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PubMed1999

Facial reanimation with jump interpositional graft hypoglossal facial anastomosis and hypoglossal facial anastomosis: evolution in management of facial paralysis.

When viable proximal facial nerve is inacessible, facial nerve paralysis has been classically managed with the hypoglossal facial anastomosis (HFA) for at least the past 70 years. While this procedure has proven its reliability, its problems with hemilingual atrophy (speech deglutition, drooling, mastication), hypertonia, synkinesis, and mimetic deficits indicate the need for a more perfect solution for facial paralysis. The jump interpositional graft hypoglossal facial anastomosis (JIGHFA) along with gold weight lid implantation and electromyographic (EMG) rehabilitation achieves substantial facial reanimation without hemilingual deficits. We present our results in 18 patients who underwent JIGHFA along with gold weight lid implantation and EMG rehabilitation for facial paralysis. These results were compared with those from published series of 30 patients treated with HFA with EMG rehabilitation evaluated with objective (House-Brackmann) criteria. Anonymous retrospective information from questionnaires from 22 of 48 patients who were treated with the classic HFA was also presented. In properly selected patients, the JIGHFA technique is capable of achieving substantial facial reinnervation (House-Brackmann grade III or better) in 83.3% of the patients without hemilingual sequelae which was seen in 45% of the HFA patients. In contrast to the HFA, this procedure can be used by patients with concomitant lower cranial nerve paralysis (except hypoglossal), and bilateral facial paralysis. Hypertonia, synkinesis, and lagophthalmus were less symptomatic in the JIGHFA patients. Mimetic expression was not improved in the JIGHFA population compared with the HFA group.

Adolescent↗
PubMed2003

Facial nerve paralysis following cochlear implant surgery.

OBJECTIVES: Facial nerve paralysis is a rare but devastating complication of cochlear implant surgery. The aims of the study were to define the incidence of facial nerve paralysis in our series and understand possible mechanisms of injury. STUDY DESIGN: Retrospective chart review and case reports. METHODS: Charts were reviewed of all 705 patients implanted between 1980 and 2002 at the authors' institutions to identify those with postoperative facial nerve weakness and determine incidence. For patients with facial nerve weakness, onset, degree, and timing of paralysis were noted; clinical findings were correlated to operative report findings. The method of treatment was noted, and the final facial nerve function outcome was recorded. RESULTS: Five patients (one child and four adults) were found to have postoperative facial nerve weakness, for an incidence of 0.71%. This complication was delayed in all cases, ranging from 18 hours to 19 days postoperatively. All patients were treated with steroids or steroids combined with antiviral medication, and all ultimately recovered normal facial function. CONCLUSIONS: In the study series, the incidence of facial nerve paralysis following cochlear implant surgery was 0.71%. Possible mechanisms of injury included heating injury and viral reactivation. All patients presented with a delayed facial nerve paralysis and did recover normal facial nerve function.

Adult↗
PubMed1992

Thyrotoxic periodic paralysis in the United States. Report of 7 cases and review of the literature.

Although hypokalemic periodic paralysis is a common complication of hyperthyroidism among Asian populations, it is an uncommon problem in the United States. The recent experience in an American medical center with 7 patients with thyrotoxic periodic paralysis (TPP) is reviewed. Compared to most descriptions of this disorder, which tend to reflect the international experience with this disease, patients with TPP in the United States reflect the ethnic makeup of the local population: the predisposition of patients of Asian origin is very evident, but whites are more frequently affected than most previous reports have recognized. Hispanics and American Indians also appear to be at increased risk, and blacks have also been affected. Except for the fact that hyperthyroidism is an absolute requirement for expression of the disease, TPP is identical to familial periodic paralysis (FPP) in its clinical presentation. TPP affects predominantly males (to an even greater degree than FPP), is rarely associated with a positive family history, and has a later onset of presentation than FPP (reflecting the need for hyperthyroidism to occur before the disorder can be expressed). Graves disease is the most common cause of hyperthyroidism in affected patients, but any cause of thyrotoxicosis (including administration of excessive amounts of exogenous thyroid hormone) can trigger attacks of TPP in susceptible subjects. Clinical features of thyroid disease may be very subtle or virtually nonexistent; as a result, thyroid function tests should be routinely monitored in patients with features of hypokalemic paralysis. The pathophysiology of the disorder is not well understood. Definitive treatment of hyperthyroidism leads to cessation of periodic hypokalemic paralysis, but symptoms can return with recurrence of the hyperthyroid condition. Potassium administration during an acute attack will shorten the duration of the episode, and treatment with propranolol, potassium supplementation, or spironolactone may prevent attacks in some patients.

