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PubMedDate not supplied

Use of botulinum toxin to lateralize true vocal cords: a biochemical method to relieve bilateral abductor vocal cord paralysis.

Using the mongrel dog as an animal model, we studied the effectiveness of botulinum toxin (Oculinum) to lateralize the true vocal cord. This experiment was undertaken in order to determine whether the toxin can improve the airway in subjects with bilateral abductor vocal cord paralysis. The toxin was injected into the cricothyroid muscle to block neuromuscular transmission at the motor end-plate. Paralysis of the cricothyroid muscle was achieved and documented by electromyography and videotaped endoscopy. Paralysis of the cricothyroid muscle decreases the tension of the true vocal cord and allows the cord to take a more lateral position. In this preliminary report, the literature is reviewed, the effect of and action of the toxin are discussed, and the results of the experimental protocol, establishment of dose-response curves, and techniques of injection are presented. Preliminary data suggest that there is an increase in the airway by lateralizing the true vocal cord with this biologic substance, and that this method may have many applications in clinical medicine for the otolaryngologist-head and neck surgeon.

Animals↗
PubMed1989

Facial nerve paralysis with benign parotid masses.

Facial paralysis in the presence of a parotid mass has been associated classically with a presumed diagnosis of malignancy. However, isolated case reports have documented the occurrence of paresis or paralysis secondary to pathologically benign, nonneurogenic parotid lesions. These previous cases have been reviewed and three additional cases are described. Comparisons are made on age, sex, symptoms, physical findings, pathologic findings, and prognosis. Involvement of the seventh nerve may be explained on the basis of compression, especially in association with local inflammation. Although facial paralysis still should be considered indicative of a malignancy, it also may be caused by benign masses, particularly those associated with rapid enlargement and/or infection.

Abscess↗
PubMed1996

Vocal fold paralysis following the anterior approach to the cervical spine.

The anterior cervical approach is commonly used for access to the cervical spine. Vocal fold paralysis (VFP), a complication of this approach, is underrepresented in the literature. A review of the database of the Vanderbilt Voice Center revealed 289 patients with VFP, including 16 patients who developed paralysis as a result of an anterior cervical approach. The paralysis was on the right side in all but 1 patient. Compared to patients who developed VFP after thyroidectomy and carotid endarterectomy, patients with VFP after an anterior cervical approach have a higher incidence of aspiration and dysphagia, suggesting the presence of trauma to the superior laryngeal and pharyngeal branches as well as the recurrent branch of the vagus nerve. Two patients had partial return and 1 patient had complete return of vocal fold movement within 10 months. Of the remaining 13 patients, 8 underwent vocal fold medialization with improvement of symptoms. Two patients are 6 and 7 months postinjury and await vocal fold medialization. Two patients are 27 months and 45 months postinjury and are considering vocal fold medialization. The remaining patient was lost to follow-up. An anatomic-geometric analysis of the right and left recurrent laryngeal nerves was performed by using measurements obtained from computed tomography scans of 8 patients with idiopathic unilateral VFP, as well as experience gained through surgical and cadaveric dissections. We conclude 1) the anterior cervical approach may place multiple branches of the vagus nerve at risk; 2) because of anatomic-geometric factors, the right-sided anterior cervical approach may carry a greater risk to the ipsilateral recurrent laryngeal nerve than does the left; and 3) an understanding of the anatomy and geometry presented herein allows relatively safe exposure from either side of the neck.

Adult↗
PubMed1996

Laryngeal electromyography findings in idiopathic congenital bilateral vocal cord paralysis.

Children with idiopathic congenital bilateral vocal cord paralysis (BVCP) were investigated by electromyography (EMG) of the posterior cricoarytenoid and thyroarytenoid muscles to determine whether laryngeal EMG findings had diagnostic or prognostic significance. Four children between 3 weeks and 33 months of age were studied. Three had abductor paralysis and were tracheostomy-dependent, while the fourth had adductor paralysis requiring a feeding gastrostomy. Two of these patients also had other anomalies. Motor unit potentials showing phasic bursts with respiration were found in all four cases, while three children developed a full interference pattern on lightening of the anesthetic. Follow-up for between 37 and 52 months showed no significant clinical improvement in any of the patients. While the diagnosis of idiopathic congenital BVCP can represent a heterogeneous group of conditions, the findings suggest that normal laryngeal EMG findings may be a feature of idiopathic congenital BVCP but do not imply a favorable prognosis for early recovery. They may, however, have implications to explain the likely site of lesion in idiopathic congenital BVCP.

