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At least 865 records · Page 48Linked to original sources
PubMed1981

Facial nerve paralysis: it is always Bell's palsy?

Most patients with facial nerve paralysis have idiopathic, or Bell's palsy. Nevertheless, other more serious causes should be carefully excluded before Bell's palsy is diagnosed. Several tests can help the physician determine the site of the lesion and the physiologic extent of involvement of the facial nerve. The type of treatment depends on the cause of the paralysis and whether it is complete or partial. Familiarity with facial nerve anatomy and the various causes of facial paralysis should facilitate early diagnosis and appropriate treatment.

Cerebrovascular Disorders↗
PubMed1984

Facial nerve paralysis. 1. General evaluation, Bell's palsy.

The correct diagnosis of facial paralysis is not easily made but is important for proper management, since such paralysis is a sign or symptom of an underlying disorder. The clinician must be able to make an accurate and complete assessment of the entire facial nerve. Once a diagnosis is made, information from the history and results of topographic and electrical testing can be used in planning management and treatment. Bell's palsy, which is idiopathic, is the most common cause of facial paralysis. It is acute in onset and can come from a variety of causes. In the large majority of patients, the condition resolves either spontaneously or with treatment. Currently available treatments include corticosteroid therapy and facial nerve decompression, although both remain controversial.

Acute Disease↗
PubMed1984

Facial nerve paralysis. 2. 'All that palsies is not Bell's'.

Management of the patient with facial nerve paralysis challenges the diagnostic skills and clinical judgment of the attending physician. The clinician should not assume that all facial paralysis is Bell's palsy; the disease possibilities are broad and fascinating. Therapeutic options are still being evaluated, debated, and assessed. Appropriate management of the patient with facial nerve paralysis requires a complete history and precise examination.

Adult↗
PubMed2003

Use of botulinum toxin in facial paralysis.

Facial paralysis triggers aesthetic and functional changes that hold significant physical and psychological repercussions to those suffering from this condition. Botulinum toxin may be used to reduce the facial asymmetry encountered in patients suffering from facial paralysis. The onset of improvement starts usually 15 days after the injection. Patients' satisfaction increases with time, especially after 30 days. Adverse events concerning the perioral area are found but resume as the patients get used to the new dynamics. The use of botulinum toxin is effective in decreasing the hyperkinesis contralateral to facial paralysis. The global aesthetic aspect of the face improves.

Botulinum Toxins, Type A↗
PubMedDate not supplied

Facial nerve paralysis and Kawasaki disease.

A case of facial nerve paralysis in a patient with Kawasaki disease is described, and 17 cases in the literature are reviewed. A female predominance and a high rate of cardiovascular involvement were noted in patients with facial nerve paralysis and Kawasaki disease. The paralysis was self-limited, resolving without treatment in all surviving patients.

Facial Paralysis↗
PubMed1986

Use of WIN 51711 to prevent echovirus type 9-induced paralysis in suckling mice.

The systemic efficacy of the antipicornavirus agent WIN 51711 was assessed in suckling mice infected with echovirus type 9 (Barty strain). Single, daily intraperitoneal doses of WIN 51711 as low as 10 mg/kg significantly (P less than .01) slowed the rate of onset of echovirus-induced paralysis and reduced the number of paralyzed animals. Intraperitoneal administration beginning 2 hr before infection or 48 hr after infection was equally effective in preventing paralysis. Oral administration of WIN 51711 twice daily beginning 72 hr after infection was the most-effective dosage regimen, with doses as low as 3 mg/kg preventing paralysis in 75% of the animals. Titers of virus in asymptomatic mice on day 6 after infection were reduced by up to 4.75 log pfu in WIN 51711-medicated mice when compared with placebo. Maximal concentrations of WIN 51711 in adult mice after oral medication with a 100 mg/kg dose were 24.3, 21.5, 10.4, 9.8, 6.9, and 4.1 micrograms/g in heart, kidney, brain, liver, serum (micrograms/ml), and muscle, respectively at 0.5-1.0 hr after medication.