Adult↗
PubMed2003

Acute otitis media and facial nerve paralysis in adults.

OBJECTIVE: The pathophysiology and treatment of facial nerve paralysis associated with acute otitis media are still under debate. The objective of this study was to review treatment strategies and extent of recovery in adult patients with the aim of defining a standard treatment protocol for this rare pathologic condition. STUDY DESIGN: Retrospective chart review. SETTING: University hospital, tertiary referral center. PATIENTS: Between 1993 and 2000, 11 patients were admitted for facial nerve paralysis secondary to acute otitis media. There were six women and five men without a history of chronic middle ear disease, who ranged in age from 21 to 71 years. Facial palsy was graded with the House-Brackmann scale: four patients had Grade III palsy, six had Grade IV palsy, and one patient had Grade V palsy. Bacteriologic examination of middle ear fluid was performed in four patients Streptococcus pneumoniae was observed in one patient, and the remaining three cultures were negative. INTERVENTIONS: All patients were treated with parenteral ampicillin-sulbactam or a third-generation cephalosporin in conjunction with oral or intravenous corticosteroids, except in a single patient with diabetes mellitus who received antibiotics alone. Myringotomy alone or with ventilation tube application was performed in eight patients. A simple mastoidectomy without facial nerve decompression was used in a patient with sudden impairment to Grade VI paralysis and worsening otitis after an initial improvement. RESULTS: Normal facial function returned in all patients, independently of the grade of the paralysis, the treatment strategy, or the outcome of the middle ear disease. The time of recovery varied from 2 weeks to 3 months, except for one patient who underwent mastoidectomy and in whom normal function returned in 10 months. CONCLUSIONS: The treatment of facial nerve paralysis secondary to otitis media should be as conservative as possible, using antibiotics and corticosteroids. Myringotomy and a ventilation tube should be added when spontaneous perforation of the tympanic membrane is not present. Mastoidectomy should be performed only when it is necessary to treat otitis media. Facial nerve decompression should not be necessary.

Adrenal Cortex Hormones↗
PubMed2004

The VlsE (IR6) peptide ELISA in the serodiagnosis of lyme facial paralysis.

OBJECTIVE: Facial paralysis is a manifestation of early disseminated Lyme neuroborreliosis. In the current study, we compared the immunoglobulin G (IgG) VlsE (sixth invariant region) peptide enzyme-linked immunosorbent assay (ELISA) with the current two-tier approach of sonicate ELISA and Western blot in the serodiagnosis of Lyme facial paralysis. STUDY DESIGN: Retrospective. SETTING: Tertiary referral center. PATIENTS: Serum samples from 47 Lyme patients with facial paralysis and 86 control subjects were analyzed for IgG antibodies to VlsE peptide of Borrelia burgdorferi and for immunoglobulin M (IgM) and IgG antibodies to sonicate antigens of B. burgdorferi using the two-tier approach. INTERVENTION: Diagnostic. MAIN OUTCOME MEASURE: Serum IgG antibody responses to VlsE (IR6) peptide. RESULTS: All 47 (100%) patients with facial paralysis and 4 (5%) of 86 controls had positive antibody responses to the VlsE peptide. In the two-tier test, 41 (87%) patients had positive IgM, 31 (66%) had positive IgG, and all 47 patients had positive IgM or IgG responses. Of the 86 control subjects, 2 (2%) had positive results with the two-tier test. Thus, the sensitivities of the VlsE and the two-tier tests were 100%; the specificity of the VlsE ELISA was 95% and the specificity of the two-tier test was 98%. CONCLUSIONS: The VlsE peptide ELISA showed a high sensitivity and specificity in the serological diagnosis of Lyme facial paralysis, similar to the two-tier test. The principal advantage of the VlsE peptide ELISA is that it requires only one test rather than four tests. However, the specificity of the VlsE test may not be as high as that of the two-tier test.

