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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Facial paralysis represents the end result of a wide array of disorders and heterogeneous etiologies, including congenital, traumatic, infectious, neoplastic, and metabolic causes. Thus, facial palsy has a diverse range of presentations, from transient unilateral paresis to devastating permanent bilateral paralysis. Although not life-threatening, facial paralysis remains relatively common and can have truly severe effects on one's quality of life, with important ramifications in terms of psychological impact and physiologic burden. Prognosis and outcomes for patients with facial paralysis are highly dependent on the etiologic nature of the weakness as well as the treatment offered to the patient. Facial plastic surgeons are often asked to manage the sequelae of long-standing facial paralysis. It is important, however, for any practitioner who assists this population to have a sophisticated understanding of the common etiologies and initial management of facial paralysis. This article reviews the more common causes of facial paralysis and discusses relevant early treatment strategies.
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PMID:Overview of facial paralysis: current concepts. 1847 Aug 26

Bell's palsy is an acute facial paralysis of unknown etiology. Infections including syphilis have been implicated as causes for peripheral facial paresis. The Jarisch-Herxheimer reaction is an acute worsening of skin manifestations and systemic symptoms occurring after administration of antimicrobial therapy for spirochetal infections. Although rare, neurological signs can present as part of the Jarisch-Herxheimer reaction. The authors report a case of Bell's palsy experienced by a patient shortly after treatment with penicillin for secondary syphilis and propose that this acute unilateral peripheral facial paralysis was a Jarisch-Herxheimer reaction in response to therapy.
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PMID:Unilateral facial paralysis after treatment of secondary syphilis. 1856 91

A 58-year-old man was admitted to our hospital with fever, vomiting and disturbance of consciousness after common cold-like symptoms for 2 days. Physical examination showed high fever, moderate hypertension and tachycardia. There were no superficial lymph nodes swelling nor skin rashes. Cerebrospinal fluid (CSF) examination revealed increased protein level (467 mg/dl) and pleocytosis (508 cells/mm3), but no glucose was detected. CSF smear test detected the pneumococcus. Intravenous cefotaxime was administered along with intravenous immunoglobulins and steroid pulse therapy. However, DIC developed, so FOY therapy was started. With these treatments, level of consciousness gradually improved and he became able to eat. At 11th days after the onset, the patient suddenly developed left facial palsy and paresis of the left arm. Head T2-weighted magnetic resonance imaging demonstrated tumor-like hyperintensity signal lesions (28 x 16.6 mm) with ring enhancements in the right frontal lobe. Acute disseminated encephalomyelitis (ADEM) was diagnosed based on MRI and CSF findings, and then additional corticosteroid pulse therapy was administered twice. Herpes simplex virus and herpes zoster virus DNA in the CSF were undetectable by PCR. After 6 days of treatment with corticosteroid pulse therapy, left facial palsy and paresis of the left arm gradually improved and MRI showed the disappearance of tumor-like hyperintense signals. Although ADEM usually develops as a complication after viral infection such as measles, rubella, mumps and herpes zoster, this case suggests that ADEM complication should be considered even after pneumococcal meningoencephalitis.
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PMID:[A case of acute disseminated encephalomyelitis (ADEM) following treatment for pneumococcal meningoencephalitis]. 1934 73

Impairment of the peripheral or central part of the facial nerve causes an ipsilateral peripheral facial nerve paresis. It is quite a common syndrome and affects 20-35 persons per 100,000 per year in Western Europe and the United States. A possible complication of facial palsy is paralytic lagophthalmos with aesthetic and functional impairment for the patient. Beside primary nerve reconstructive procedures plastic-reconstructive procedures play a major role in correcting paralytic lagophthalmos. The eyebrow, upper and lower lids, medial and lateral lid angle as well as the lacrimal system need to be seen as functional units and can be corrected with local surgical procedures. Restoration of eye closure is the most important goal in treating the affected eye. Due to the significant aesthetic limitations and resultant psychological stress for the patient cosmetic aspects must be included in the surgical concept.
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PMID:[Surgical treatment of paralytic lagophthalmos]. 2011 5

Idiopathic facial palsy (IFP), or Bell's palsy, is an acute peripheral unilateral paresis of the facial nerve with an abrupt onset of unknown origin. Primary infection or reactivation of the Herpes simplex virus is suggested as a possible mechanism in some but not all patients. Since IFP is a diagnosis of exclusion, all other causes, especially other neurological diseases or Herpes zoster reactivation need to be excluded, as does Lyme disease in children and endemic areas. If recovery or defective healing has not taken place within 6-12 months, it is mandatory to exclude malignant disease. Severity of the paresis and electromyography are to date the best prognostic markers for defective healing. Steroid application is the only evidence-based therapy to date with recovery rates >90%. The spontaneous recovery rate is about 80%. There is a lack of well defined diagnostic procedures to detect those patients who will recover spontaneously. On the other hand, patients with severe complete paresis might profit from additional antiviral drugs. There is an urgent need for further clinical trials in patients with severe IFP.
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PMID:[Idiopathic facial palsy]. 2045 80

