Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Paralysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1994

Diaphragmatic paralysis in children: diagnosis by TM-mode ultrasound.

Diaphragmatic paralysis, a difficult diagnosis in the pediatric age group, has classically been made by fluoroscopy or B-mode ultrasound. We report our experience with TM-mode exploration. Twenty-seven patients suspected to have diaphragmatic paralysis were examined by means of inspiratory and expiratory chest radiography, fluoroscopy and B-mode ultrasound. The diaphragmatic echo was recorded on TM-tracing during spontaneous breathing using coronal oblique scans. Direction, excursion and the pattern of the transition between inspiration and expiration were analysed. In 7 patients examination was normal and TM mode demonstrated movement of normal direction and excursion with a sharp aspect of the transition zone. Diaphragmatic paralysis was present in 11 patients: unilateral in 9 and bilateral in 2 cases. TM mode demonstrated paradoxical movement, reduced excursion and a smooth transition zone. In 9 patients with diaphragmatic dysfunction TM mode demonstrated movement in the normal direction but with reduced excursion and a smooth transition zone. Compared to other imaging modalities, TM-mode records diaphragmatic movements more objectively. It can identify direction of the movement even if they are fast and of weak amplitude and in the case of bilateral paralysis. TM can differentiate paralysis from dysfunction. Moreover, this low-cost, non-irradiating made of imaging can be performed at the bedside and is available on all basic devices.

Adolescent↗
PubMed1989

Diaphragmatic weakness and paralysis.

Diaphragmatic weakness implies a decrease in the strength of the diaphragm. Diaphragmatic paralysis is an extreme form of diaphragmatic weakness. Diaphragmatic paralysis is an uncommon clinical problem while diaphragmatic weakness, although uncommon, is probably frequently unrecognized because appropriate tests to detect its presence are not performed. Weakness of the diaphragm can result from abnormalities at any site along its neuromuscular axis, although it most frequently arises from diseases in the phrenic nerves or from myopathies affecting the diaphragm itself. Presence of diaphragmatic weakness may be suspected from the complaint of dyspnea (particularly on exertion) or orthopnea; the presence of rapid, shallow breathing or, more importantly, paradoxical inward motion of the abdomen during inspiration on physical examination; a restrictive pattern on lung function testing; an elevated hemidiaphragm on chest radiograph; paradoxical upward movement of 1 hemidiaphragm during fluoroscopic imaging; or reductions in maximal static inspiratory pressure. The diagnosis of diaphragmatic weakness is confirmed, however, by a reduction in maximal static transdiaphragmatic pressure (Pdimax). The diagnosis of diaphragmatic paralysis is confirmed by the absence of a compound diaphragm action potential on phrenic nerve stimulation. There are many causes of diaphragmatic weakness and paralysis. In this review we outline an approach we have found useful in attempting to determine a specific cause. Most frequently the cause is either a phrenic neuropathy or diaphragmatic myopathy. Often the neuropathy or myopathy affects other nerves or muscles that can be more easily investigated to determine the specific pathologic basis, and, by association, it is presumed that the diaphragmatic weakness or paralysis is secondary to the same disease process.

Diaphragm↗
PubMed1998

[Recurrent laryngeal nerve paralysis after thyroid gland operations. Etiology and consequences].