Adolescent↗
PubMed2004

Expression of emotion and quality of life after facial nerve paralysis.

OBJECTIVE: To investigate the facial expression of emotion and quality of life in patients after long-term facial nerve paralysis. STUDY DESIGN: Cross-sectional. SETTING: Facial nerve paralysis clinic. PATIENTS: Twenty-four patients with facial nerve paralysis and 24 significant others (partner, relative, friend). INTERVENTION: Patients were assessed using Sunnybrook, Sydney, and House-Brackmann grading scales and SF-36, Glasgow Benefit Inventory, and Facial Disability Index quality-of-life measures. RESULTS: When patients identified themselves as either effective or not effective at facially communicating each of Ekman's primary emotions (happiness, disgust, surprise, anger, sadness, and fear), 50% classified themselves as not effective at expressing one or more of the six emotions. Significant others of the not effective patients rated the emotions as more difficult for their partner-patients to communicate facially than did the significant others of effective patients. The SF-36 quality-of-life survey revealed lower social functioning relative to physical functioning for not effective patients. From the Sunnybrook Facial Grading System, more synkinesis was found for those patients not effective at expressing happiness, less brow and eye movement for patients not effective at expressing sadness, and less voluntary movement for those not effective with surprise. CONCLUSION: Movement deficits associated with expressing specific emotions and an association with quality-of-life measures were identified in patients with long-term facial nerve paralysis who saw themselves as not effective at facial expression of emotions. To improve management of emotional expression in patients with facial nerve paralysis, a broader approach is recommended, linking the practitioner's treatment goals with patient-driven outcome goals.

Adolescent↗
PubMed2006

Early diagnosis of thyrotoxic periodic paralysis: spot urine calcium to phosphate ratio.

OBJECTIVES: To identify a clinically reliable index of thyrotoxic periodic paralysis (TPP), a life-threatening emergency with unique and effective therapies. DESIGN: Diagnostic study. SETTING: University teaching hospital. PATIENTS: Fifty-three consecutive patients with hypokalemic paralysis during a 3-yr period and 30 thyrotoxic patients without paralysis as the thyrotoxic control group. INTERVENTIONS: For patients with hypokalemic paralysis, blood and second-void spot urine samples were obtained and measured by routine laboratory prior to therapy. For the thyrotoxic control group, blood and spot urine were collected when they visited outpatient clinics. MEASUREMENTS AND MAIN RESULTS: Twenty-nine patients fulfilled the criteria for TPP. Compared with the thyrotoxic control group, the TPP group had significant decreases in plasma potassium (K) and phosphate concentrations associated with very low urine K and phosphate excretion. Compared with the non-TPP group, the TPP group had significantly lower plasma creatinine and phosphate levels, a significantly higher urine calcium to creatinine ratio (0.25 +/- 0.12 vs. 0.08 +/- 0.07 mg/mg, p < .001), and a significantly lower urine phosphate to creatinine ratio (0.08 +/- 0.05 vs. 0.31 +/- 0.23 mg/mg, p < .001). The urine calcium to phosphate ratio had greater discriminatory power between TPP and non-TPP hypokalemic paralysis (4.1 +/- 2.3 vs. 0.5 +/- 0.6 mg/mg, p < .001). Using a urine calcium to phosphate ratio cutoff value of 1.7 mg/mg, sensitivity and specificity for TPP were 100% and 96%, respectively. CONCLUSIONS: Hypercalciuria and hypophosphaturia are characteristic features of TPP.

