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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1976

[Prognostic assessment in peripheral facial nerve paralysis with particular reference to electroneurography (author's transl)].

Electrophysiological investigations were carried out on 20 healthy controls and 130 patients with peripheral facial nerve paralysis. The aetiology was as follows: idiopathic (Bell's palsy) in 60 cases, viral in 29, traumatic in 18, postoperative in 4, in connexion with chronic otitis media in 6, diabetes mellitus in 4, positive rheumatological tests in 3, disturbed lipid metabolism in 2, the Melkersson-Rosenthal syndrome in 1, as a complication of pregnancy in 2, and in association with a tumour in 1 case. The compound action potential (CAP) of the orbicularis oris muscle was determinedi n 370 occasions in a right/left comparision, the record of the muscle response was intergrated over the time of action (IAR) on 32 occasions and trison of 255 occasions. The normal values are given in the first place and their dependence of the age of the subject. Then, the prognostic sifnficance of the above-mentioned parameters is investigated in cases of peripheral facial nerve paralysis. It is apparent that the determination of the CAP in a right/left comparison is a valuable prognostic guide as early as the 4th day, insofar as a decrease in this parameter of under 50% can be interpreted as a favourable sign and satisfactory reversal of the paralysis can be expected within 6-8 weeks. By contrast, a decrease of over 70% in the CAP is a bad prognostic sign, indicative of presumably only a poor trend to reversal of the paralysis. An intermediate depression of the CAP in the range of 50-70% signifies an expected moderate recovery within 6-8 weeks ahe case of CAP determination at the time of maximum amplitude depression (as opposed to the 4th day), then a decrease of less than 70% is taken to be indicative of satisfactory functional recovery within 6-8 weeks; a decrease of 95-100% signifies a bad prognosis, whilst a decrease amounting to between 70 and 95% carries an uncertain prognosis. The maximum decrease in amplitude was registered on the 8th day on average; the range lay between the 4th and the 14th day. An exception to these figures was the delayed response of the CAP in the case of 6 patients, 5 of whom showed a maximum decrease during the 3rd week and the last patient as late as the 4th week following the onset of facial nerve paresis. Similar reliance can be placed on the prognostic value of the IAR. however, the decrease in the IAR is smaller than that of the CAP measured on the same potential in a right/left comparison, so that a decrease in the IAR of over 60% can already herald a poor recovery. Repeated determination of the latency in cases of facial nerve paralysis showed that the mean latency value for the entire group of patients was slightly prolonged at the end of the 1st week, but the latency values obtained in any one particular patient are of no prognostic significance. A comparison between CAP and latency values obtained with the opposite (i.e...

Action Potentials↗
PubMed1978

Peripheral facial nerve paralysis of dental origin.

The aetiology, diagnosis and treatment of peripheral facial nerve palsy are discussed. Four cases of facial nerve palsy following dental procedures are reported. Following a revision of the world literature during the last 23 years, the 25 cases of facial nerve palsy documented are analysed and divided into four groups on the basis of aetiology, speed of onset and recovery and modes of treatment suggested.

Adolescent↗
PubMed1979

Idiopathic facial palsy. Viral, hereditary, or both?

Two cases of acute peripheral facial paralysis occurring in two siblings in a family of six members, who all developed influenza-like symptoms, are reported. Both patients with facial paralysis, as well as two other members of the family had elevated titers against herpes simplex virus, even though it was not possible to demonstrate any raise in titers between the acute and convalescent phase. The "epidemic" occurrence is from a statistical point of view more than just a coincidence, and it is concluded that these findings support the hypothesis that Bell's palsy may be caused by reactivation of herpes simplex virus, probably facilitated by some hereditary component. The authors suggest that a combination of infectious (most likely viral) and hereditary factors may be etiologically important for the occurrence of acute peripheral facial paralysis.

Acute Disease↗
PubMed1978

Neurinoma of the facial nerve.

This paper deals with 2 cases of peripheral facial paralysis, due to intratemporal facial neuroma of tympanic (case No. 2) and vertical (case No. 1) segments of the Fallopian canal. The authors present a literature review of the intratemporal facial neuromas with special reference to clinical-surgical and differential diagnostic aspects. It is difficult to detect a Schwannoma of the facial nerve during a peripheral facial paralysis; radiological studies of the mastoid and Fallopian canal are essential for this diagnosis. Treatment of neurinomas of the VIIth nerve is always surgical, the authors emphasize the necessity of an 'en masse' tumor-nerve removal and the use of a nerve graft.