Child, Preschool↗
PubMed1998

Cervicomedullary compression: an unrecognized cause of vocal cord paralysis in rheumatoid arthritis.

Cervicomedullary compression (CMC) from traumatic, infectious, or congenital processes of the atlanto-axial joint is a known cause of vocal cord immobility. Cervicomedullary compression can also occur from destructive arthritic changes and inflammatory pannus formation at the occipito-atlanto-axial joint in patients with rheumatoid arthritis (RA). We present findings suggesting that CMC in patients with RA is an unrecognized cause of vocal cord immobility. Previously, vocal cord immobility in patients with RA has been assumed to be cricoarytenoid arthritis with joint fixation. We report 3 patients with RA and radiographically demonstrated CMC with vocal cord immobility. One patient had bilateral vocal cord immobility and airway obstruction; 2 patients had unilateral cord paralysis and contralateral paresis without airway compromise. All patients had myelopathy and neck pain in addition to brain stem symptoms. All patients underwent transoral-transpharyngeal decompression of the anterior craniocervical junction with subsequent posterior fusion. These patients demonstrated full return of vocal cord function within 3 months of decompression. We propose that CMC is a cause of vocal cord paralysis in patients with RA that may go unrecognized without appropriate imaging studies of the skull base and physician awareness of symptoms of occipito-atlanto-axial subluxation and/or basilar invagination with brain stem compression. Our results demonstrate that CMC in RA is a potentially reversible cause of vocal cord paralysis.

Aged↗
PubMed1978

Tick paralysis in three children. The diversity of neurologic presentations.

Reviewed are 3 cases of tick paralysis in children each with a different presentation. One child presented with an ascending flaccid weakness, another with weakness and cerebellar signs, and a third with pure cerebellar signs. Ixodes scapularis, the black-legged deer tick, was the offending tick in Case 3 and apparently has not been previously reported to cause paralysis in humans. Because of the potential for a fatal outcome, it is imperative to consider tick paralysis in any child with an ascending flaccid weakness or acute ataxia.

Ataxia↗
PubMedDate not supplied

Facial paralysis in children: differential diagnosis.

The differential diagnosis in 170 patients between birth and 18 years of age is reviewed. There are a number of obvious physical findings and historical features that allow one to make a diagnosis rather quickly. Pain, vesicles, a red pinna, vertigo, and sensorineural hearing loss suggest herpes zoster oticus. Slow progression beyond three weeks, recurrent facial paralysis involving the same side, facial twitching, weakness, or no return of function after six months indicate a neoplasm. Bilateral simultaneous facial paralysis indicates a cause other than Bell's palsy, such as Guillain-Barré syndrome, pseudobulbar palsy, sarcoidosis, and leukemia. Recurrent facial paralysis associated with a fissured tongue, facial edema, and a positive family history should suggest Melkersson-Rosenthal syndrome.

Abnormalities, Multiple↗
PubMedDate not supplied

Medullary carcinoma of the thyroid masquerading as idiopathic vocal cord paralysis.

The following conclusions may be drawn as a result of our study: 1. Serum calcitonin by radioimmunoassay proved to be the only valid preoperative indicator in a case of medullary carcinoma of the thyroid occurring with vocal cord paralysis. This test should be considered in all cases of idiopathic recurrent laryngeal nerve paralysis, especially when obscure thyroid pathology is suspected. 2. Provocative calcitonin testing, such as a calcium infusion test, may help verify presence or absence of disease in equivocal cases of calcitonin assay. 3. Vocal cord paralysis may be the first sign of intrathroid malignancy. 4. In the furture, serum calcitonin assay (drawn posttreatment) may be a valuable prognostic indicator and may guide the need for additional treatment.

Adult↗
PubMed1983

The facial paralysis prognostic index.

The treatment of facial paralysis requires a reliable estimate of prognosis as well as an accurate diagnosis. Although the majority of patients recover, the degree of subsequent facial function varies. An estimation of the risk of nerve degeneration and subsequent disability is needed to guide therapy and to advise patients. Currently, prognosis is obtained by clinical evaluation of initial signs and symptoms, specific nerve excitability and function testing, and response to medical therapy. This study attempts to identify and quantitate factors that predict the outcome of facial paralysis. In 1214 patients with Bell's palsy, we identified factors associated with a severe course or poor outcome. We analyzed the predictive value of each item in an extensive research protocol, estimating the relative contribution to the total risk of unfavorable outcome by means of multiple regression models. With the use of these data, we have developed the facial paralysis prognostic index (FPPI). The FPPI can assist otologists to more accurately estimate outcome based on physical examination and electrical testing.

