Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “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 253 records · Page 14Linked to original sources
PubMed1990

Neuropathy of the facial nerve in chronic otitis media without associated facial paralysis. A human temporal bone study.

In the present study we examined whether pathologic changes can exist in the facial nerve in chronic otitis media (COM) when facial nerve function is clinically normal. In so doing, 20 human temporal bones were examined. Each case had a premortem history of COM without facial paralysis. Nine normal temporal bones were also studied. Signs of degenerative neuropathy involving the facial nerve were found in 2 out of the 20 cases studied. In the first of these 2 cases the tympanic segment of the facial nerve showed focal areas of demyelinization, as well as hypertrophy and proliferation of the Schwann cells but without loss of the axons. These areas were also occasionally associated with increased numbers of mast cells. In the second case the most striking finding was the presence of small dark globules in the mastoid segment of the facial nerve. These formations were assumed to be products of cellular and myelin degeneration. Our studies suggest that COM may be associated with degenerative changes in the facial nerve without clinical impairment of its function. Nonetheless these changes may have the potential for the development of facial paralysis during COM.

Aged↗
PubMed1989

Peripheral facial paralysis and HIV infection: report of four African cases and review of the literature.

Four cases of infranuclear facial palsy associated with infection by the human immunodeficiency virus in young heterosexual African patients are reported. Two cases were healthy HIV carriers, one patient manifested AIDS-related complex, and one case fulfilled the CDC criteria for AIDS. Two patients had a typical Bell's palsy, one presented with manifest cephalic Herpes zoster infection and one, who suffered from facial diplegia, could be considered to have a cephalic form of Guillain-Barré syndrome. A review of the literature confirmed that peripheral facial palsy can occur at any stage of HIV infection and in various clinical contexts. In stages I and II of the HIV infection, patients may develop either Bell's palsy or Guillain-Barré syndrome. In stages III and IV, when the cellular immunity has begun to decline, Herpes zoster-related facial paralysis, seventh cranial nerve involvement secondary to meningeal lymphomatosis, and peripheral facial paralysis as one aspect of widespread chronic peripheral neuropathy may also occur.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Objective facial paralysis grading based on Pface and eigenflow.

To provide physicians with an objective and quantitative measurement of single-sided facial paralysis, the paper presents a computer-based approach that is different from the nine existing, subjective and hand-performed international scales, such as House-Brackman. For voluntary expressions of a patient, this approach used Pface, which stems from Dface, to measure the asymmetry between two sides of the face and used eigenflow to measure the expression variations between the patient and normal subjects. The results from Pface and eigenflow were then combined by the support vector machine produce to Pdegree. A study of 25 subjects revealed that Pdegree could differentiate paralysis states (Pdegree > or = 0) and normal states (Pdegree < 0), with the ability to grade facial paralysis automatically. Moreover, the Pface of specific facial areas can be used in the supervision of the rehabilitation process.

Adolescent↗
PubMed1978

Acoustic reflex and loudness discomfort in acute facial paralysis.

An extensive research protocol was used to evaluate the conditions of 48 consecutive patients with acute facial paralysis. The results indicated that after nerve excitability testing, the acoustic reflex was the most efficient indicator of impending nerve degeneration and predictor of recovery. The presence of increased sensitivity to intense acoustic stimuli (loudness discomfort level) indicated poor prognosis. The data demonstrate that dysacusis (hyperacusis) is not related to stapedial muscle paralysis and also question the validity of "topographic diagnosis" in determination of the site of the lesion in facial paralysis.

Adolescent↗
PubMed2025

A Multi-omics Exploration Revealing SLIT2 as a Prime Therapeutic Target for Peripheral Facial Paralysis: Integrating Single-Cell Transcriptomics and Plasma Proteome Data.