Adult↗
PubMed1989

The prognosis and management of idiopathic vocal cord paralysis.

If a vocal cord paralysis is termed idiopathic, no cause has been identified. The aim of this study was to assess the prognosis and management of patients with an idiopathic vocal cord paralysis. Data of 42 such patients have been stored prospectively. During follow-up 4 patients were found to have malignancies that in retrospect had been responsible for their vocal cord paralysis. Of the remainder approximately half either recovered vocal cord function or regained a near normal voice due to compensatory movement by the non-paralysed cord. No patient over the age of 60 compensated. No patient either recovered vocal cord function or compensated more than 12 months after the onset of his paralysis. In conclusion, patients with an idiopathic vocal cord paralysis should be suspected of harbouring a malignancy unless vocal cord mobility recovers, and management of the laryngeal dysfunction should be expectant for up to 12 months.

Adult↗
PubMed1997

Hemidiaphragmatic paralysis following subclavian vein catheterization.

The right subclavian artery was inadvertently punctured during attempted preoperative insertion of a right subclavian venous catheter in a 59-yr-old woman undergoing radical hysterectomy. Large supraclavicular swelling became apparent soon after the arterial puncture. The postoperative chest X-ray obtained approximately 24 h after the catheterization revealed significant elevation of the right hemidiaphragm, which was further augmented on the 2nd to 4th postoperative days; oxygenation was concurrently impaired during these days. It was clinically judged that the hemidiaphragmatic paralysis was responsible for the elevated diaphragm. Both chest roentogenogram and arterial blood gas analyses started to improve on the 5th day, finally returning to normal on the 6th day. It is unlikely that the surgical procedure caused the paralysis, because it dealt only with the lower abdomen. Rather, the attempts at the subclavian venous catheterization probably caused the phrenic nerve paralysis, because the phrenic nerve travels very close to the subclavian vessels. Both the large haematoma formation following the arterial puncture and the time course of the paralysis suggest that compression of the right phrenic nerve by the haematoma, rather than needle trauma, was responsible for the paralysis.

Catheterization, Central Venous↗
PubMed1977

Electromyographic (EMG) study in thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP) is produced by a different metabolic disorder than familial periodic paralysis. In the familial disorder, a myopathic cause is well known, but although electromyography can be used to demonstrate the site of the lesion in TPP, such studies are rare in the medical literature and the results are conflicting. In this report, EMG studies were carried out on eight Chinese patients with thyrotoxic periodic paralysis during the attack and the results compared with studies repeated during a remission. Most cases showed a myopathic pattern during an attack of paralysis which disappeared during remission. The myopathic changes noted were a decrease in duration of muscle action potentials, an increase in polyphasic potentials, a satisfactory interference pattern with reduced amplitude and a reduced amplitude of the evoked muscle action potential on nerve stimulation. Peripheral nerve function was normal in the cases studied. It is concluded that the weakness in TPP is myopathic and that the peripheral nerve function during paralysis is normal.

Action Potentials↗
PubMed2000

Spontaneous laryngeal paralysis in four white-coated German shepherd dogs.

Four cases of spontaneous laryngeal paralysis in juvenile white-coated German shepherd dogs are described. The presenting signs were typical for laryngeal paralysis, with stridor present in all four cases. Laryngoscopy revealed bilateral laryngeal paralysis in three cases, and unilateral paralysis in one. Concurrent megaoesophagus was also identified in one dog. All dogs underwent surgical treatment for laryngeal paralysis. Euthanasia was performed in one case due to intractable regurgitation and aspiration pneumonia. A possible association with white coat colour is discussed.

Animals↗
PubMed1975

Cattle and the paralysis tick Ixodes holocyclus.

