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Results for “Facial Paralysis”

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At least 181 records · Page 10Linked to original sources
PubMed1993

Anti-Borrelia burgdorferi antibodies in patients with facial paralysis.

Ninety-eight patients with facial paralysis were studied by an indirect enzyme-linked immunosorbent assay (ELISA) employing two types of Borrelia burgdorferi antigen, namely sonic extract and flagellum protein of B. burgdorferi. IgG or IgM antibodies were detected by sonic extract ELISA in 22 (32.4%) of 68 patients with Bell's palsy, and in 2 (10.0%) of 20 patients with varicella-zoster virus infection. This difference was statistically significant (P < 0.05). A positive reaction was more frequent with the sonic extract antigen, while the positive rates were significantly increased in Bell's palsy patients with hyperglobulinemia (P < 0.05). IgM antibodies were also significantly more frequently observed in patients who developed Bell's palsy between October and March (P < 0.05). Since none of the patients had a history suggestive of Lyme disease, some kind of non-specific reaction and certain undefined factors linked to a positive reaction against B. burgdorferi could be involved in Bell's palsy.

Adolescent↗
PubMed1992

Electromyographic feedback in the treatment of bilateral facial paralysis: a case study.

Electromyographic feedback in the treatment of facial paralysis has been shown to be a useful alternative to surgical procedures. In this paper we report on the partial recovery of a 7-year-old patient with congenital bilateral facial paralysis (Moebius syndrome) that had been considered untreatable by medical specialists. Biofeedback of electromyographic activity was provided together with specific instructions, social reinforcement, and exercises that the patient carried out at home. The rehabilitation training lasted 1 year, during which there was a substantial increase in the electromyographic activity of the muscles on both sides of the face. A follow-up after 1 year of discontinuing the treatment showed that the muscle activity had been maintained and that there was a marked improvement in the patient's mood and facial expression.

Abducens Nerve↗
PubMed1980

Maximal nerve excitability testing versus neuromyography: prognostic value in patients with facial paralysis.

Neuromyography (NMG) is compared with maximal nerve excitability testing (NET) as a prognostic tool in facial paralysis. Normal latencies, summation muscle action potentials, and test/retest reliability were determined in three groups of subjects. NMG was performed in 33 control subjects of Group 1 to determine test/retest reliability. To determine the range of normal facial nerve conduction latency and amplitude and configuration of the summation muscle action potentials, NMG was performed in 172 otolaryngologic control patients without facial paralysis. NMG and NET were then compared in Group 3, which consisted of 43 patients with Bell's palsy. Fluctuations in NMG were then analyzed in a fourth test series of three subjects from Group 1, in whom summatin muscle action potentials at various positions of the electrodes were compared. The high rate of fluctuations observed indicates the need for further assessment of test/retest reliability and standardization of normal values in NMG. Our results indicate that maximal NET is more reliable than NMG for prognosis of facial paralysis.

Adolescent↗
PubMed2004

[Effects of aminoguanidine on the expression of NOS in facial nerve and surrounding tissues of traumatic facial paralysis rats].

OBJECTIVE: To study the effects of inducible NOS inhibitor aminoguanidine on the expression of NOS in facial nerve and surrounding tissue of traumatic facial paralysis rats. METHODS: A small dose of aminoguanidine were intraperitoneally injected into rats before and after facial paralysis. The facial nerve and surrounding tissues were cut at different time point. Immunohistochemical ABC method was used to study the changes of NOS expression in facial nerve and surrounding tissues. RESULTS: The inducible NOS immunoreactivity was obvious inhibited in the facial nerve and surrounding tissues in aminoguanidine group. CONCLUSION: Aminoguanidine chronic treatment can obvious inhibit the inducible NOS expression in the facial nerve and surrounding tissues. Aminoguanidine can improve the regeneration of facial nerve and the recovery of traumatic tissues.

Animals↗
PubMed1991

[Measurement and clinical using of motor conduction latency time and motor conduction latency rate of facial nerve in health subjects and facial paralysis patients].

The motor conduction latency time (MCLT) and rate (MCLR) of facial nerve in 70 cases of health subjects and 60 cases of facial paralysis patients were measured using evoke EMG. The results showed that MCLT is below 4 ms and MCLR is above 25 m/sec in 70 cases of health subjects, while the MCLT is above 4 ms and MCLR is below 25 m/sec in 60 cases of facial paralysis patients. We have observed the difference of MCLR and MCLR on different age groups in health subjects. The results showed that MCLT is prolonged gradually and MCLR is gradual reduced after 50 years old groups. But the MCLT does not exceed 4 ms and MCLR is not slower than 25 m/sec. The results of this studies suggested that if MCLT is above 4 ms, and MCLR is below 25 m/sec, it is a index of facial nerve paralysis.

Adolescent↗
PubMed2000

Facial paralysis: is there a role for a therapist?