Administration, Oral↗
PubMed2001

Identification of genetic loci associated with paralysis, inflammation and weight loss in mouse experimental autoimmune encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE), a model for human multiple sclerosis, is an inducible inflammatory and demyelinating disease of the central nervous system (CNS). Susceptibility to this disease is heritable and is demonstrated by the development of an ascending paralysis accompanied by a loss in body wt 2-3 weeks following immunization with proteins derived from CNS myelin. In a previous genetic analysis of susceptibility to EAE in a cross between susceptible SJL/J mice and resistant B10.S mice, we found suggestive evidence of linkage with disease susceptibility at the telomeric end of chromosome 2 and in the central region of chromosome 3. To define these associations more precisely and to investigate the genetic factors controlling measurable phenotypes of EAE, we performed a new analysis with a larger number of mice. The results now indicate that the chromosome 2 locus significantly influences EAE-related weight loss (P = 6.7 x 10(-5)) and that the chromosome 3 locus is linked with the development of paralysis. In addition, an intriguing inheritance pattern was revealed in which female backcross mice generated from B10.S female x (B10.S x SJL/J)F(1) male parents experienced significantly more EAE-related weight loss (P = 1.2 x 10(-4)) than females generated from F1 female x B10.S male parents. After controlling for this inheritance, a new locus at the centromeric end of chromosome 8 was identified that significantly influences both the development of paralysis (P = 8.2 x 10(-6)) and the incidence of CNS inflammation (P = 7.0 x 10(-5)) in EAE.

Animals↗
PubMed1977

Lower limb paralysis induced in mice by a temperature-sensitive mutant of Moloney leukemia virus.

A temperature-sensitive mutant of Moloney murine leukemia virus defective in an early function and injected into newborn mice produced lower limb paralysis. Susceptible mice were inbred strains CFW/D, CBA/H, C3H/Bi/Ka, and outbred NIH Swiss stock. Inbred W/Fu rats and C57BL/Ka mice did not develop the paralysis, though the latter were infected with virus; the sera from these mice produced paralysis in susceptible CFW mice.

Animals↗
PubMed2003

An unusual cause of hypokalemic paralysis: chronic licorice ingestion.

Long-term licorice ingestion is a well-known cause of secondary hypertension and hypokalemia. Nevertheless, its initial presentation with a very severe degree of hypokalemia and paralysis is exceedingly rare. We report an elderly Asian man who presented to the emergency department with marked muscle weakness that progressed to paralysis. His blood pressure was 160/96 mm Hg. The major biochemical abnormalities were hypokalemia (plasma K+ concentration, 1.8 mmol/L) and metabolic alkalosis (HCO - 3 , 36 mmol/L). His renal potassium excretion was higher (transtubular potassium gradient of 9). Plasma renin activity and aldosterone concentration were suppressed and cortisol concentration was normal. A detailed history revealed that he had ingested tea flavored with 100 g of natural licorice root containing 2.3% glycyrrhizic acid daily for 3 years. Note that renal potassium wasting and hypertension persisted for 2 weeks after discontinuing licorice consumption along with KCl supplement and spironolactone. Long-term licorice ingestion should be kept in mind as a cause of paralysis with an extreme degree of hypokalemia to avoid missing this recognizable and curable medical disorder.

Acid-Base Imbalance↗
PubMed1997

Decreased paralysis and better motor coordination with microspinal versus PE10 intrathecal catheters in pain study rats.

We compared the standard PE10 catheter to a smaller microspinal catheter for intrathecal (IT) catheterization in rats. The PE10 or microspinal catheter was implanted in the lumbar subarachnoid space through the atlantooccipital membrane in rats (21 each group). Surviving rats without paralysis were tested on a rota-rod treadmill for motor function on Postoperative Days (POD) 3-6. Different doses of IT butorphanol were injected to demonstrate the functionality of the catheters by measuring tail-flick antinociception. Methylene blue was injected IT immediately before the spinal necropsy in each rat to identify the catheter tip location. For PE10 and microspinal catheters, the immediate death rate after the catheter implantation was 4 of 21 and 3 of 21 (no significant difference); paralysis rate was 8 of 21 and 2 of 21 (P < 0.05), and motor coordination recovery on POD6 was 67% and 91% (P < 0.01), respectively. Rats in both groups showed a dose-dependent response to IT butorphanol. Intrathecal methylene blue stained the lumbar spinal cord but not the surrounding tissue in both groups. Therefore, the microspinal catheter is better than the PE10 for IT catheterization in rats because it causes less paralysis and provides faster recovery of motor function.