Peripheral facial paralysis (PFP) is a common neurological disorder characterized by facial-nerve dysfunction. Identifying therapeutic targets and understanding the molecular and cellular mechanisms underlying PFP are crucial for developing effective treatment strategies. This study combined Mendelian randomization (MR) analysis and single-cell RNA sequencing (scRNA-seq) to explore potential therapeutic candidates and their roles in PFP pathophysiology. The MR analysis included 1925 publicly available plasma protein cis-heritability instruments. Instrumental variables were selected for MR analysis to identify plasma proteins associated with PFP, followed by colocalization analysis to evaluate shared genetic variants between the identified proteins and PFP. After the initial identification of plasma proteins associated with Bell's palsy using MR analysis, a rat model of facial-nerve injury was established to further dissect underlying mechanisms at cellular and molecular levels. Using scRNA-seq technology, we delved deeply into cellular Heterogeneity and dynamic changes in gene expression in the facial-nerve nucleus tissues under both injured and control conditions, thereby achieving a systematic study ranging from macroscopic genetic associations to microscopic cellular functions. Finally, expression patterns were preliminarily validated by performing in vitro immunofluorescence analysis on the facial-nerve nucleus samples of SD rats. The MR analysis results identified 30 plasma proteins significantly associated with PFP, with nine target genes showing differential expression in the scRNA-seq data. Colocalization analysis demonstrated that slit guidance Ligand 2 (SLIT2), semaphorin 4D (SEMA4D), EGF containing fibulin extracellular matrix protein 1 (EFEMP1), and sprouty related EVH1 domain containing 2 (SPRED2) shared causal variants with PFP. SLIT2 was highly expressed in the microglia and inhibitory neurons in the experimental group, whereas SEMA4D showed elevated expression across multiple glial cell types in the same group. In contrast, EFEMP1 and SPRED2 showed distinct expression patterns in fibroblasts and oligodendrocytes. The role of SLIT2 has been previously well-documented in many central nervous system diseases. However, for the first time, this study detected SLIT2 alteration after facial-nerve injury. Altered intercellular signaling, particularly enhanced SLIT2-ROBO signaling between neurons and glial cells, was observed in the PFP group. Pseudotime analysis revealed dynamic SLIT2 expression during microglia and inhibitory neuron differentiation, mirroring changes in ROBO1 expression. Immunofluorescence analysis of rat facial-nerve nucleus samples verified that SLIT2 protein levels were significantly increased in the facial-nerve nuclei of injured samples. In conclusion, despite the fact that this study is primarily founded on animal models and despite notable differences existing between animals and humans in terms of the facial motor nucleus, this study successfully identified SLIT2 as potential therapeutic targets for PFP. The SLIT2-ROBO axis stands out as a particularly promising candidate. SLIT2 may play a role in modulating neuroimmune interactions and promoting nerve repair. These findings provide a foundation for future clinical studies and targeted interventions to enhance recovery from PFP. Future research should focus on human sample validation to enhance clinical translation.

Animals↗
PubMed2006

Temporal bone rhabdomyosarcoma presenting as acute peripheral facial nerve paralysis.

Facial palsy is not an uncommon presentation to an emergency department. Whereas most patients will ultimately receive a diagnosis of Bell palsy (idiopathic peripheral seventh cranial nerve palsy), a subset will have an identifiable cause for their facial paralysis. Children are more likely to have an identifiable cause than are adults. We present a case in which a child presented with acute peripheral facial nerve palsy and was found to have temporal bone rhabdomyosarcoma. The key clinical finding was the presence of both 7th and 12th cranial nerve palsy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1983

Recurrent alternobaric facial paralysis resulting from scuba diving.

Only one detailed case of alternobaric (referring to alternating pressure changes) facial paralysis resulting from scuba diving has been reported in the world literature. This article describes the dive profile and clinical course of a commercial diver who developed facial paralysis after scuba diving on three different occasions. Probable pathophysiologies, identification of the diver at risk, treatment and prophylactic measures are reviewed. Additional cases from the literature due to scuba diving and flying are cited.

Acoustic Impedance Tests↗
PubMed1996

A histomorphometric analysis of the cross-facial nerve graft in the treatment of facial paralysis.

One of the most unsettling sequela of facial paralysis (FP) is the loss of the blink reflex, leading to both a functional and aesthetic deformity. A successful method of treating FP and, in particular, loss of eye-sphincter function, is the use of the cross-facial nerve graft (CFNG) to reinnervate the previously denervated orbicularis oculi muscle. The present study examined the histomorphometric aspects of the entire CFNG, with respect to axon diameter and myelin area. The axon profile of the CFNG had a positive correlation with motor end-plate counts and electrophysiologic recordings. These results should help in further understanding the number of motor axons needed to restore adequate function to the paralyzed eye sphincter, and establish more rational reconstructive procedures.

Animals↗
PubMedDate not supplied

[Association of peripheral facial paralysis in patients with human immunodeficiency virus infection].

INTRODUCTION: Neurological disorders are common in patients infected with the human immunodeficiency virus (HIV). The objective of this study is to show the possible association of peripheral facial paralysis (PFP) in persons who test positive for HIV, which because of the characteristics of outpatient management is important in basic medical attention. PATIENTS AND METHODS: The scope of our study included all patients observed in 1998 and the first six months of 1999 who had PFP, and in whom detailed clinical history, physical examination by a neurologist, laboratory tests and HIV serological tests were done. RESULTS: We found that 89.1% of the patients with PFP were seropositive. The facial paralysis showed similar characteristics to Bell s palsy, with complete recovery after four weeks in 66.6% of this group of patients. The seronegative patients also recovered completely but took longer to do so. In two cases the PFP was associated with obvious features of AIDS. CONCLUSIONS: In the literature reviewed we have not found such a large group of patients with PFP associated with HIV+. However, it is obvious that there is an increase in facial paralysis which is in proportion to the increase in HIV+ persons. The results of our study suggest to us that HIV should be tested for in patients with PFP.