In the period of 1 January 1990 to 31 December 1996 the thyroidectomy cases we performed were immediately followed by vocal cord evaluation using a flexible bronchoscope while the patient was still on the operating table. If an obvious cord paralysis was discovered, an exploration of the recurrent laryngeal nerve, to the level of the larynx, was performed. If the nerve was found to be intact, no further measures were taken. A severed nerve underwent suture repair. If an otolaryngologist diagnosed a vocal cord paralysis 1-5 days after surgery, a reoperation was recommended except in the cases where postoperative bronchoscopy had shown an easily mobile cord or the recurrent nerve was completely dissected during the operation. Within this 7-year period, we performed 3492 thyroidectomy operations. The diagnosis of subsequent unilateral postoperative vocal cord paralysis occurred in 48 cases. In 33 of these cases the status of the nerve in the surgical field was known: 4 patients had an intact nerve proved by complete dissection during thyroidectomy, in two patients the lesions of the nerve were detected intraoperatively (1 transsection, 1 partial resection), and 27 cases were followed by reoperation. Of the 33 patients mentioned above, in 19 instances the recurrent laryngeal nerve was found to be intact; 3 displayed signs of local trauma, and 11 were found to be severed with total discontinuity. Those patients with an intact nerve, or local nerve trauma only, went on to develop normal function within 6 months in 20 (91%) of 22 cases. Of the 11 with a severed nerve, 8 showed "autoparalysis" with good voice within 4-8 months, after suture repair in 10 cases. The patient with partial resection had no repair of the nerve. If immediate postoperative evaluation showed mobility of the vocal cords but a paralysis was detected later by an otolaryngologist and repeat intervention was not done, vocal cord function was spontaneously restored in 9 of 11 patients. Four patients refused reoperation. From 1990 to 1991, the recurrent laryngeal nerve was not always dissected during our thyroidectomy operations. However, this was done routinely from 1991 to 1996. Routine intraoperative dissection of the vocal cord nerve reduced the rate of postoperative cord paralysis from 2.0% to 1.2%. It also reduced the frequency of intraoperative nerve injury with total discontinuity from 0.58% to 0.23%.

Follow-Up Studies↗
PubMed2004

[Hypokalemic paralysis with thyrotoxicosis].

Hypokalemic periodic paralysis as a complication of thyrotoxicosis (thyrotoxic periodic paralysis) most often occurs in east Asian men. It is characterised by recurrent episodes of flaccid paralysis, hypokalemia, and underlying hyperthyroidism. It needs to be distinguished from sporadic and familial forms of periodic hypokalemic paralysis. No disturbances in the acid-base state and no extracorporal potassium loss are present. We report on the typical case of a young Chinese man presenting with hypokalemic periodic paralysis associated with yet unknown Graves' disease. Intravenous substitution of potassium and oral propranolol were administered. Complete remission was achieved after 10 hours. After medical therapy had normalised thyroid hormone levels, no further hypokalemic paralytic attacks occurred.

1-Propanol↗
PubMed2001

Post-intubation vocal cord paralysis: the viral hypothesis. A case report.

After digestive surgery, a 20-year-old man presented dysphonia and fever. Indirect laryngoscopy revealed a left vocal cord paralysis with no structural lesion. IgM and IgG were positive for cytomegalovirus and negative for human immunodeficiency virus, herpes simplex virus, varicella zoster virus and Epstein-Barr virus. The patient recovered spontaneously with a normal voice, and the mobility of vocal cord recovered within 3 months. The aetiology of post-intubation vocal cord paralysis (VCP) remains controversial. Vocal cord paralysis with cytomegalovirus has been reported in two cases associated with acquired immunodeficiency syndrome. Vocal cord paralysis secondary to viral disease has also been described in other circumstances. panied by polyneuritis, especially in immunocompromised patients. We report the case of a patient with transitory unilateral post-intubation vocal cord paralysis which could have been related to a virus infection.

Adult↗
PubMed2003

Problems with eating and drinking in patients with unilateral peripheral facial paralysis.

Patients with facial paralysis not only suffer from asymmetry of the face, but also from problems with eating and drinking. To demonstrate that these patients have many problems with activities such as eating and drinking, we examined 17 outpatients with a unilateral peripheral facial paralysis for the presence of problems in these functions. To collect data, all patients completed a questionnaire concerning the problems they had directly following onset of the paralysis and at the moment of this study. In addition, they were examined to determine the severity of the paralysis, the problems with eating and drinking, their experiences regarding impairments and disabilities, and the compensatory behavior. The result of the study is a portrayal of problems and conscious or unconscious compensations. Furthermore, we concluded that the Sunnybrook Facial Grading System score does not predict the number of problems in eating and drinking, the number of compensations, and the emotional impact. Significant correlations are found only between various scores on Visual Analog Scales and the number of compensatory actions. Patients differ in how they experience the extensive problems due to the facial paralysis and in the extent to which they are successful in adaptation. Consulting a speech therapist for treatment of functional problems is a meaningful adjunct to regular therapy. The treatment of deglutition disorders can be best based upon the detailed information of the questionnaire and the examination of eating, drinking, and compensatory behavior.

Adaptation, Physiological↗
PubMed2005

A case report and review of hypokalemic paralysis secondary to renal tubular acidosis.

