Cases reported "Facial Paralysis"

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1/15. Bell's palsy during interferon therapy for chronic hepatitis c infection in patients with haemorrhagic disorders.

    Two adult patients with life-long severe haemorrhagic disorders commenced on interferon-alpha2b therapy for chronic hepatitis c infection. Both developed Bell's palsy several weeks after commencing therapy, They were started on steroids and, in addition, the first patient discontinued interferon-alpha2b therapy while the second patient elected to continue with therapy. In both cases facial paralysis improved over the ensuing weeks. Bell's palsy is often idiopathic but has been reported. in association with herpesviruses. It is not a recognised complication of chronic hepatitis b or C infection, or interferon-alpha2b therapy. However, the interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of nerve palsies, including optic tract neuropathy, occurring during interferon therapy, and immune-based mechanisms are thought to play a role in the aetiopathogenesis. No reports of Bell's palsy in association with interferon therapy were identified in our literature search, although one possible case has been reported to the Committee of safety in medicine. Although Bell's palsy in our patients may have occurred by chance, a neuropathic effect of interferon-alpha2b on the facial nerve cannot be excluded and we urge physicians using interferons to be aware of this potential side-effect.
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2/15. Dynamic restoration in Mobius and Mobius-like patients.

    mobius syndrome is classically characterized by bilateral facial nerve and abducens nerve paralysis in combination with limb defects. In the past 110 years, physicians diagnosed children as having the syndrome on the basis of heterogeneity of symptoms and used the term "mobius syndrome" or "Mobius-like syndrome" for patients with multiple cranial nerve involvement. The cause and the exact pathogenesis of the syndrome still elude understanding. Genetic work-ups, radiological findings, and data from autopsies differ in their approaches and their findings of the basic causes of mobius syndrome. In the international literature, about 301 case reports are found scattered through the past century. The appearance of the facial deformity is easy to recognize, because the Mobius patient is impaired in his or her ability to communicate nonverbally. Despite ophthalmologic problems, it is the search for a smile that brings these patients to the reconstructive surgeon. Over the past 100 years, surgical efforts attempted to improve the mask-like appearance by static and dynamic procedures, usually local muscle transpositions. Today, combinations of microsurgical procedures and aesthetic techniques are being used to restore some movement to the expressionless face of these patients by nerve and muscle transplantation. This article discusses the heterogeneity of mobius syndrome, advocates a new classification system, presents the clinical findings of 42 patients who were seen and examined in consultation, and discusses the surgical management of 20 patients who underwent dynamic restorative microsurgery. Exemplary cases illustrating the preoperative work-up regimen and possible outcomes are reported.
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3/15. facial paralysis caused by tuberculosis in a 2.5-month-old infant.

    We describe an infant who presented with a cervical mass and ear discharge that did not respond to broad-spectrum antibiotics. Tuberculous infection was diagnosed after the onset of respiratory distress. Persistent otorrhoea that does not respond to conventional antibiotics or facial paralysis in a child with a discharging ear should alert the physician to a diagnosis of tuberculosis.
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4/15. Pontine hemorrhage presenting as an isolated facial nerve palsy.

    We report a case of an isolated facial nerve palsy in a young, otherwise healthy man who was found to have a pontine hemorrhage on computed tomography. Pontine hemorrhage is a rare cause of facial nerve palsy and has been reported in the literature as an isolated neurologic finding in only 1 other instance. This case reminds the emergency physician to remain vigilant for alternative causes of facial nerve palsy other than "idiopathic" Bell's palsy.
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5/15. facial paralysis as a presenting symptom of leukemia.

    facial paralysis may occur as a complication of central nervous system leukemias in children, but it is rarely a presenting symptom. This report describes an 8-month-old child who presented with peripheral facial palsy, failure to thrive, anemia, and otitis media. Antibiotic and steroid treatment led to an improvement in the clinical condition, but not the paralysis. At readmission 3 weeks later, physical examination revealed bluish, firm, palpable masses on the scalp and facial areas, and laboratory and imaging studies confirmed the diagnosis of acute myeloid leukemia. This case should alert physicians to consider hematologic malignancies in children with facial paralysis.
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6/15. facial nerve paralysis associated with Kawasaki disease.

    Kawasaki disease is a multisystem disorder with varying clinical expression. This is a report on one case of Kawasaki disease which during its clinical course developed facial nerve palsy and spontaneous recovery without specific treatment. It is hoped that this report will serve to remind physicians of the association of facial nerve paralysis with Kawasaki disease.
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7/15. Bell's palsy.

    Idiopathic facial (Bell's) palsy is an affliction commonly seen and managed by the family physician. Although the prognosis is generally good, steroids and cromolyn sodium have each been advocated to enhance full recovery. Surgical exploration of the nerve is indicated when the diagnosis is unclear. Various measures may be necessary to protect the eye.
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8/15. Patterns of degeneration of the facial nerve.

    Facial palsy is a distressing nonfatal disorder that creates an emotional crisis for the patient and often a therapeutic enigma for the physician. Among the causes for facial palsy are neoplasia, infection, trauma, and dysmorphogenesis. Histologic studies of the temporal bones of twelve subjects with facial nerve pathology demonstrate the susceptibility of the nerve to pressure atrophy in its course in the temporal bone. Lesions located central to the genu cause degeneration of the motor component distally and the sensory component medially. Lesions located peripheral to the genu cause degeneration of both sensory and motor bundles distally.
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9/15. 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.
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10/15. Familial recurrent peripheral facial palsy. Observations of the pediatric population.

    Idiopathic peripheral facial palsies in the pediatric population have been noted to carry a favorable prognosis. We describe three members of a family, including two children with recurrent facial palsy, and review the relevant literature. As recurrent peripheral facial palsies carry a relatively poor prognosis, the physician should be alerted to this possibility in any child who has an idiopathic peripheral facial palsy and a positive family history.
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