Cases reported "Bell Palsy"

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1/29. Bell's palsy in an older patient with uncontrolled hypertension due to medication nonadherence.

    OBJECTIVE: To describe and inform pharmacists of a rarely reported occurrence of facial palsy in an elderly patient with uncontrolled hypertension resulting from nonadherence to blood pressure medications. CASE SUMMARY: A 62-year-old Hispanic woman presented to the hypertension clinic with left facial weakness, mild eyelid lag, and auricular pain for two days. The patient self-discontinued fosinopril and minoxidil six days and two days prior to developing these symptoms, respectively. A diagnosis of idiopathic peripheral VII cranial nerve lesion was made after ruling out other possible causes. Corticosteroids were not initiated because of this patient's labile hypertension. Palliative therapy was initiated and the left facial paralysis continuously improved during the six months after discharge. DISCUSSION: patients have rarely presented with facial paralysis as the initial feature of severe hypertension. The relationship between facial paralysis and hypertension has been reported in a small number of cases, including several reports of recurrence of paralysis during acute exacerbations of hypertension. A variety of physiologic theories to explain the relationship between facial paralysis and hypertension have been published, including small hemorrhages into the facial canal which have been confirmed by two autopsies. However, the true etiology remains unknown. CONCLUSIONS: The possible relationship between facial paralysis and uncontrolled hypertension has not been reported in pharmacy literature and has been reported only twice in subspecialty medical journals since 1990. pharmacists should be aware of the complications of hypertension and should question patients about signs and symptoms at each visit. While Bell's palsy complicating hypertension does not appear to be a serious complication, pharmacists must appreciate that the patient should be immediately evaluated to rule out a more serious neurologic event.
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2/29. Vagal and hypoglossal Bell's palsy.

    A 7-year-old boy was referred because of a sudden change to nasal speech, dysarthria for words with explosive consonants in speech, and nasal regurgitation of fluids. The symptoms arose over 1 week following a capricious episode of acute asthmatic bronchitis. Physical and neurologic examinations were normal except for a left deviation of the uvula, accompanied by a "curtain" movement of the posterior pharyngeal wall against the opposite side, and a left deviation of the protruded tongue. No vascular, traumatic, infectious, neoplastic, or neurologic causes could be identified. No therapy was administered. Full recovery occurred 4 months later. The diagnosis was idiopathic vagal and right hypoglossal nerve palsy (Bell's palsy).
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3/29. 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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4/29. Bell's palsy: a 10-year experience with antiphlogistic-rheologic infusion therapy.

    OBJECTIVE: Treatment of idiopathic peripheral facial paralysis has remained controversial in many aspects. The authors report their experience with a protocol based on high-dose prednisolone with intravenous low-molecular-weight dextran and pentoxifylline. For this regimen, the term antiphlogistic-rheologic infusion therapy (ARIT) has been coined. STUDY DESIGN: Retrospective case-series review. SETTING: University-based hospital of otorhinolaryngology/head and neck surgery. patients: 334 patients suffering from sudden facial paralysis of unknown cause. INTERVENTION: Treatment consisted uniformly of prednisolone in a starting dosage of 250 mg tapering over 18 days and accompanying infusion of dextran and pentoxifylline. MAIN OUTCOME MEASURES: facial nerve function after 6 months, adverse effects of therapy and comorbidity. RESULTS: From 239 patients with nonrecurrent palsy having received treatment within 12 days after onset, 92% recovered completely (House-Brackmann [HB] Grade I) without sequelae. In incomplete palsy (HB Grade II-V), normal facial function was restored in 97% of cases. Results were significantly better in the group in which therapy had been started within 3 days after the onset of palsy. Other factors such as old age, hypertension, or diabetes did not seem to influence the functional outcome in this series. Serious adverse effects requiring termination of therapy were observed in 1.2% of cases. CONCLUSION: ARIT for Bell's palsy is safe and leads to recovery rates superior to the most optimistic observations of the natural course.
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5/29. facial nerve palsy following intra-oral surgery performed with local anaesthesia.

    The precise cause of Bell's palsy remains unclear. A variety of mechanisms have been linked to this palsy, including viral re-activation, demyelination, oedema, vasopasm and trauma. A link with dental treatment has been suggested previously, and a series of seven cases of facial nerve palsy following intra-oral surgery are reported. All of the patients had local anaesthetic solution containing adrenaline as the vasoconstrictor administered. There may be under-reporting of this association, as patients with facial nerve palsy are treated by specialists from several disciplines, not only maxillofacial surgeons. An association with local anaesthesia administered to permit dental treatment would have important medicolegal consequences, and perhaps go some way to explaining the pathophysiology of Bell's palsy.
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6/29. magnetic resonance imaging findings in bilateral Bell's palsy.