Paralysis of domestic stock by the paralysis tick Ixodes holocyclus is chiefly a disease of young animals (especially calves) and of non-habituated stock introduced into tick-infested country in spring. The tick has a wide host range, but its principal hosts are bandicoots. The tick has one generation per year and the adult female, which causes almost all paralysis, is abundant in spring and early summer and occurs most commonly in overgrown or regrowth country where bandicoots are abundant. The distribution and behavior of the long and the short-nosed bandicoots are reviewed. The number of ticks required to induce paralysis in cattle and the protection from paralysis afforded by prior experience of the tick are discussed.

Animals↗
PubMed1984

Physical mapping of the paralysis-inducing determinant of a wild mouse ecotropic neurotropic retrovirus.

We have recently shown that a molecularly cloned ecotropic retrovirus, initially isolated from the brain of a paralyzed wild mouse, retained the ability to induce hind limb paralysis when inoculated into susceptible mice (Jolicoeur et al., J. Virol. 45:1159-1163, 1983). To map the viral DNA sequences encoding the determinant of paralysis, we constructed chimeric viral DNA genomes in vitro between parental cloned infectious viral DNA genomes from this neurotropic murine leukemia virus (MuLV) and from nonneurotropic amphotropic 4070-A MuLV. Infectious chimeric MuLVs, recovered after microinjection of NIH 3T3 cells with these recombinant DNAs, were inoculated into newborn SIM.S and SWR/J mice to test the paralysis-inducing potential. We found that the 3.9-kilobase-pair SalI-ClaI fragment of the neurotropic MuLV comprising the 3' end of pol and all env sequences was sufficient to confer the paralysis-inducing potential to chimeric viruses. Therefore, this region of the neurotropic MuLV genome most likely harbors the primary determinant of paralysis.

Animals↗
PubMed1984

Role of immunity in age-related resistance to paralysis after murine leukemia virus infection.

Resistance to the paralytic effects of a wild mouse (Cas-Br-M) murine leukemia virus infection develops with age and is complete by 10 days of age in susceptible NFS mice. The possibility that cell-mediated immunity plays a significant role in this resistance was suggested by the observation that treatment of 10-day-old mice with antithymocyte serum rendered them susceptible to paralysis. By comparison, mice rendered incapable of generating a humoral immune response by treatment from birth to 1 month of age with anti-immunoglobulin M serum did not develop paralysis after challenge with virus at day 10. Transfer of unseparated and T-cell-enriched populations of Cas-Br-M murine leukemia virus-immune spleen cells protected neonatally infected NFS recipients from paralysis; transfer of Cas-Br-M murine leukemia virus-immune populations enriched for B cells delayed the onset but did not ultimately protect neonatally infected NFS mice from paralysis. Transfer of naive adult spleen cells had no protective effect in neonatally infected NFS mice. High-level virus replication occurred in the spleens and brains of all mice that developed paralysis regardless of treatment; low-level virus replication in spleen and barely detectable replication in brain occurred in mice that remained clinically normal. These studies suggest that the age-acquired resistance to the paralytic effect of Cas-Br-M murine leukemia virus infection is immunologically mediated and that T cells may play a major role.

Age Factors↗
PubMed2001

Genetic control of neuroadapted sindbis virus replication in female mice maps to chromosome 2 and associates with paralysis and mortality.

