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Results for “Peripheral facial paralysis”

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At least 73 records · Page 4Linked to original sources
PubMed1984

[Glossitis in the area supplied by the chorda tympani nerve in peripheral facial paralysis. Early symptom of the Melkersson-Rosenthal syndrome?].

The case is reported of a patient with incomplete peripheral facial palsy. In addition to hyperacousia and gustation disturbance, he presented with signs of glossitis limited to the region supplied by the chorda tympani. Clinical and laboratory investigations excluded the possibility of a viral infection. Possible connections between this combination of symptoms (apparently "idiopathic" facial palsy and regional glossitis) and the Melkersson-Rosenthal syndrome are discussed.

Adult↗
PubMed1989

[Lyme borreliosis--the most frequent cause of acute peripheral facial paralysis in childhood].

A prospective hospital-based multicentre study in Lower Saxony allowed to investigate the frequency of acute peripheral facial palsy due to Lyme borreliosis and its clinical and laboratory characteristics. Diagnosis of Lyme Borreliosis was based on detection of IgM antibodies against Borrelia burgdorferi in serum and CSF as well, using an IgM capture ELISA. Between June 1986 and October 1987 27 consecutive cases with acute peripheral facial palsy were studied. Lyme borreliosis is the main cause of peripheral facial palsy in childhood. It was verified serologically in two thirds of the cases. All cases with a positive history for a tick bite and/or an erythema migrans in the head-neck region showed ipsilateral neurological affection suggesting a direct invasion via the affected nerve by Borrelia burgdorferi. Peripheral facial palsy due to Lyme borreliosis represents a monosymptomatic meningoradiculitis. All children with Lyme borreliosis revealed a lymphocytic CSF pleocytosis, whereas in cases of unknown etiology CSF findings usually were normal. Therefore, in any case of facial palsy with an inflammatory CSF syndrome Lyme borreliosis has to be suspected unless proven otherwise.

Adolescent↗
PubMed1988

Viral infections in acute peripheral facial paralysis. Nationwide analysis centering on CF.

The degree of participation and regional specificity of virus infection in relation to atraumatic acute peripheral facial palsy was studied, placing particular emphasis on change in the CF titre of varicella zoster virus (VZV), herpes simplex virus (HSV) and adenovirus (adeno). The subjects of the study were 91 patients with Hunt's syndrome and 396 patients with Bell's palsy treated at 17 institutions all over Japan in the period between April 1985 and November 1986. Among the cases of Hunt's syndrome, the positive conversion rate of CF antibody titre of VZV was 81%. In Bell's palsy cases, virus participation was detectable in 8% with VZV, 4% with HSV and 4% with adeno. With regard to the age distribution, Bell's palsy cases with possible virus involvement tended to be observed in younger patients than those without that possibility. As to regional specificity, the incidence of Bell's palsy with possible virus involvement tended to be higher in densely populated areas. With regard to the main cause of acute peripheral facial palsy, virus infection has been implicated, as well as insufficient blood circulation (ischemia). Even in cases of acute peripheral facial palsy, in which herpes zoster oticus is not observed, the participation of varicella zoster virus (VZV) as a cause of paralysis has been pointed out in some cases (zoster sine herpete). Furthermore, it is known that the serum antibody titres of various viruses such as herpes simplex virus (HSV) change significantly in some cases of Bell's palsy (2, 5-13).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1979

Peripheral facial paralysis secondary to metastatic malignant melanoma. A clinicopathologic report.

We report a case of disseminated malignant melanoma in which the initial sign was an isolated peripheral facial palsy on the left side. The cause of the palsy was established five months later, with the appearance of metastatic axillary nodes. The temporal bones demonstrated tumor infiltration within the marrow spaces of the petrous apices bilaterally. The left facial nerve was also extensively involved with melanoma to the level of the geniculate ganglion.

Autopsy↗
PubMed1994

[The Poland anomaly with unilateral peripheral facial paralysis].

The authors present the clinical history and physical findings in a 16-month baby girl with the diagnosis of Poland's syndrome associated with another congenital anomaly: unilateral peripheral facial palsy, on the opposite side. The authors believe this is the first report of such an association.

Facial Paralysis↗
PubMed1993

[Isolated acute peripheral facial paralysis in children. Etiological and prognostic study].