Animals↗
PubMed1978

Antibiotic-induced paralysis of the mouse phrenic nerve-hemidiaphragm preparation, and reversibility by calcium and by neostigmine.

Certain antibiotics can induce neuromuscular paralysis, but the mechanism of this action is largely unknown. The purpose of this study was to compare the neuromuscular blocking potencies and reversibilities of 16 antibiotics in the isolated mouse phrenic nerve-hemidiaphragm preparation. The antibiotics tested were five aminoglycosides (neomycin, gentamicin, streptomycin, dihydrostreptomycin and kanamycin), tetracycline and oxytetracycline, polymyxins B and E, penicillins G and V, cephradine, cephaloridine, erythromycin, lincomycin, and clindamycin. Reversibility of the muscle paralysis by calcium and neostigmine was assessed. All the aminoglycosides resembled magnesium in blocking neuromuscular transmission, the neuromuscular blockade being almost completely reversed (to 64-77 per cent of control) by calcium but only poorly reversed by neostigmine (to 20-67 per cent of control). Neuromuscular blockade produced by the tetracyclines was also reversed by calcium (44-104 per cent) but not by neostigmine (0-15 per cent). Neuromuscular blockade produced by the polymyxins or by lincomycin was only partially reversed by calcium (0-34 per cent). Penicillin V, erythromycin, clindamycin, polymyxin B and the tetracyclines could also produce muscle paralysis by decreasing muscle contractility. This effect on contractility was irreversible by pharmacologic means. Penicillin G, cephradine and cephaloridine possessed negligible paralyzing effects on the nerve-muscle preparation. It is concluded that the different groups of antibiotics tested act by different mechanisms and that only the calcium-induced reversal of aminoglycoside block is predictable.

Animals↗
PubMed2005

Single acceleromyographic train-of-four, 100-Hertz tetanus or double-burst stimulation: which test performs better to detect residual paralysis?

BACKGROUND: Acceleromyography is regularly used as an isolated test to detect residual paralysis. The performance of acceleromyography, however, has not been investigated for the setting where calibration is impossible. This study first evaluated the reliability of a single acceleromyographic train-of-four (TOF) ratio (T4/T1) to detect residual paralysis and compared it with tactile estimation of fade after double-burst stimulation and 100-Hz, 5-s tetanus. The second part of the study investigated whether uncalibrated acceleromyographic TOF ratio can predict time to complete recovery. METHODS: Anesthesia was induced and maintained with propofol and sufentanil. In the first part of the study (n = 40) neuromuscular blockade was assessed by mechanomyography. After signal stabilization 0.15 mg/kg cisatracurium was given. At the end of surgery a first physician evaluated manual fade after double-burst stimulation, then, in the same patient, a single acceleromyographic TOF ratio was recorded; thereafter a second physician, unaware of the results, assessed fade after a 100-Hz, 5-s tetanus. Sensitivity, specificity, and negative and positive predictive value of the three tests to detect a mechanomyographic TOF > or =0.9 were calculated. In the second part of the study (n = 25) neuromuscular recovery was assessed simultaneously with mechanomyography and uncalibrated acceleromyography (current set manually at 60 mA); the time intervals from acceleromyographic TOF ratios of 0.6, 0.7, 0.8, and 0.9 until complete recovery, i.e., adductor pollicis mechanomyography 0.9 TOF ratios, were determined. RESULTS: The sensitivity of double burst stimulation was 29% (95% confidence interval [CI], 13-45%), its specificity was 100%, the negative predictive value was 29% (95% CI, 13-45%), and the positive predictive value was 100%. For a single acceleromyographic TOF ratio the respective values were 70% (95% CI, 54-86%), 88% (95% CI, 67-100%), 47% (95% CI, 23-71%) and 95% (95% CI, 86-100%). The respective values for 100-Hz, 5-s tetanus were 74% (95% CI, 59-89%), 55% (95% CI, 23-88%), 38% (95% CI, 12-64%), and 85% (95% CI, 72 -99%). At an uncalibrated acceleromyographic TOF ratio was 0.6, complete recovery occurred within 16 min (95% CI, 13.5-17.8 min). At acceleromyographic TOF ratios of 0.7, 0.8, and 0.9 this time interval was 12.5 min (95% CI, 10.2-14.8 min), 8 min (95% CI, 6.1-9.9 min), and 4 min (95% CI, 2.7-5.8 min), respectively. CONCLUSIONS: Acceleromyographic TOF performed better than double-burst stimulation or 100 Hz tetanus, but it did not reliably detect low degrees of residual paralysis when used as an isolated test at the end of surgery. The uncalibrated acceleromyographic TOF ratio, however, did predict the time to complete recovery.

