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At least 19 recordsLinked to original sources
PubMed1979

Lip transposition in patients with facial paralysis.

Since facial reanimation is not always possible in patients with facial paralysis, one must have alternate methods of reconstruction available. Satisfactory static reconstruction of the face may be accomplished with the use of a brow lift, tarsorrhaphy, and correction of the paralyzed mouth. Transposition of the corner of the mouth utilizing the Z-plasty technique has proven to be an effective method to correct the drooling and garbled speech associated with facial paralysis. When combined with a brow lift and tarsorrhaphy, symmetry of the facial appearance while at rest has also been obtained.

Aged↗
PubMed1977

Delayed facial paralysis after a condylar fracture.

Facial paralysis following facial injuries during childhood is rare. The literature is reviewed and the mechanisms of facial nerve injuries are discussed. The case of a five-year-old boy with facial paralysis 48 hours after a condylar fracture is presented. The surgical and conservative treatment of traumatic facial paralysis is discussed.

Child, Preschool↗
PubMed1977

Preoperative facial paralysis in malignant parotid tumours.

Preoperative paralysis of the facial nerve was found in 145 of 1,029 patients with malignant parotid tumours (14%) treated at nine university clinics in Scandinavia. The incidence of facial paralysis varied between the different clinics. A parellelism between the incidence of the facial paralysis and the impairment of the prognosis of the different tumour types is shown. The presence of preoperative facial nerve paralysis in malignant parotid tumours implies a very poor prognosis but the situation is not as hopeless as has been suggested and therefore one must rely on very radical surgery.

Adenoma↗
PubMed1979

Idiopathic facial paralysis in the dog.

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.

Animals↗
PubMed1977

Surgical and nonsurgical management of facial paralysis following closed head injury.

The outcomes of facial nerve decompression, surgical exploration, and nonsurgical treatment for facial paralysis following closed head injury were analyzed in 30 patients with an intact facial nerve, and complete evaluation. Objective evaluation of outcome was achieved by calculation of a Facial Paralysis Recovery Profile and Recovery Index (Profile minus complications). Twelve of 15 patients with incomplete facial paralysis were treated medically. All followed patients with incomplete paralysis and bilaterally equal facial nerve excitability had a Recovery Index of + 10 (complete recovery of function, no complications). Three with partial denervation had a Recovery Profile of + 10 with mild contracture and synkinesis. The average Recovery Profiles for all patients treated by decompression, exploration, or nonsurgically were respectively 4.0, 5.7, and 5.7. The Recovery Indices were +1.8, +3, and +2.7, respectively. Where nerve excitability had become abnormal, facial nerve decompression was of no benefit in traumatic facial paralysis due to closed head injury. Nerve excitability tests of peripheral branches are of great value for prognosis and selection of patients who do not need surgical intervention. Substitution of facial nerve exploration for facial nerve decompression seems reasonable. Polytomography of the facial canal is invaluable in selection of patients for operation.

Adolescent↗
PubMed1977

Auditory symptoms associated with herpes zoster or idiopathic facial paralysis.

Auditory symptoms (hyperacusis, tinnitus, decreased hearing) have long been recognized to accompany herpetic or idiopathic facial paralysis. Twenty-nine percent of 1,080 patients with idiopathic facial paralysis and 37 percent of 172 with herpes zoster oticus facial paralysis had auditory symptoms. Abnormal related sensori-neural hearing loss was documented in only 11 of these 377 patients with auditory complaints. All of the 11 had a diagnosis of herpes zoster oticus. Sensori-neural hearing loss occurs in only about 6.5 percent of patients with herpes zoster facial paralysis, and no confirmed case of such loss in idiopathic facial paralysis has been reported. In patients presenting with sensori-neural hearing loss accompanying facial paralysis believed to be idiopathic, herpes zoster should be suspected even in the absence of vesicles. Factors favorable for recovery of auditory function include age 64 years or younger, mild initial hearing loss, a cochlear pattern of hearing loss, and absence of vertigo. Recovery of auditory function does take place; however, a high-tone sensori-neural loss may persist except in younger patients.

Adolescent↗
PubMed1979

The opercular syndrome--diagnostic trap in facial paralysis.

We describe a patient with a left facial paralysis and hemotympanum following left parieto-occipital skull trauma. The initial admission diagnosis of intratemporal facial nerve injury secondary to temporal bone fracture was incorrect. Normal facial movements during involuntary activity (yawning, laughing at a joke) and focal seizure activity on the paralyzed side of the face, seen subsequently, indicated the site of lesion as supranuclear. The diagnosis of opercular syndrome was made. This syndrome can result when the contralateral frontal lobe is injured. Supranuclear weakness of muscles supplied by the hypoglossal or spinal accessory nerves is also present. Unlike other central paralyses, the facial paralysis in operculum syndrome may not demonstrate "forehead sparing" and consequently it may be mistaken for a peripheral paralysis. The neuroanatomic basis for the syndrome is discussed. Signs and symptoms are outlined to help the otolaryngologist avoid this diagnostic pitfall.