Adolescent↗
PubMed1995

Symmetry and synkinesis during rehabilitation of unilateral facial paralysis.

We evaluated biofeedback rehabilitation in patients with severe chronic unilateral facial paralysis, who had intact facial-motor innervation (House grades 3 to 5). Recovery of facial function was characterized (1) by grading facial movement symmetry, and (2) by counting the number of muscles exhibiting synkinesis during maximal execution of selected facial movements (e.g., smiling). Facial function in 21 patients typically improved by one House grade. Facial symmetry recovered rapidly during the first 5 months of treatment, and then improved more slowly. However, during this latter period, examination of the relationship between symmetry and synkinesis (visualized by a graph plotting symmetry grades on the x-axis, against the number of synkinetic muscles on the y-axis) indicated that overall facial control was improving even when House grading suggested that it was not. Such information should aid facial retraining and may clarify understanding of underlying rehabilitation mechanisms.

Adult↗
PubMed1990

Pathologic findings in the labyrinthine segment of the facial nerve in a case of facial paralysis.

The histopathologic findings for a patient with acute facial paralysis caused by herpes zoster oticus who obtained no return of active facial function after 1 year are presented. All imaging studies were nondiagnostic. Biopsy of the labyrinthine segment was performed. Histopathologic analysis showed a sharp line of demarcation between sclerotic nerve proximal to and necrotic nerve distal to the meatal foramen area of the fallopian canal. This finding is consistent with observations that the lesion producing Bell's palsy and herpes zoster oticus usually is situated at the meatal foramen.

Adult↗
PubMedDate not supplied

[Peripheral facial paralysis and HIV infection. 2 case reports].

Two cases of peripheral facial paralysis in subjects with HIV infection are reported. On the basis of these two cases and data from the literature, the clinical and paraclinical features of this facial nerve lesion are described. The various aetiological hypotheses put forward are discussed, but it is probable that the paralysis results from a direct effect of the virus on the nerve. HIV-associated peripheral facial paralysis may occur irrespective of the number of CD4 lymphocytes and does not seem to have a prognostic significance. However, it appears by preference in stages I, II and III and may then reveal the HIV infection.

Adrenal Cortex Hormones↗
PubMed2005

[Clinical observation on electroacupuncture for treatment of peripheral facial paralysis at different stages].

OBJECTIVE: To probe into the optimal opportunity of electroacupuncture for treatment of peripheral facial paralysis. METHODS: One hundred and twenty cases were randomly divided into group A and B, 60 cases in each group. The group A were treated by electroacupuncture and ultrashort-wave from the acute stage and the group B were treated by ultrashort-wave at the acute stage and ultrashort-wave plus electroacupuncture at the resting stage. RESULTS: The cured and markedly effective rate was 85.0% and the total effective rate was 98.3% in the group A, and 68.3% and 91.7% in the group B respectively (P < 0.05); there was no significant difference between the two groups in abnormal myoelectrogram before treatment and at the 8th day (P > 0.05); but at the 30th day the number of cases in whom BR wave turned to normal or mild abnormal in the group A were more than those in the group B (P < 0.05), and the shortening of the latent period of M wave and increase of the wave amplitude were significantly better than those in the group B (P < 0.05). CONCLUSION: Electroacupuncture at acute stage can significantly increase the cured and markedly effective rate, and the acute stage is the optimal opportunity for acupuncture treatment of peripheral facial paralysis.

Acupuncture Therapy↗
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↗
PubMed2004

Varicella zoster virus: beyond facial paralysis.

J. Ramsay Hunt's hypothesis that herpes zoster oticus results from a reactivation of the herpes zoster virus in the geniculate ganglion, has been supported by the demonstration of varicella zoster viral DNA in the geniculate ganglion of the side with facial paralysis in patients with Ramsay Hunt syndrome, with the use of the polymerase chain reaction. Similarly, DNA of the varicella zoster virus has been identified in the spiral and vestibular ganglion as well. We report on three patients with cochleovestibular symptoms as the first manifestations of Ramsay Hunt syndrome. A 64-year old woman and a 72-year old man presented with vertigo and an auricular herpetiform eruption. Only the woman developed later on a mild facial paralysis. A 58-year old man presented with an acute cochleovestibular syndrome, serologically proven to be a varicella zoster viral reactivation, which was followed three weeks later by the typical cutaneous recrudescence. We believe that these cases result from reactivation of latent varicella zoster virus in the spiral and/or vestibular ganglion. As the varicella zoster virus is dormant in the non-neuronal satellite cells, the facial symptoms in our patients as well as the high incidence of cochleovestibular symptoms in classical Ramsay Hunt syndrome can be explained by viral transmission across the nerves inside the internal auditory canal. Therefore, we think there are grounds to recommend a prompt treatment with an antiviral and a corticosteroid agent, not only in case of an acute facial paralysis but also when confronted with an acute cochleovestibular syndrome.

Acyclovir↗