Rehabilitation for peripheral facial paralysis is often neglected and patients are left untreated. This article explains how nonsurgical rehabilitation, specifically facial neuromuscular retraining, restores function in these patients. Patients with facial paralysis resulting from viral causes, postsurgical tumor resection, traumatic injury, or congenital paresis may be candidates for treatment. Typical patients present with flaccid paralysis acutely and may develop abnormal movement patterns (synkinesis) as recovery progresses. Neuromuscular retraining is effective. It provides specific strategies that inhibit synkinesis based on individual function and unique facial nerve and muscle properties. Successful rehabilitation results in improved patient satisfaction, self-esteem, and quality of life. Electrical stimulation should not be used at any time in facial rehabilitation. There is evidence that it may be contraindicated, and it is unnecessary. The imperative in treating synkinesis is to inhibit abnormally contracting muscles, not stimulate flaccid ones. The unfounded use of electrical stimulation is an unnecessary expense for patients and third-party payers.

Allied Health Personnel↗
PubMed2004

Aciclovir or valaciclovir for Bell's palsy (idiopathic facial paralysis).

BACKGROUND: The most common disorder of the facial nerve is acute idiopathic facial paralysis or Bell's palsy and there may be significant morbidity or incomplete recovery associated with severe cases. OBJECTIVES: To assess the efficacy of aciclovir or similar agents for treating Bell's palsy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register (searched April 2003), MEDLINE (from January 1966 to April 2003), EMBASE (from January 1980 to April 2003) and LILACS (from January 1982 to April 2003). We also contacted authors of identified trials. SELECTION CRITERIA: Randomised or quasi-randomised trials of aciclovir or valaciclovir therapy, alone or in combination with any other drug, in patients with Bell's palsy. DATA COLLECTION AND ANALYSIS: We identified six randomised trials. MAIN RESULTS: Three studies met our inclusion criteria, including 246 patients. One study evaluated aciclovir with corticosteroid versus corticosteroid alone, another study evaluated aciclovir alone versus corticosteroid and a further study evaluated valaciclovir with corticosteroid versus corticosteroid alone or versus placebo alone. Incomplete recovery after one year: data were not available. An analysis was performed on data reported at the end of the study period in each trial. The results from one study four months after the start of treatment significantly favoured the treatment group, whilst the results of the study three months after the start of treatment significantly favoured the control group. The results from the second study at four months showed no statistically significant difference between the three groups. Adverse events: relevant data were not reported in any of the three trials. Complete facial paralysis six months after start of treatment: only one patient had complete paralysis upon entering one of the studies. This patient was assigned to the control group and the level of recovery attained was not reported. Motor synkinesis or crocodile tears one year after start of treatment: data were available up to a maximum of four months after onset of paralysis. One study reported a significant difference between the treatment groups in favour of the aciclovir plus corticosteroid group over corticosteroid alone, another demonstrated an inconclusive result with no difference between the aciclovir and corticosteroid. The third study did not comment upon these sequelae. REVIEWERS' CONCLUSIONS: More data are needed from a large multicentre randomised controlled and blinded study with at least 12 months' follow up before a definitive recommendation can be made regarding the effect of aciclovir or valaciclovir on Bell's palsy.

Acyclovir↗
PubMed1992

Facial paralysis in temporal bone trauma.

A retrospective review of 36 patients with delayed-onset (19 patients) and immediate-onset (17 patients) traumatic facial paralysis was performed. We hypothesized that traumatic delayed-onset facial paralysis does not necessitate surgical decompression under any routine circumstances. Of 19 patients in this group, normal recovery (House grade 1) occurred in 94 percent of the patients without surgical intervention. The small percentage (6%) of these patients who failed to recover completely demonstrated mild degrees of weakness and synkinesis (House grade 2). Immediate-onset paralysis occurred in 17 patients. It has a much poorer prognosis. Seven patients with penetrating wounds had facial nerve transections, usually of the vertical portion of the facial nerve. Closed head injured patients with immediate-onset facial paralysis sustained injuries usually to the horizontal and perigeniculate portion of the facial nerve. For those cases in which surgical exploration of the traumatized facial nerve is indicated, the operating surgeon should have the capacity to enlarge the exposure with a translabyrinthine or middle-fossa dissection.

Adolescent↗
PubMed1990

Slowly progressive facial paralysis due to vascular malformation of the brain stem.

Slowly progressive facial paralysis is suggestive of a diagnosis other than Bell's palsy. A case of slowly progressive facial paralysis caused by a cavernous angioma of the brain stem is presented. The classification of vascular malformations of the central nervous system is described with emphasis on the MRI appearance of these lesions.

Brain Neoplasms↗
PubMedDate not supplied

Peripheral facial paralysis as initial manifestation of hypertension in a child.

Hypertension is one of the rare causes of peripheral facial paralysis in children. The unawareness of this association at presentation may cause serious medical errors and result in delays in the diagnosis of hypertension, which may worsen with corticosteroid therapy given for Bell's palsy. We describe a severely hypertensive child who was first seen with peripheral facial paralysis and given corticosteroid therapy in another hospital. She presented to our clinic during the second facial paralysis attack with hypertensive pontine hemorrhage.

Cerebellopontine Angle↗