    Bell's palsy (idiopathic facial paralysis) is the most common cause of unilateral peripheral facial neuropathy. Bilateral involvement occurs in less than 10% of cases. The authors describe a 20-year-old man with bilateral idiopathic facial weakness. brain magnetic resonance imaging (MRI) showed abnormal bilateral enhancement of the proximal intracanalicular segments of VII/VIII nerve complexes. The enhancement was most prominent in the leptomeningeal regions. There was no facial nerve swelling. Three months later he had improving residual bifacial weakness. To the authors' knowledge, this is the first report of abnormal MRI findings in bilateral Bell's palsy.
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7/29. Facial diplegia as the presenting manifestation of acute lymphoblastic leukemia.

    A 36-year-old man with recent onset of unilateral peripheral 7th nerve paresis presented ten days later with involvement of the other side of his face. physical examination was otherwise normal, and since blood tests and imaging were also normal, he was considered to have bilateral Bell's palsy. However, unexpected headaches and worsening of the paresis led to a gallium-67 scan which revealed uptake in the mediastinum. A repeat lumbar puncture revealed cells which were identified as lymphoblasts. T-cell acute lymphoblastic leukemia (T-ALL) was diagnosed, although the peripheral blood smear was normal. The differential diagnosis of bilateral 7th nerve palsy and of mononuclear cerebrospinal fluid pleocytosis is discussed, as well as this rare central nervous system presentation of acute leukemia.
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8/29. Recurrent idiopathic familial facial nerve palsy and ophthalmoplegia.

    INTRODUCTION: Idiopathic facial nerve palsy is a common neurologic condition but episodes of ophthalmoplegia in these patients are uncommon. MATERIALS AND methods: Retrospective case series. RESULTS: Three patients with facial nerve palsy with unusual features, including ophthalmoplegia, are described. CONCLUSION: Recurrent episodes, familial tendency, and associated ophthalmoplegia are uncommon in patients with idiopathic facial nerve palsy.
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9/29. Botulinum toxin treatment for hyperlacrimation secondary to aberrant regenerated seventh nerve palsy or salivary gland transplantation.

    AIM: To investigate the potential of botulinum toxin A for treating hyperlacrimation. methods: Three patients with unilateral symptoms of hyperlacrimation (diagnosed as "crocodile tearing") and one patient with a submandibular salivary gland transplant (SMGT) were studied. Tear production was quantified in the resting and stimulated (chewing or following exercise) state, using Schirmer's test and tear clearance. Lacrimal scintigraphy was used to assess outflow. Intraglandular injections (for patients with "crocodile tears") or periglandular injections (for the SMGT patient) of Dysport were administered in divided doses. RESULTS: Two of the three eyes with reported gustatory lacrimation had a higher Schirmer test result than their fellow eye following gustatory stimulation. Scintigraphy, with and without stimulation, confirmed a patent drainage system in these patients. The other patient demonstrated a functional obstruction to tear flow. After treatment patients with confirmed gustatory lacrimation and the SMGT patient had a marked reduction in tearing at 2 weeks. This effect lasted 3-4 months. There was no demonstrable improvement in the patient with epiphora secondary to functional obstruction. Two patients who had received intraglandular injections developed a ptosis, which resolved spontaneously. CONCLUSIONS: This study illustrates that gustatory lacrimation is a difficult diagnosis. In post-facial nerve palsy a functional element must always be considered. However, in confirmed hyperlacrimation botulinum toxin treatment is effective but side effects may occur.
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10/29. Blink reflex and discomplete facial nerve palsy.

    BACKGROUND: Electrophysiologic findings of the blink reflex in patients with Bell's palsy are usually said to be either prolonged latencies and/or absent early and middle responses of it. methods: facial nerve conduction and blink reflex studies were performed on a 42-year-old male patient with right-side Bell's palsy. Studies were done using protocols previously validated and published elsewhere. RESULTS: The right compound muscle action potential was not found after stimulation of the right facial nerve as expected. Absence of the short (R1) and middle (R2) responses of the blink reflex were also noted after right and left supraorbital nerve stimulation. Further, the late (R3) response of the blink reflex was displayed on the abnormal side when electrical stimuli were applied to the right supraorbital nerve while the patient attempted to perform voluntary movement of the paralyzed facial muscles including eye closing. CONCLUSIONS: The recording of R3-a late response following fibers and using motoneurons other than those employed by R1 and R2-on the paralyzed side after performing some reinforcement maneuvers allows us to suggest that, in some facial nerve palsies, there are some structures remaining alive that may be useful for carrying out a more timely and accurate diagnosis and follow-up.
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