A 5-year-old girl with distal renal tubular acidosis (RTA) and hypokalemic muscle paralysis is reported. RTA is a known cause of hypokalemia, but in spite of the presence of persistent hypokalemia muscular paralysis is uncommon, rarely described in children, and the onset of paralysis may initially be misinterpreted particularly if the patient is attended by a physician who is not a pediatric nephrologist. Therefore parents must be informed about this possibility. Still, as the clinical appearance of hypokalemic paralysis is quite similar to familial hypokalemic periodic paralysis, and because the emergent and prophylactic treatment of the two disorders are quite different, we discuss the diagnostic evaluation and the treatment for both of them.

Acidosis, Renal Tubular↗
PubMed2005

Recovery from paralysis with succinylcholine increased Response entropy and EMG but not State entropy.

OBJECTIVE: It is reported that the electromyogram is an indicator of patient arousal during pain stimulation if anesthesia is inadequate. This may not be true during recovery from succinylcholine induced paralysis. We evaluated State entropy of the electroencephalogram (EEG, 0.8-32 Hz) and Response entropy, a combined measure of the electromyogram (EMG) and EEG (0.8-47 Hz), during recovery from paralysis with succinylcholine. METHODS: Twenty patients were randomized to receive either 0.8% (n = 10) or 1.4% isoflurane (n = 10), with 2 mg/kg succinylcholine administered for paralysis in all patients. State entropy and Response entropy were evaluated using a Datex-Ohmeda Entropy module. Frontal EMG was measured separately by an EEG module. State entropy, Response entropy, and EMG were measured in awake patients, during isoflurane anesthesia and paralysis, and after 100% recovery to train of four stimulation. RESULTS: Response entropy and State entropy decreased from awake levels in a dose related manner during 0.8% or 1.4% isoflurane and succinylcholine. Recovery from succinylcholine significantly increased Response entropy and EMG in 5 of 10 patients with 0.8% isoflurane and 8 of 10 with 1.4% isoflurane without a change in State entropy. CONCLUSION: Although RE and EMG increased during recovery from paralysis with succinylcholine, SE, an indicator of EEG, was not stimulated. EMG activity may not be an indicator of patient arousal after succinylcholine treatment.

Anesthetics, Inhalation↗
PubMed1991

Diaphragm paralysis following cardiac surgery: role of phrenic nerve cold injury.

Diaphragm paralysis has been reported radiologically after cardiac surgery with an incidence ranging from 30% to 75% of patients. We studied 100 consecutive patients undergoing open heart operations, half of whom received ice/slush topical hypothermia (group 1) and half of whom did not (group 2). Chest radiology and diaphragm screening were performed at 1 week, 1 month, and every 6 months thereafter in all patients with an elevated diaphragm. Phrenic nerve conduction time was measured in all patients in whom there was radiological evidence of diaphragm paralysis 1 week postoperatively. The two groups were similar in terms of age and sex. Aortic cross-clamp time was less in group 1 (61.5 +/- 15.6 minutes) compared with group II (74.4 +/- 20.8 minutes), although this difference was not significant. Significant differences, however, were found for radiological evidence of partial left lower lobe collapse (82% in group 1 versus 32% in group 2; p less than 0.01) and for radiological evidence of diaphragm paralysis (32% in group 1 versus 2% in group 2; p less than 0.001) within the first postoperative week. Unilateral diaphragm paralysis developed in 16 group 1 patients (15 left sided, 1 right sided) compared with only 1 patient in group 2. In these 16 group 1 patients, diaphragm paralysis was still present in 12 (75%) at 1 month and in 5 (31.3%) at 1 year postoperatively. There were no significant differences between the two groups in terms of postoperative arrhythmias, myocardial infarction, or mortality. Phrenic nerve conduction time was found to be a sensitive indicator of phrenic nerve cold injury and recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Surgical Procedures↗
PubMed1996

Diaphragmatic paralysis: a complication of lung transplantation.