Adult↗
PubMed1979

[Prognosis and therapy of peripheral facial nerve paralysis. Electrodiagnostic ways of evaluation].

The function of the facial nerve can be examined by four electrodiagnostic methods. In the nerve excitability test and electroneurography with determination of the distal latency the facial nerve is stimulated over the stylomastoid foramen. Chronaximetry and electromyography are performed in the muscles. Whereas chronaximetry renders an impression of the severity of neural lesion, electromyography can also determine the onset of reinnervation activity. Early prognosis within 6 days of onset can be determined only by nerve excitability test and electroneurography, preferred by us, which assesses the muscle potential. If the potential amplitude decreases more than 35% within two days and the muscle potential disappears between the fourth and sixth day, total degeneration of the nerve with poor prognosis is indicated. Such data can be gathered by at least two electrodiagnostic investigations preferably on the third day after onset and one to three days later. The cosmetic disfigurement through peripheral facial nerve palsy poses immediately the question of prognosis and of the therapeutic possibilities. Usually, this question can be answered by clinical examination alone. As soon as paralysis of facial muscles exists, prognostical statements can be made by electrodiagnostical methods alone. Because of the possiblility of operative treatment it is necessary to assess the infavorable courses early.

Action Potentials↗
PubMed1976

[Orbicularis oculi reflex after facial paralysis: decreased amplitude of reflex response and spreading to all hemifacial muscles after reinnervation (author's transl)].

After the acute stage of peripheral facial paralysis with nerve degeneration we find some signs of paresis after reinnervation due to insufficient motor recovery and associated movements due to faulty reinnervation. Electromyographical investigation of the orbicularis oculi reflex can be used for the objective evaluation of these two phenomena. This shows the following typical signs: 1. The amplitudes of the early and late reflex response are decreased on the affected side proportionate to the degree of paresis. 2. The response occurs in all reinnervated hemifacial muscles as a result of misdirection of fibres which originally innervated the orbicularis oculi muscle.

Eyelids↗
PubMed1975

Central functional changes after facial-spinal-accessory anastomosis in man and facial-hypoglossal anastomosis in the cat.

A left facial-spinal-accessory anastomosis was performed for peripheral facial paralysis in an 8-year-old boy. By the fourth postoperative year, the corneal reflex showed a normal latency, and left arm and face movements could be executed independently. The possibility of neural plasticity playing a role in establishing new central relationships which enable the achievement of a "normal" latency corneal reflex and independent face and arm movements is discussed. The latency of the corneal reflex recorded as electrical response of the orbicularis oculi muscle to electrical stimulation of the ipsilateral cornea was measured in normal cats and cats which had undergone a facial-hypoglossal anastomosis 12 to 14 months previously. The latency of the reflex was 8 to 22 msec in normal animals and 200 to 300 msec in the operated cats, while conduction times in the regenerated hypoglossal nerve fibers were found to be within normal limits. This suggests that the long latency of the corneal reflex following the cross anastomosis is due to the time required for transmission across newly-formed connections between the trigeminal terminals and the hypoglossal neurons.

Accessory Nerve↗
PubMed1979

Bilateral facial palsy associated with Stevens-Johnson syndrome.

A 22-year-old man developed acute bilateral peripheral facial paralysis in association with Stevens-Johnson syndrome, probably as a result of ampicillin allergy. All symptoms cleared except the facial paralysis. He is the first patient in whom acute facial palsy and Stevens-Johnson syndrome have occurred simultaneously.

Adult↗
PubMedDate not supplied

Acute facial palsy. Some clinical and virological observations.

A prospective clinical and virological study on 44 patients with acute, peripheral facial paralysis was carried out in consecutive cases during one year. In 9 cases varicella-zoster infections were serologically established. In 5 additional patients an associated varicella-zoster, or herpes simplex, infection was possible. Of the 9 confirmed cases, 6 were clinically diagnosed as zoster oticus, whereas on clinical grounds, 3 were regarded as Bell's palsy. No evidence was obtained of associated enterovirus, mumps, measles, cytomegalovirus, tick-borne encephalitis virus, para-influenza virus, mononucleosis or Mycoplasma pneumoniae infection.

Acute Disease↗