Adolescent↗
PubMed1984

Experimental studies for correction of superior laryngeal paralysis by fusion of the thyroid to cricoid cartilages.

Contraction of the cricothyroideus muscles (CTMs), innervated by the superior laryngeal nerves (SLNs), modulates the voice by tilting the thyroid cartilage anteriorly onto the top of the cricoid and tensing the vocal cords. Either unilateral or bilateral paralysis of the SLNs is disabling for individuals with above-average voice demands. Some patients never compensate for this paralysis; there is no surgical procedure recognized to correct it. This study tested the hypothesis that surgical fusion of the thyroid and cricoid cartilages anteriorly can correct the problems of SLN injury by duplicating the mechanical tilt of the thyroid onto the cricoid cartilage normally produced by the CTMs. The SLNs were cut in 12 dogs. In six the cricoid and thyroid cartilages were fused anteriorly. Vocal cord and airway function was assessed preoperatively, immediately postoperatively, and 6 to 10 weeks after surgery. Following surgery there was no airway compromise and there appeared to be a more satisfactory compensation for the SLN paralysis in the fused larynges as compared with the unfused controls as determined by cinelaryngoscopic analysis.

Animals↗
PubMed1987

Laryngeal chondrosarcoma as a late-appearing cause of "idiopathic" vocal cord paralysis.

A case of laryngeal chondrosarcoma is presented as a late-appearing cause of idiopathic vocal cord paralysis. Twelve cases are cited from the literature in which the cause of so-called idiopathic vocal cord paralysis was discovered with long-term followup. The natural history of idiopathic vocal cord paralysis is addressed, and recommendations for patient management are discussed.

Chondrosarcoma↗
PubMed1993

Transcutaneous Teflon injection for vocal cord paralysis.

In 1989, I reported a series of 19 cases of unilateral vocal cord paralysis treated by transcutaneous Teflon injection. At that time it was shown that unilateral vocal cord paralysis could be effectively treated in the office in the unanesthetized patient using a transcutaneous route of injection. Since that time, an additional 43 patients have been treated using a similar technique. The initial impression of safety and efficacy has been confirmed in this subsequent series. Several refinements in this technique have simplified its use and improved its reliability. No airway complications have been observed to date and no patients have required hospital admission. Transcutaneous Teflon injection can be considered a useful method for treatment of vocal cord paralysis in selected patients.

Adult↗
PubMed2005

Maintaining support in people with paralysis: what works?

Social support is a protective factor for well-being in the risk-and-resilience framework, yet people with paralysis report lower levels of support compared to people without paralysis. Rather than examine deficits, in this study, the authors conducted in-depth interviews with individuals who report high levels of social support to examine what sustains this protective factor. Because relationship equity affects social support, the authors also examined this. They selected participants who reported high levels of support from a survey sample of 299 U.S. adults experiencing some form of paralysis. Seventeen participants completed the in-depth interview. The importance of reciprocity, maintaining autonomy, and a positive outlook for sustaining support were themes identified in the content analysis. In their responses, people with high support emphasized that they do all they can to affect their environment positively, so that ideally, the only assistance that they cannot provide themselves is successfully obtained from others.

Adaptation, Psychological↗
PubMed2003

Cold induces shifts of voltage dependence in mutant SCN4A, causing hypokalemic periodic paralysis.

BACKGROUND: The authors reported a mutation, P1158S, of the human skeletal muscle sodium channel gene (SCN4A) in a family with cold-induced hypokalemic periodic paralysis (hypoKPP) and myotonia. OBJECTIVE: To identify mechanisms of temperature dependency in this channelopathy. METHODS: Using the amphotericin B perforated patch clamp method, sodium currents were recorded at 22 and 32 degrees C from the wild-type (WT) and P1158S mutant SCN4A expressed in tsA201 cells. Computer simulation was performed, incorporating the gating parameters of the P1158S mutant SCN4A. RESULTS: P1158S mutant SCN4A exhibited hyperpolarizing shifts in voltage dependence of both activation and inactivation curves at a cold temperature and a slower rate of inactivation than the WT. Computer simulation reproduced the abnormal skeletal muscle electrical activities of both paralysis at a low potassium concentration in the cold and myotonia at a normal potassium concentration. CONCLUSIONS: Both paralysis and myotonia are attributable to the biophysical properties of the SCN4A mutation associated with hypoKPP. This is the first report of an SCN4A mutation that exhibits temperature-dependent shifts of voltage dependence in sodium channel gating.