BACKGROUND: Damage to the phrenic nerve, either unilaterally or bilaterally, is a well-documented complication of cardiac operation, but less commonly reported after lung transplantation. METHODS: A retrospective review of 185 single and sequential single lung transplant procedures was performed at The Toronto Hospital. Objective confirmation (fluoroscopy or ultrasound) of diaphragmatic paralysis was found in 6 patients. Paralysis was unilateral in 5 patients (all were left sided) and bilateral in 1 patient. RESULTS: The average length of ventilation was 8.2 +/- 9.2 days with an average intensive care unit stay of 11.2 +/- 10.6 days. Mean duration in the hospital was 37.5 +/- 11.1 days. The average length of intensive care unit stay and hospitalization were compared with all other sequential single transplantations performed from approximately the time of the first documented case of diaphragmatic paralysis. Intensive care unit stay and hospitalization for the other (no diaphragmatic paralysis) transplant recipients were significantly shorter (5.3 +/- 2.7 and 29.1 +/- 12.9 days, respectively; p < 0.05). One patient required noninvasive ventilatory assistance via bilevel positive airway pressure in the hospital. One other patient used bilevel positive airway pressure in the hospital and overnight for 6 months after discharge. All patients obtained acceptable lung function and were ambulatory upon discharge from the hospital. CONCLUSIONS: Clinically detectable diaphragmatic paralysis is an infrequent complication of lung transplantation and is associated with longer intensive care unit stay and hospitalization, but is not associated with significant adverse outcomes.

Adult↗
PubMed1981

Influence of early phases of paralysis on microcirculation of rat skeletal muscle.

By combining tissue pO2 measurements with morphological visualization and counting of perfused capillaries, early microvascular changes were investigated in paralysis of skeletal muscle of the rat. The models included experimental allergic encephalomyelitis (EAE), experimental allergic neuritis (EAN), 6-aminonicotinamide intoxication, and peripheral denervation. The results showed that in all models tissue oxygenation was either normal or elevated. In most cases this was accompanied by a reduced perfusion of the capillary bed, supporting the hypothesis of a dysfunction in oxidative metabolism. The effects of paralysis on capillary perfusion were more marked in red than in white muscles, except in spastic paresis. Flaccid paralysis had more deleterious effects on muscle microcirculation than spastic paralysis. Our data suggest that: (1) microvascular changes occur very early after the onset of paralysis and (2) later developing changes in the skeletal muscle such as atrophy cannot be ascribed to a lack of oxygen supply but rather, at least in part, to a dysfunction in oxidative metabolism.

6-Aminonicotinamide↗
PubMed1985

Motor paralysis in rats after repeated electroconvulsive shock: comparison between aural and corneal stimulation.

Daily transaural electroshock treatment of rats results in a reversible hindlimb paralysis. Assuming there is a relationship between current pathway and the route of electroshock administration we compared both the type of convulsive behavior and the incidence of paralysis produced by transcorneal shock with that of transaural stimulation. Both transaural and transcorneal stimulation induced clonic and tonic convulsions, whereas, only transaural stimulation induced a body flexion (twisting and writhing). The use of transaural electrodes induced a higher incidence of paralysis than the use of corneal electrodes. These data demonstrate that both (1) the type of convulsive behavior produced and (2) the incidence of paralysis is related to electrode placement suggesting that paralysis is a function of current pathway.

Animals↗
PubMed1982

Botulinum toxin type A: kinetics of calcium dependent paralysis of the neuromuscular junction and antagonism by drugs and animal toxins.

The effect of botulinum Toxin (BoTx), which blocks the mechanism of release of acetylcholine at neuromuscular junctions and induces paralysis of muscles stimulated by nerves, is known to be Ca2+-dependent. Amplitude of muscular contractions evoked by nerve impulse was studied in BoTx poisoned preparations. The present report notes that an increase in Ca2+ concentration in vitro delays paralysis of muscular contractions of the frog evoked by nerve impulse. The restorative effect of different drugs on this paralysis has been tested: 4-aminopyridine, ATXII (toxin isolated and purified from the sea anemone Anemonia sulcata tentacles) and a crude venom isolated from the scorpion Androctonus australis antagonize the BotX induced paralysis at physiological concentrations of Ca2+ (Cao2+ = 2 mM), whereas the restorative effect observed with tetra-ethylammonium or guanidine occurs at higher concentrations of Ca2+ (Cao2+ = 4 mM), as in mammals. ATXII restores in vivo the activity of a BoTx paralysed muscle of guinea pig and this effect is more efficient if the interval between the injection of BoTx and ATXII is shortened. These results on the frog and guinea pig are in agreement with those obtained on other biological preparations by several investigators. Moreover it is suggested that the antagonism of BoTx induced paralysis is a consequence of the increase in Ca2+ at the nerve ending. The efficiency of 4-aminopyridine and animal toxins is explained by an action on the nerve ending, by increasing Ca2+ from an interval compartment of the cell, whereas antagonism produced by guanidine and tetraethylammonium involves uptake of Ca2+ from the external medium. The bathing medium must be at a higher concentration of Ca2+ than usual. This explains the differences in antagonism obtained by these drugs and toxins in vitro and in vivo.