Adult↗
PubMed1995

Paramyotonia congenita without paralysis on exposure to cold: a novel mutation in the SCN4A gene (Val1293Ile).

The autosomal dominantly inherited phenotype of paramyotonia congenita (PC) without paralysis on exposure to cold MIM 168350) was originally described by De Jong in 1955. This phenotype is clearly different from classical paramyotonia congenita Eulenburg, which has been shown to be a sodium channelopathy resulting from mutations in the gene for the alpha-subunit of the human skeletal muscle sodium channel gene (SCN4A). From the clinical picture it has always been assumed that PC without paralysis to cold and PC Eulenburg are allelic disorders. In this study we present three German families with PC without cold paralysis, provide evidence that the disorder is linked to the SCN4A gene and report a novel SCN4A mutation (Val1293Ile) segregating in these families.

Base Sequence↗
PubMed1979

Olivopontocerebellar atrophy with velopharyngolaryngeal paralysis: a contribution to the somatotopy of the nucleus ambiguus.

The authors report a case of olivopontocerebellar atrophy (OPCA) with velopharyngolaryngeal paralysis. The cerebellar syndrome appeared in a 66 year-old woman and ran its course until her death at 75. The velopharyngolaryngeal paralysis occured two years after the beginning of the cerebellar symtomatology and was limited for 6 months to a Gerhardt syndrome. Postmortem examination showed typical lesions of OPCA, and on serial sections of the medulla a massive loss of neurons in the lower two thirds of the nucleus ambiguus, bilaterally. The association of OPCA with velopharyngolaryngeal paralysis is exceptional. The anatomical findings in this case contribute to the somatotopy of the nucleus ambiguus in man by demonstrating the location of the velopharyngolaryngeal centers in this formation. The upper third plays only an accessory role in the velopharyngolaryngeal functions, and in the two lower thirds one finds, from the oral to the caudal extremity, first the velopharyngeal, then the laryngeal centers.

Aged↗
PubMed1999

CO2 laser endoscopic posterior partial transverse cordotomy for bilateral paralysis of the vocal fold.

OBJECTIVE/HYPOTHESIS: A clinical evaluation of CO2 laser endoscopic posterior partial transverse cordotomy (EPPTC) in patients with severely compromised airway due to bilateral paralysis of the vocal fold. STUDY DESIGN: An inception cohort of 25 patients over a 10-year period. METHODS: The CO2 laser EPPTC was unilateral in 15 patients and bilateral in 10. Variables were tested for potential statistical relation to successful rehabilitation of the airway. RESULTS: The use of the CO2 laser never resulted in adverse side effects. Complications were not encountered. A one-step, successful restoration of the airway was achieved in 68% (17/25) of patients. In univariate analysis, the CO2 laser EPPTC was statistically more likely to be successful if bilateral EPPTC was performed (P = .018). None of the following variables--age, sex, cause of bilateral paralysis, prior treatment, laser parameters, and duration of postoperative antibiotherapy and oral steroids--was statistically related to a successful restoration of the airway. Revision CO2 laser EPPTC, performed in six patients, resulted in an overall 92% (23/25) rate for a successful restoration of the airway. The overall tracheotomy rate was 8% (2/25). CONCLUSION: The authors' data confirm the safety, ease of performance, and efficiency of the CO2 laser EPPTC in patients with bilateral vocal fold paralysis. This report also suggests that the completion of bilateral CO2 laser EPPTC statistically increases the likelihood of restoring the airway in a one-step surgical procedure.

