each of the 5 patients showed different features of PVVN. CONCLUSIONS: Respiratory infection can trigger or cause vocal fold paresis, laryngopharyngeal reflux, and neuropathic pain.
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ranking = 1
keywords = paresis
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8/85. Congenital hypomyelination neuropathy in a newborn infant: unusual cause of diaphragmatic and vocal cord paralyses.

    We report a case of congenital hypomyelination neuropathy presenting at birth. The infant had generalized hypotonia and weakness. There was decreased respiratory effort along with a right phrenic nerve and left vocal cord paralyses. tongue fasciculations were present. Deep tendon reflexes were absent in the upper extremities and hypoactive (1 ) in the lower extremities. magnetic resonance imaging of the head revealed no intracranial abnormalities, including normal cerebral myelination. Nerve conduction study showed absence of motor and sensory action potentials in the hands when the nerves in the upper limbs were stimulated. A motor response could be elicited only in the proximal leg muscles. Needle electromyography study was normal in the proximal limb muscles, but showed active denervation in the distal muscles of the arm and leg. These findings were thought to be consistent with a length-dependent sensorimotor peripheral polyneuropathy of axonal type with greater denervation of the distal muscles. A biopsy of the quadriceps muscle showed mild variability in fiber diameter, but no group typing or group atrophy. The muscle fibers showed no intrinsic abnormalities. biopsy of the sural nerve showed scattered axons with very thin myelin sheaths. There was also a nearly complete loss of large diameter myelinated fibers. No onion bulb formations were noted. These findings were thought to be consistent with congenital hypomyelination neuropathy with a component of axonopathy. dna analysis for identification of previously characterized mutations in the genes MPZ, PMP22, and EGR2 was negative. Several attempts at extubation failed and the infant became increasingly ventilator-dependent with increasing episodes of desaturation and hypercapnea. He also developed increasing weakness and decreased movement of all extremities. He underwent surgery at 2 months of age for placement of a gastrostomy tube and a tracheostomy. He was discharged from the hospital on a ventilator at 6 months of age. The infant was 13 months old at the time of submission of this report. Although he appears cognitively normal, he remains profoundly hypotonic and is on a home ventilator. There was no evidence of progressive weakness. Congenital hypomyelination neuropathy is a rare form of neonatal neuropathy that should be considered in the differential diagnosis of a newborn with profound hypotonia and weakness. It appears to be a heterogeneous disorder with some of the cases being caused by specific genetic mutations.
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ranking = 0.014607712259091
keywords = muscle
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9/85. Vocal fold paresis of charcot-marie-tooth disease.

    No cohesive overview of vocal fold abnormalities associated with charcot-marie-tooth disease (CMT) has been presented in the literature. This study examines a patient in depth and compares the findings with those of published reports to characterize the features of vocal fold paresis in CMT. The affected patient was investigated with nerve conduction testing, laryngeal electromyography, endoscopy, and laryngeal sensory testing. Ten published cases were reviewed for similarities and differences. Vocal fold paresis has been observed in 11 CMT patients ranging in age from 8 to 80 years. Two cases have occurred in the context of CMT type 1, and 9 in CMT type 2. Seven of the 11 cases (64%) were clearly bilateral; only 2 of the 7 cases (29%) required tracheotomy, and both were in children. The electromyographic findings were typical of reinnervation. Sensory findings were present, but did not represent significant disability in the 1 patient so studied. We conclude that CMT does not spare the cranial nerves, as has been previously thought. Furthermore, vocal fold paresis is not restricted to CMT type 2 and should not be considered a hallmark of that category. The available evidence suggests that the neural deficit evolves gradually, may exhibit partial recovery, and often escapes notice for a time. Vocal fold abnormalities are most often bilateral. Because the deficit is generally well tolerated in adults, many cases have probably been overlooked, and no conclusion regarding incidence is possible. Nevertheless, the potential for airway compromise exists, especially in children. Respiratory complaints of CMT patients should be thoroughly investigated.
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ranking = 7
keywords = paresis
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10/85. myotonic dystrophy type 1 (DM1) presenting with laryngeal stridor and vocal fold paresis.

    myotonic dystrophy type 1 (DM1) is the most common inherited muscle disorder and may present in numerous ways due to characteristic multisystem involvement. We report a 47-year-old man who presented with an 8-year history of slowly progressive dyspnea and episodic stridor. The laryngeal paresis was documented with videostroboscopy and laryngeal electromyography, and treated with tracheostomy and antimyotonia agents.
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ranking = 5.0024346187098
keywords = paresis, muscle
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