Action Potentials↗
PubMed2006

Hypokalemic paralysis due to Gitelman syndrome: a family study.

Hypokalemic paralysis is rarely seen as the presenting feature in patients with Gitelman syndrome. We report a Chinese man who presented with periodic paralysis, in whom molecular analysis revealed compound heterozygous inheritance of three mutations of the thiazide-sensitive sodium chloride cotransporter. Family history revealed intrafamilial variation in phenotypes. Gitelman syndrome should be considered as a cause of hypokalemic paralysis, and molecular analysis may help establish the diagnosis.

Adult↗
PubMed1999

A novel sodium channel mutation in a family with hypokalemic periodic paralysis.

OBJECTIVE: To identify the cause of hypokalemic periodic paralysis (HOKPP) in a family whose disease is not caused by a mutation in the dihydropyridine-sensitive (DHP) receptor alpha1-subunit gene (CACNA1S). BACKGROUND: Hypokalemic periodic paralysis is primarily caused by mutations within CACNA1S. Genetic heterogeneity for HOKPP has been reported, but no other locus has been identified. METHODS: Single-stranded conformational polymorphism (SSCP) analysis and PCR direct sequencing were used to screen the skeletal muscle alpha1-sodium channel gene (SCN4A) for a mutation in our family. RESULTS: SSCP analysis showed an abnormally migrating conformer in exon 12. Direct sequencing of the conformer showed a guanine to adenine transition at position 2006 in the cDNA sequence; this results in an amino acid substitution of a highly conserved arginine (Arg) to histidine (His) at position 669. This sequence alteration segregated only with the affected members of the kindred and was not found in a panel of 100 DNA samples from healthy controls. The amino acid substitution alters the outermost positive charge in the membrane spanning segment DII/S4, which is involved in voltage sensing. CONCLUSIONS: The first arginine in DII/S4 and in DIV/S4 within the skeletal muscle sodium channel and the L-type calcium channel genie CACNA1S appear to be critical for normal function. In all four cases, Arg to His mutations result in a disease phenotype. The identification of a mutation within the skeletal muscle sodium channel resulting in hypokalemic periodic paralysis represents a novel finding.

Adult↗
PubMed2004

Acute laryngeal paralysis induced by the migration of a totally implantable venous access device's catheter tip.

The authors report a case of acute vagus nerve paralysis that appeared during a course of chemotherapy. The drugs had been administered through a totally implantable venous access device (TIVAD), whose catheter tip had migrated into the right internal jugular vein (IJV) and was surrounded by a complete venous thrombosis. The supposed aetiology of this paralysis was a leakage of the cytotoxic drug (5-fluorouracil) from the vessel wall into the surrounding carotid space, because of the stagnation of the chemotherapeutic agent above the thrombosis. Four months after cessation of chemotherapy, the laryngeal paralysis was still evident.

Aged↗
PubMed2005

General practitioners' referral pattern for children with acute facial paralysis.

INTRODUCTION: The relative incidence of paediatric Bell's palsy is two to four times less than the condition in adults. The number encountered in our otolaryngology department falls short of the above prediction. This could either reflect the general practitioners' (GPs) patterns of referral or a lower incidence in our locality. METHODS: Postal questionnaires were sent to our local GPs to determine their referral practice when managing children presenting with acute facial paralysis. RESULTS: Of 233 questionnaires, 172 (74 per cent) were returned and analysed. Fifty-four per cent of GPs referred their patients to the local paediatric services, 22 per cent to an otolaryngologist, and the remaining 24 per cent of GPs were confident in diagnosing and managing Bell's palsy in children themselves. DISCUSSION AND CONCLUSION: Of the GPs surveyed 78 per cent did not refer children presenting with acute facial paralysis to an otolaryngologist. We suggest minimum investigations for acute facial paralysis in children before diagnosing Bell's palsy and stipulate otolaryngology referral for all.

Acute Disease↗