BACKGROUND: As facial nerve palsy is usually of sudden onset and of obscure etiology, a survey of large series may provide new information. PATIENTS AND METHODS: The files of 40 children suffering from acute facial nerve palsy seen in 3 pediatric and 1 otorhinolaryngologic (ORL) departments between 1980 and 1990 were analysed. Patients with congenital palsy and those with paralysis that appeared after injury or in the course of acute or chronic disease (otitis media, tumor) were excluded from the study. The children were 9 months-16 years old (mean: 7 year 1 month). There were 22 left and 18 right facial nerve palsies. The palsy was moderate in 17 children, severe in 15, and total in 5. Etiologic factors (viral serologic studies, CSF examination), ORL studies and electromyogram of the facial nerve were analyzed in the majority of cases. Corticosteroids were used in 30 patients. RESULTS: A viral etiology was suspected and/or confirmed in 13 children; abnormalities were seen in 6 of the patients who underwent lumbar puncture. A familial facial nerve palsy was seen in 1 case and kidney disease in 2 cases. 23 cases appeared to be idiopathic. A moderate permanent residual weakness was seen in only 4 children. The mean time for recovery was 32 days (4-140 days). Corticosteroids did not influence the incidence of complete recovery, but decreased the time for recovery (26 versus 37 days) only in the patients who were treated before the 3rd day of the disease. Patients with idiopathic palsy recovered 23 days before those with viral etiology. CONCLUSIONS: Idiopathic and post-viral facial nerve palsies seem to have an excellent prognosis. Corticosteroids seem to have no effect although there is some evidence of benefit when treatment is begun early.

Acute Disease↗
PubMed1989

[Prognosis of peripheral facial paralysis in Lyme borreliosis (Garin-Bujadoux, Bannwarth meningopolyradiculitis)].

Meningopolyradiculitis (Garin-Bujadoux syndrome, Bannwarth syndrome) is the second stage of Lyme disease, a tick-borne Borrelia infection. Almost 60% of these patients develop an acute peripheral facial paresis. The disease can be differentiated from Bell's palsy only by finding the specific Borrelia antibodies in serum and CSF. Other cranial nerve lesions can be found besides facial paresis. The follow-up of seven Borrelia-infected patients is described: one showed bilateral, the others unilateral, facial paresis. High dosage of penicillin or tetracycline for 10-14 days is the appropriate therapy. The prognosis of facial paresis in tick-borne Borrelia infection is considered to be good. All our patients showed complete recovery of motor nerve function.

Adolescent↗
PubMedDate not supplied

[The role of heredity in the genesis of idiopathic peripheral facial paralysis. A case report].

After a study of a family with 9 members who had one or more episodes of idiopathic facial palsy at some point in life, we reviewed the literature for the role of heredity as an etiopathogenetic factor in peripheral facial palsy. Differential criteria for the most controversial aspects were considered, such as incidence and the type or mechanism of transmission which conditions the appearance of peripheral facial palsy in patients with possible genetic factors.

Adult↗
PubMedDate not supplied

[Our technique of hetero-lateral facio-facial anastomosis by means of nerve autografting in the treatment of permanent peripheral facial paralysis].

The authors describe the technique used in 12 surgical cases of heterolateral facio-facial anastomosis by nerve autograft in the treatment of permanent peripheral facial paralyses. Their main contention is that section of 50 p. 100 of the neurones of the peripheral branches of the facial nerve on the unaffected side does not impair motricity to any extent and that it therefore is possible to anastomose the proximal portion of some healthy branches to the corresponding distal portion of the affected side by placing between them a graft from the external saphenous nerve. The principles for fascicular suture as defined by Seddon and later by Millesi are followed. The technique differs from that made popular by Smith and later by Smii inasmuch as: --the bilateral, hidden face-lift incision makes possible a final passive musculotegumentary suspension of the paralysed side immediately improving the patient's appearance while the nerve re-establishes itself; --retrograde interfascicular dissection on the paralysed side allows precious centimetres to be gained; --pinpointing of the nerve suture area is possible by the placing of a silicone-coated ring with a clip some distance away.

Facial Nerve↗
PubMed1998

Cat scratch disease presenting with peripheral facial nerve paralysis.

Acquired peripheral facial nerve paralysis is a relatively common disorder that affects both children and adults. The most frequent nontrauma-related etiologies in otherwise neurologically intact patients are idiopathic (Bell's palsy) and infectious, which includes otitis media, herpes zoster, Lyme disease, herpes simplex virus, Epstein-Barr virus, and Mycoplasma pneumoniae. Cat scratch disease (CSD) is typically a subacute, regional lymphadenitis caused by Bartonella henselae that is seen in children and young adults. CSD most often has a benign, self-limited course. However, 11% of CSD patients may present atypically, most commonly with Perinaud's oculoglandular syndrome or acute encephalopathy. We present a child with the first reported case of acute facial nerve paralysis in serologically proven CSD with typical lymphadenitis.

Cat-Scratch Disease↗
PubMed1988

[Isolated and recurrent peripheral facial paralysis in human infection with human immunodeficiency virus (HIV)].

Unilateral facial palsies were observed in three patients with positive serology for HIV. Two patients presented a second unilateral peripheral seventh nerve palsy after extraction of a tooth. Recovery was complete in each case. Peripheral neuropathies are present in 20% of cases with AIDS but cranial neuropathies are uncommon, affecting only 2 to 3% of patients. The seventh and the fifth are the most frequent cranial nerves involved. The reported isolation of HIV in the cerebrospinal fluid and from the nerve suggests a direct role of this agent. In this study an indirect mechanism such as a vascular spasm may also favour the occurrence of these facial palsies.

Acquired Immunodeficiency Syndrome↗
PubMed1995

[2'-5' olygoadenylate synthetase activity in peripheral facial paralysis].