Neuroadapted Sindbis virus (NSV) infection of mice causes hindlimb paralysis and 100% mortality in the C57BL/6 mouse strain, while adults of the BALB/cBy mouse strain are resistant to fatal encephalomyelitis. Levels of viral RNA are higher in the brains of infected C57BL/6 mice than in BALB/cBy mice (D. C. Thach et al., J. Virol. 74:6156-6161, 2000). These phenotypic differences between the two strains allowed us to map genetic loci involved in mouse susceptibility to NSV and to find relationships between mortality, paralysis, and viral RNA levels. Analysis of percent mortality in H2-congenic and F(1) mice suggested that the H2 locus, sex linkage, and imprinting were not involved in determining susceptibility and that resistance was partially dominant over susceptibility. Segregation analysis using CXB recombinant inbred (RI) mice indicated that the percent mortality was multigenic. Interval mapping detected a suggestive quantitative trait locus (QTL) on chromosome 2 near marker D2Mit447. Analysis of paralysis in the RI mice detected the same suggestive QTL. Viral RNA level in F(1) mice was intermediate. Interval mapping using viral RNA levels in RI mice detected a significant QTL near marker D2Mit447 that explained 69% of the genetic variance. This QTL was confirmed in F2 mice and was designated as Nsv1. Viral RNA level, percent paralyzed, and percent mortality were linearly correlated (r = 0.8 to 0.9). These results indicate that mortality, paralysis, and viral RNA levels are related complex traits and that Nsv1 controls early viral load and determines the likelihood of paralysis and death.

Adaptation, Physiological↗
PubMed2004

The exercise test as a monitor of disease status in hypokalaemic periodic paralysis.

OBJECTIVE: To evaluate exercise test responses in hypokalaemic periodic paralysis (HPP), to determine its value as a diagnostic tool and the factors that could affect the responses. METHODS: 22 subjects were studied from two families with HPP caused by R528H mutation, four patients with thyrotoxic periodic paralysis, 15 normal controls, and four controls with hyperthyroidism. All family members were submitted to clinical evaluation, electrophysiological exercise testing, and DNA analysis. Patients with thyrotoxic periodic paralysis had exercise tests before and after treatment of their hyperthyroidism. RESULTS: Abnormal responses to the exercise tests were obtained only in subjects with recent attacks of weakness. They were not correlated with genotype, as asymptomatic carriers were unaffected. Patients with thyrotoxic periodic paralysis showed pronounced impairment while they were hyperthyroid, but improved when they were euthyroid. One patient with HPP and chronic KCl use had an increase in amplitude potentials over approximately 20 minutes, possibly related to alteration of potassium homeostasis. CONCLUSIONS: The exercise test is a useful diagnostic test for periodic paralysis, but in the absence of recent weakness negative results must be viewed with caution. It has advantages over the DNA test in being a non-invasive functional test that can provide insights into abnormalities of muscle excitability.

DNA↗
PubMed1979

Idiopathic facial paralysis in the dog.

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.

Animals↗
PubMed1984

Respiratory response to partial paralysis in anesthetized dogs.

The ability to maintain alveolar ventilation is compromised by respiratory muscle weakness. To examine the independent role of reflexly mediated neural mechanisms to decreases in the strength of contraction of respiratory muscles, we studied the effects of partial paralysis on the level and pattern of phrenic motor activity in 22 anesthetized spontaneously breathing dogs. Graded weakness induced with succinylcholine decreased tidal volume and prolonged both inspiratory and expiratory time causing hypoventilation and hypercapnia. Phrenic peak activity as well as the rate of rise of the integrated phrenic neurogram increased. However, when studied under isocapnic conditions, increases in the severity of paralysis, as assessed from the ratio of peak diaphragm electromyogram to peak phrenic activity, produced progressive increases in inspiratory time and phrenic peak activity but did not affect its rate of rise. After vagotomy, partial paralysis induced in 11 dogs with succinylcholine also prolonged the inspiratory burst of phrenic activity, indicating that vagal reflexes were not solely responsible for the alterations in respiratory timing. Muscle paresis was also induced with gallamine or dantrolene, causing similar responses of phrenic activity and respiratory timing. Thus, at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle partial paralysis results in a decrease in breathing rate without changing the rate of rise of respiratory motor activity. This is not dependent solely on vagally mediated reflexes and occurs regardless of the pharmacological agent used. These observations in the anesthetized state are qualitatively different from the response to respiratory muscle paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