Animals↗
PubMed2006

Functional and physiologic results of video-assisted thoracoscopic diaphragm plication in adult patients with unilateral diaphragm paralysis.

BACKGROUND: Plication of the hemidiaphragm for unilateral diaphragm paralysis is infrequently performed in adults. Barriers to diaphragm plication have included the perceived need for thoracotomy and uncertainty of the potential benefits. The purpose of this investigation was to assess the effects of video-assisted thoracoscopic diaphragm plication in symptomatic adult patients with unilateral diaphragm paralysis. METHODS: Patients with unilateral diaphragm paralysis underwent an evaluation that included a chest radiograph, fluoroscopic sniff test, pulmonary spirometry, and the Medical Research Council (MRC) dyspnea score. Patients with symptomatic unilateral diaphragm paralysis present for at least 6 months were offered video-assisted thoracoscopic diaphragm plication. Patients who underwent diaphragm plication as well as those who declined surgery were reassessed at 6 months with a chest radiograph, spirometry, and the MRC dyspnea score. RESULTS: Twenty-five patients underwent left (19) or right (6) diaphragm plication through video-assisted thoracoscopic diaphragm plication (22) or thoracotomy (3). There were no operative deaths. Mean hospital length of stay for diaphragm plication was 3.7 days for video-assisted thoracoscopic diaphragm plication and 5.4 days for thoracotomy. After diaphragm plication, mean forced vital capacity, forced expiratory volume at 1 second, functional residual capacity, and total lung capacity improved by 17%, 21.4%, 20.3%, and 16.1%, respectively (p < 005) at 6 months. Mean MRC dyspnea scores also significantly improved in the operative cohort (p < 0001). Seventeen patients in the surgical cohort had returned to work at 6 months. Seven patients treated without surgery displayed a trend toward more frequent hospitalizations and deteriorating pulmonary spirometry and MRC dyspnea scores during the follow-up period. CONCLUSIONS: Plication of the hemidiaphragm using minimally invasive techniques produced significant improvements in patients' functional status, pulmonary spirometry, and MRC dyspnea scores. Video-assisted thoracoscopic diaphragm plication should be considered appropriate therapy in symptomatic adult patients with unilateral diaphragm paralysis.

Adult↗
PubMed2006

Radiology findings in adult patients with vocal fold paralysis.

AIM: To compile imaging findings in patients with vocal fold paralysis. MATERIALS AND METHODS: A retrospective analysis of the medical charts of 100 consecutive patients, admitted to our department with vocal fold paralysis was undertaken. After laryngoscopy, patients were referred for radiological work-up depending on their clinical history and clinical findings. Ultrasound of the neck and/or contrast-enhanced spiral computed tomography (CT) of the neck and mediastinum was performed, extending to include the whole chest if necessary. In one patient, CT of the brain and in two patients, magnetic resonance angiography was undertaken. Analysis of the clinical and radiological data was performed to assess the most frequent causes for vocal fold paralysis. RESULTS: In 66% of patients, the paralysis was related to previous surgery. Thirty-four percent of cases were labelled idiopathic after clinical examination. After imaging and follow-up, only 8% remained unexplained. Nine patients suffered from neoplasms, four from vascular disease, and 12 from infections. One patient developed encephalomyelitis disseminata on follow-up. CONCLUSION: Thorough radiological work-up helps to reduce the amount of idiopathic cases of vocal fold paralysis and guides appropriate therapy.

Adult↗
PubMed2005

Comparisons of steroid, acyclovir, lipoprostoglandin E1 and steroid + acyclovir treatments in facial paralysis: a rat study.