Facial nerve palsy is rarely associated with an inflammatory parotid process. We present a case of peripheral facial palsy initiated by infection of a cystadenolymphoma of the parotid gland. The paresis progressed rapidly despite abating inflammation and 48-h antibiotic therapy. Following total parotidectomy the facial nerve paresis persisted for a period of 4 months. Histological work-up yielded a diagnosis of Warthin's tumor with necrotic changes. This case indicates that even benign processes can be associated with facial nerve palsy.
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PMID:[Facial nerve palsy due to a benign parotid gland tumor]. 2060 2

We report on a previously healthy 11-year-old boy with unilateral periorbital mild headache and facial nerve palsy, followed during the next 5 months by recurrent unilateral headaches and subsequent extrinsic paresis of the third cranial nerve and paresis of the sixth cranial nerve, each of which improved with steroids. Cranial magnetic resonance imaging revealed increased thickening of the left cavernous sinus and adjacent structures, with marked gadolinium enhancement. Eight months after the initial signs, he developed left retro-orbital headache that lasted 16 days and was relieved 24 hours after resuming steroid treatment. Recurrent multiple cranial neuropathies, neuroimaging findings, and long-lasting headache that responded to steroids indicated Tolosa-Hunt syndrome, further confirmed by extensive investigation and a long follow-up to exclude other causes. This patient illustrates the complexity of disorders with multiple cranial nerve palsies, and adds to the sparse literature on Tolosa-Hunt syndrome in children, describing the first pediatric case preceded by facial palsy.
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PMID:Tolosa-Hunt syndrome preceded by facial palsy in a child. 2155 63

The term Bell's palsy is used for the peripheral paresis of the facial nerve and is of unknown origin. Many studies have been performed to find the cause of the disease, but none has given certain evidence of the etiology. However, the majority of investigators agree that the pathophysiology of the palsy starts with the edema of the facial nerve and consequent entrapment of the nerve in the narrow facial canal in the temporal bone. In this study the authors wanted to find why the majority of the paresis are suprastapedial, i.e. why the entrapment of the nerve mainly occurs in the proximal part of the canal. For this reason they carried out anatomical measurements of the facial canal diameter in 12 temporal bones. By use of a computer program which measures the cross-sectional area from the diameter, they proved that the width of the canal is smaller at its proximal part. Since the nerve is thicker at that point because it contains more nerve fibers, the authors conclude that the discrepancy between the nerve diameter and the surrounding bony walls in the suprastapedial part of the of the canal would, in cases of a swollen nerve after inflammation, cause the facial palsy.
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PMID:Anatomical study of the facial nerve canal in comparison to the site of the lesion in Bell's palsy. 2166 56

The traditional access route for cochlear implantation was initially proposed by William House in 1961. Alternatives to this surgical approach have been suggested by many authors. The combined approach technique (CAT) is a variation of the traditional mastoidectomy-posterior tympanotomy method, which uses a transcanal approach to cochleostomy combined with a small mastoidectomy and an equally small posterior tympanotomy for the insertion of electrodes. This paper presents a detailed description of this alternative procedure, reporting our experience with 50 cases, and adds our contribution regarding possible advantages and implications of using a transcanal cochleostomy. The subjects had profound and severe bilateral hearing loss and had not benefited from external hearing aids. They underwent cochlear implantation at Hospital de Clinicas de Porto Alegre from May 2003. The median follow-up was 29 months. All cases were successfully implanted using CAT. No major complications, such as facial paralysis or paresis, meningitis, cholesteatoma, or cerebrospinal fluid leaks, were observed in any patient. The CAT is a safe and efficient variation of cochlear implantation surgery, which is especially appropriate if cochlear calcification or malformations are present, or whenever cochleostomy has to be performed anteriorly, and when the position of the facial nerve prevents an adequate posterior tympanotomy.
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PMID:Transcanal cochleostomy in cochlear implantation: experience with 50 cases. 2175 9

We report a case of infarction of the anterior inferior cerebellar artery (AICA) with peripheral facial palsy following vertigo and acute sensorineural hearing loss. A 39-year-old female presented with vertigo and sudden hearing loss, tinnitus, and aural fullness of the right ear. An audiogram revealed a severe hearing loss at all tested frequencies in the right ear. Spontaneous nystagmus toward the left side was also observed. Otoneurological examinations showed sensorineural hearing loss of the right ear and horizontal and rotatory gaze nystagmus toward the left side, and a caloric reflex test demonstrated canal paresis. Initially, we diagnosed the patient for sudden deafness with vertigo. However, right peripheral facial palsy appeared 2 days later. An eye tracking test (ETT) and optokinetic pattern test (OKP) showed centralis abnormality. The patient's brain was examined by magnetic resonance imaging (MRI) and magnetic resonance angioglaphy (MRA) and showed an infarction localized in the pons and cerebellum. MRI and MRA revealed infarction of the right cerebellar hemisphere indicating occlusion of the AICA. Consequently, the patient was diagnosed with AICA syndrome but demonstrated regression following steroid and edaravone treatment. We suggest that performing MRI and MRA in the early stage of AICA syndrome is important for distinguishing cerebellar infarction resulting from vestibular disease.
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PMID:AICA syndrome with facial palsy following vertigo and acute sensorineural hearing loss. 2186 60


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