Interferons are produced in response to viral infection and play an important part in defense by their antiviral effects. An interferon-induced enzyme, 2'-5' oligoadenylate synthetase (2-5AS) also takes an important part of the system of defense against viral infections, and its activity elevates in nonspecific viral infections. This study was designed to evaluate the usefulness of examining serum 2-5AS activity and peripheral blood WBC 2-5AS (WBC 2-5AS) as diagnostic aids of viral infections that cause facial paralysis. Samples were obtained from 83 patients with Bell's palsy, 20 with Ramsay Hunt syndrome, 74 healthy individuals, and a total of 177 subjects. In 177, we measured serum 2-5AS level in 123 subjects, WBC 2-5AS level in 57, and both in 25. Serum 2-5AS levels in Bell's palsy (60 cases) ranged from 20 to 146 pmol/dl (average: 38.5). The range in Ramsay Hunt syndrome (13) was 20-333 (average: 59.0), and in healthy controls (50), it was 20-128 (average: 41.4). WBC 2-5AS level ranged from 20 to 5900 pmol/dl (average: 733.2) in Bell's palsy (23 cases), from 20-4540 (average: 1371.4) in Ramsay Hunt syndrome (7), and from 20-903 (average: 294.5) in healthy individuals (24). There were no statistically significant differences in serum 2-5AS activities. Otherwise, there was significant difference (p < 0.01) between healthy individuals and Patients with Ramsay Hunt syndrome in WBC 2-5AS activity. In Bell's palsy, 3 cases (13.0%) with markedly high WBC 2-5AS levels existed.(ABSTRACT TRUNCATED AT 250 WORDS)

2',5'-Oligoadenylate Synthetase↗
PubMed2004

[Bilateral peripheral facial paralysis secondary to Lyme disease].

Simultaneous bilateral facial paralisis (SBFP) occurs in 0.3-2% of all facial paralisis. We report a case of SBFP in association with Lyme disease. A review of literature about SBFP is made, studing specially the one caused by Borrelia burgdorferi. We present a diagnostic guideline of SBFP. Suspect diagnosis of Lyme disease is based on clinical and epidemiological criteria. Culture isolation of this bacteria is difficult, therefore serologic testing is required. Neuroborreliosis treatment is intravenous Ceftriaxone or Cefotaxime. Oral Doxycycline is useful in the treatment of neuritis without central nervous system involvement.

Facial Paralysis↗
PubMedDate not supplied

[Peripheral facial paralysis and post-antirabies-vaccination polyneuroradiculitis (author's transl)].

A case of facial diplegia with albuminocytologic dissociation of cerebrospinal fluid after antirabies vaccination prompts the author to attempt a retrospective study of post-antirabies-vaccination neuropathies, with facial or extensive involvement. Fifty-seven cases are considered. Irrespective of vaccine type, certain clinical similarities emerge, notably the age of occurrence (adult), the early onset of the paralysis (during vaccine therapy or in the following week), and the prognosis (good survival rate, severity of functional impairment varying with extent of involvement). The author attributes the main pathogenic role to the peripheral myelinic basic protein contained in varying proportions in conventional vaccines, the corollary being that such accidents should disappear completely with the new vaccination based on tissue culture material. A therapy programme comprising the discontinuation of vaccine therapy and administration of corticoids is proposed.

Culture Techniques↗
PubMedDate not supplied

[The development of a clinical protocol for the study of peripheral facial paralysis. A computerized database version].

We present a protocol for the management and follow up of facial palsies, in which, the clinical, diagnosis and therapeutical informations are obtained in order to evaluate the clinical assessment and pathology of this cranial nerve. We also present a computerized database system in order to develop statistical analysis and further studies on this peripheral nerve lesion.

Clinical Protocols↗
PubMed1998

[Bilateral peripheral facial paralysis and Guillain-Barré syndrome].

The Guillain-Barrè syndrome is a polyneuropathy of acute onset that initially tends to produce motor damage of the lower limbs, albumin-cytological dissociation in cerebrospinal fluid and electrophysiological findings suggestive of demyelination. This entity produces a wide variety of symptoms, including damage to the facial nerve in as many as half of all episodes, which means that this syndrome should be considered in the differential diagnosis of facial palsy, particularly bilateral and synchronous cases. In a review of six cases of Guillain-Barrè syndrome in which bilateral facial palsy occurred at some point, a history of immediate infection was confirmed in five, mainly related to Herpesvirinae and Campylobacter. One case began with bilateral palsy, whereas palsy appeared almost simultaneously with the rest of the symptoms in the other cases. High protein levels without cells in cerebrospinal fluid and electrophysiological patterns of slow facial nerve conduction were confirmed in every patient. Treatment with intravenous immunoglobulins resolved all episodes in less than six months. We conclude by reiterating the need for awareness of this syndrome in every case of peripheral VIIth nerve palsy, especially bilateral cases, although the associated symptoms were not very useful, if at all useful.

Adult↗