OBJECTIVE: To induce experimental peripheral facial paralysis by inoculation of HSV1 and to compare the effects of steroid, acyclovir, lipoprostoglandin E2 and steroid + acyclovir treatments in terms of clinical recovery, electrophysiologically and histopathologically. MATERIALS AND METHODS: A total of 132 adult female rats were used in this study. HSV type 1 strain was inoculated at the back of the left ear by using 27 gauge needle. Of all animals, 70 (53%) rats which developed facial paralysis were divided into five groups (n = 14 for each group) as control, steroid + acyclovir, lipoprostaglandin E1, steroid only and acyclovir only. At the end of the 21 days period, the rats were clinically examined and electrophysiological tests were performed, then decapitated and the nerve specimens were obtained. RESULTS: A modified electroneurography (ENoG) test was performed and the latencies and the amplitudes were compared. The findings of the intact side were better, but with no significant difference. Histopathologicaly edema was significantly smaller in all groups compared to the controls (p < 0.05). Similarly, no difference was seen in terms of vacuolar degeneration and Schwann cell hyperchromatisation among the groups and no significant difference in recovery period and rate of facial paralysis when all groups were compared. CONCLUSION: Facial paralysis induced by HSV1 recovered spontaneously within a week. In the treatment of facial paralysis, steroid alone, acyclovir alone, steroid + acyclovir, or lipoprostaglandin E1 all reduced edema in the infected facial nerve but there was no statistical difference in of the rate or degree of recovery.

Acyclovir↗
PubMed2006

Mutation screening in Chinese hypokalemic periodic paralysis patients.

Thyrotoxic periodic paralysis (TPP), familial periodic paralysis (FPP), and sporadic periodic paralysis (SPP) are the most common causes of hypokalemic periodic paralysis (hypoKPP). The patients present with similar clinical features characterized by episodic attacks of muscle weakness and a decrease in blood potassium. Mutations in the gene encoding the voltage-sensor coding regions of the skeletal muscle sodium channel gene (SCN4A) and the alpha-1 subunit of the skeletal muscle calcium channel gene were analyzed in 23 Chinese hypoKPP patients, including 1 FPP pedigree, 14 TPP patients, and 8 SPP patients. In addition, R83H mutation of the potassium channel subunit gene which was originally published as periodic paralysis mutation was also analyzed. A heterozygous CGT-TGT mutation at codon 672 in SCN4A gene was identified to segregate with the disease in the FPP family. Mutations in these regions were excluded in those patients with SPP and TPP. The results suggest that a likely genetic basis for FPP does not contribute to TPP and SPP, despite close similarities among FPP, TPP, and SPP.

Adult↗
PubMed2003

Utility of laryngeal electromyography in predicting recovery after vocal fold paralysis.

OBJECTIVES: To determine the value of laryngeal electromyography in predicting recovery after vocal fold paralysis and to determine what elements of laryngeal electromyography are most predictive of outcome. DESIGN: Cohort study with retrospective data review. SETTING: University voice center. PARTICIPANTS: Consecutive sample of 31 patients with vocal fold paralysis diagnosed by indirect laryngoscopy, using either nasal insertion with a flexible nasopharyngoscope or peroral with a 70 degrees Hopkins rod. Inclusion criteria were that laryngeal electromyography had to have been performed between 21 days and 6 months from the onset of symptoms and patients must have been followed a minimum of 6 months. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Vocal fold motion at 6 months from onset of symptoms. RESULTS: Nine subjects (29%) had resolved vocal fold motion, whereas 22 (71%) had persistent vocal fold paralysis. By using our laryngeal electromyography paradigm, 4 of 6 patients with a laryngeal electromyography prognosis of excellent resolved. The predictive value for a negative test was 66.7%. For patients with a fair or poor prognosis, 5 of 25 resolved. The predictive value for a positive test was 80%. Only 8 of 22 patients with persistent vocal fold paralysis had fibrillations, and spontaneous activity was not significantly related to outcome. Patients with absent or greatly decreased motor unit recruitment had a significantly higher proportion of permanent vocal fold paralysis (P<.05). Stepwise forward logistic regression determined that prognosis by laryngeal electromyography and onset time were significant predictors of outcome (P<.01). The model predicted 44.4% of resolved cases, which represents a moderate prediction. CONCLUSIONS: This study confirms the utility of laryngeal electromyography in assessing prognosis for recovery of vocal fold motion after laryngeal nerve injury. The results support our hypothesis that preset decision rules based on laryngeal electromyography data can be effectively used to determine a prognosis for recovery of vocal fold motion.

Electromyography↗