Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Peripheral facial paralysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed2004

Bilateral changes in cortical motor representation of the tongue after unilateral peripheral facial paralysis: evidence from transcranial magnetic stimulation.

Motor evoked potentials of the lingual muscles due to focal cortical transcranial magnetic stimulation were investigated in 5 patients with unilateral total facial paralysis with regard to amplitude as a function of the coil position on the interaural line. Maximum bilateral responses could be obtained at mean stimulus positions of about 6 to 8 cm lateral to the vertex. In comparison with healthy subjects, the patient group had significantly smaller mediolateral calculated centers for ipsilateral and contralateral responses. At the optimum stimulus positions, the patients' mean motor evoked potential amplitudes were significantly lower than those in healthy subjects. These alterations could be observed on both cortical hemispheres, but were more pronounced for the hemisphere contralateral to the side of facial paralysis. Thus, we provide strong evidence of bilateral changes in lingual cortical motor representation following facial paralysis with an invasion of the facial motor area by the tongue motor representation.

Adult↗
PubMed1985

[Topodiagnosis in peripheral facial paralysis].

The topodiagnosis allows the physician to determine the topographic localization of pathology involving the facial nerve. It is based on clinical tests that evaluate the function of each one of the rami of the facial nerve. With a statistic of 873 patients, the Facial Nerve Group of Hospital das Clínicas, São Paulo University, found that suprageniculate lesions are responsible for 50% of the facial nerve involvement of several etiologies. Based on these results, the physician is able to develop a rationale for therapy and surgical access for facial nerve lesions.

Facial Paralysis↗
PubMed1988

Pathological features of peripheral facial paralysis caused by malignant tumour.

It has been reported that tumour invasion of the facial canal does not necessarily produce facial paralysis. The purpose of this paper is to present the facial nerve pathology in cases of facial paralysis caused by malignant neoplasms. Forty-seven temporal bones acquired from patients who died of malignant neoplasms were used for this analysis. Of the 47, 18 temporal bones (38.3%) had temporal bone metastasis or invasion. In 6 cases, the tumour destroyed the bony facial canals exposing the facial nerves to the invading tumour cells. The records of the patients showed that only half of the patients had facial paralysis. Those in whom tumour cells invaded the facial nerve beyond the epineural sheath had complete facial paralysis before death.

Bone Neoplasms↗
PubMed2002

[Changes in the F wave during recovery from peripheral facial paralysis].

OBJECTIVE: We studied normal F wave parameters and F wave changes in patients with longstanding facial paralysis. SUBJECTS: Controls were 11 healthy volunteers studied to estimate normal F wave parameters. Subjects were 8 patients with Hunt's syndrome and 12 with Bell's palsy available for F wave detection among outpatients at our department between April 1999 and March 2000. They had ENoG of 0% within 2 weeks of paralytic onset. The test was repeated 68 times. DIAGNOSTIC INTERVENTION: Results of 68 tests were classified into 5 groups based on the course after paralysis developed and their F wave parameters were compared with controls. F wave parameters were minimal latency, maximum latency, mean latency, and frequency of F wave development. Stimulation was repeated 20 times in a test. RESULTS: No significant difference was noted in minimal latency in each group compared to controls. Maximum and mean latency were prolonged significantly in each group compared to controls. The frequency of F wave development was significantly reduced in groups in which examinations were done in less than 6 months and for 6 months to 1 year. CONCLUSIONS: Nerve fibers with fast conduction were considered to have recovered with on 6 months. This suggested that nerve conduction velocity in facial paralysis patients does not recover the same as normal conduction velocity. The maximum and mean latency in each of the postpalsy group was significantly longer than that in the normal control group. We therefore concluded that regenerated nerve fibers include some with a conduction velocity significantly slower than normal. The frequency in groups A and B was significantly lower than that in controls, but after 1 year or more had elapsed after the onset of palsy, the frequency was approximately the same as that in controls.

Adult↗
PubMed2000

[EBV infection as etiology of otomastoiditis with peripheral facial paralysis in the child].

Case report on a 15-month-old girl with acute bilateral otomastoiditis with facial nerve palsy in the course of an EBV infection. Although the initial mononucleosis blood test was negative the diagnosis was established by the presence of blastic transformed lymphocytes with immunoreaction for the latent membrane protein of EBV, and the presence of EBV-mRNA in the majority of lymphocytes in the biopsy specimen. The occurrence of facial nerve palsy in the course of an EBV infection is relatively rare but well known. The present case involved a viral otomastoiditis with a typical course, which was complicated by facial nerve palsy after a few days of illness. A case of this kind has only once been described in an adult patient and has never been reported in a child.

Adult↗