Adult↗
PubMed1999

Combined arytenoid adduction and laryngeal reinnervation in the treatment of vocal fold paralysis.

OBJECTIVE/HYPOTHESIS: Glottal closure and symmetrical thyroarytenoid stiffness are two important functional characteristics of normal phonatory posture. In the treatment of unilateral vocal cord paralysis, vocal fold medialization improves closure, facilitating entrainment of both vocal folds for improved phonation, and reinnervation is purported to maintain vocal fold bulk and stiffness. A combination of medialization and reinnervation would be expected to further improve vocal quality over medialization alone. STUDY DESIGN: A retrospective review of preoperative and postoperative voice analysis on all patients who underwent arytenoid adduction alone (adduction group) or combined arytenoid adduction and ansa cervicalis to recurrent laryngeal nerve anastomosis (combined group) between 1989 and 1995 for the treatment of unilateral vocal cord paralysis. Patients without postoperative voice analysis were invited back for its completion. A perceptual analysis was designed and completed. METHODS: Videostroboscopic measures of glottal closure, mucosal wave, and symmetry were rated. Aerodynamic parameters of laryngeal airflow and subglottic pressure were measured. A 2-second segment of sustained vowel was used for perceptual analysis by means of a panel of voice professionals and a rating system. Statistical calculations were performed at a significance level of P = .05. RESULTS: There were 9 patients in the adduction group and 10 patients in the combined group. Closure and mucosal wave improved significantly in both groups. Airflow decreased in both groups, but the decrease reached statistical significance only in the adduction group. Subglottic pressure remained unchanged in both groups. Both groups had significant perceptual improvement of voice quality. In all tested parameters the extent of improvement was similar in both groups. CONCLUSION: The role of laryngeal reinnervation in the treatment of unilateral vocal cord paralysis remains to be established.

Adult↗
PubMed2002

Long-term follow-up of fat injection laryngoplasty for unilateral vocal cord paralysis.

OBJECTIVE: The objective of the study was to evaluate the results of autologous fat injection laryngoplasty in the long-term management of unilateral vocal cord paralysis. STUDY DESIGN: A retrospective chart review and clinical voice re-evaluation of patients treated for unilateral vocal cord paralysis with autologous fat injection at the University of Iowa Hospitals and Clinics (Iowa City, IA) between May 1992 and September 1999. METHODS: The data analyzed included patient demographics, early and long-term vocal outcomes, additional surgical treatments, and patient survival. RESULTS: Fifty patients were treated with fat injection laryngoplasty, which included 44 treated for unilateral vocal cord paralysis. Thirty-one of the patients had fat injection as their primary procedure for permanent voice restoration. Eight patients treated had preoperative and postoperative voice data available. Using the GRBAS subjective voice assessment scale (0, normal; 3, severely abnormal), mean grade improved from 2.1 to 1.3 and breathiness improved from 1.4 to 0.5, at a mean period of 52 days. Thirteen of the 31 patients (41%) required additional procedures to achieve acceptable vocal outcomes. The median time to failure for these patients was 163 days. The initial treatment failure rate at 2 years was 30%, and the rate reached 45% by 4 years. CONCLUSION: Although fat injection laryngoplasty reliably improves the voice over the short term, the long-term voice outcome is unpredictable. Additional surgeries to deal with subsequent vocal deterioration are common. The role of autologous fat injection laryngoplasty in the modern era is limited.

Adipose Tissue↗
PubMed1989

Confirmation by magnetic resonance imaging of Bell's cruciate paralysis in a young child with Chiari type I malformation and minor head trauma.

We report the case of a young girl who suffered bilateral upper extremity paralysis after minor head trauma. Her clinical picture, as well as radiographic evidence of a fracture at C1, led to the diagnosis of Bell's cruciate paralysis, caused by a small lesion in the rostral part of the pyramidal decussation. Magnetic resonance images showed, in addition to a Chiari Type I malformation, an abnormality in the medulla. All previous cases of cruciate paralysis lack both pathological and radiographic supporting evidence.

Arnold-Chiari Malformation↗