Adult↗
PubMed1979

Auditory dysfunction with facial paralysis.

A series of 58 patients with idiopathic facial paralysis were studied to determine if a concomitant cochlear or eight nerve auditory dysfunction could be identified with traditional audiologic tests. Results indicated that only those patients with a facial nerve lesion, proximal to the stapedius branch, experienced reduced tolerance for loud sounds, reduction of speech discrimination at high-intensity levels, and abnormal loudness growth. Such findings suggest that changes in auditory function, accompanying facial nerve paralysis, are a mechanical effect due to absence of stapedial action. Site of lesion tests in this sample failed to demonstrate eighth nerve dysfunction and, thus, does not support a theory of polyneuropathy that involves the auditory nerve.

Adolescent↗
PubMed1979

Herpes zoster oticus. Uncommon but recognizable cause of facial paralysis.

Three cases of herpes zoster oticus illustrate the manifestations of this relatively uncommon cause of facial paralysis. Topographic analysis, in which functions of facial nerve branches are assessed, helps establish the level of facial nerve involvement. Sequential faradic stimulation testing often is a sensitive prognostic indicator of recovrey of facial nerve function, particularly if nerve excitability persists. A few recent reports support the use of systemic steroid therapy for herpes zoster oticus; opinions vary regarding the efficacy of surgical decompression for facial paralysis. Although general principles cannot be deduced from three cases, each case discussed exemplifies an important aspect of management. The prognostic significance of results of nerve stimulation tests is illustrated by the complete return of facial nerve function in our first patient. Our second patient's response to systemic steroid therapy supports recent reports of the value of such agents in herpes zoster oticus. Partial return of facial nerve function in our third patient two months after onset of paralysis accentuates the importance of a period of observation before a nerve graft or other rehabilitative procedures are undertaken.

Adult↗
PubMed1976

[Facial paralysis with inverse autonomic-voluntary dissociation from a frontal lesion. Cortical origin. Relation to supplementary motor area].

As a result of 6 cases of frontal tumour presenting central facial paralysis with inverse dissociation this symptom was investigated in patients subjected to cortical excisions for intractable epielpsy. A study of 8 cases of frontal cortical excision, 6 of them affecting the internal and posterior portion, and two the prefrontal region, has provided evidence of a link between inverse automatic-voluntary dissociation facial paralysis and lesions affecting the Penfield supplementary motor area. In such cases, facial palsy is usually associated with motor disorders in the limbs, the most characteristic of which is unilateral motor under-utilisation. The possibility of inverse dissociated facial paralysis occurring as a result of a rostral premotor lesion cannot be ruled out in our present state of knowledge.

Aged↗
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↗
PubMed1978

[Facial paralysis during progressive chronic otitis. Reflections apropos of 32 cases].

The authors report their experience of 32 cases of facial paralysis occurring during progressive chronic otitis. Twenty were pre-operative. The conclusions which may be drawn are as follows: 1) It occurs in general in cases of severe chronic otitis with large destructive cholesteatomatous and osteitic lesions. 2) Surgery is often difficult, long full of unexpected findings and risks. 3) The development of facial paralysis in a case of progressive chronic otitis is an indication for immediate surgery, on the same basis as a fistula of the H.S.C.C., which is, in fact, oftan present in association. 4) The lesions encountered are much more extensive at the time of secondary (11) rather than at primary surgery (9). 5) The extent of the lesions (13 cases of fistula or laybrinthine destruction) and auditory impairment (16 cophoses or sub-cophoses) are such that tympanoplasty is useless. The authors report their long term results: 13 cases of complete recovery, 4 nil, 3 partial (2 as a result of a superficial cervical plexus graft). They raise the problem of the management when a markedly contused nerve is discovered: simple liberation with incision of its sheath or immediate graft? The other twelve were postoperative. Five were cases operated upon by the autor. There was 100% recovery in all cases, but one patient, in whom the nerve followed an atypical course, required decompression surgery. In the other seven, the autors performed 3 decompressions followed by an excellent result, apart from in one case in which the nerve was markedly contused. In 2 cases a superficial cervical plexus graft and a XII-VII anastomosis proved necessary.

Adolescent↗
PubMed1977

Vestibular disease, and its relationship to facial paralysis in the horse: a clinical study of 7 cases.

The signs observed in 6 cases of peripheral vestibular disease included incoordination, head tilt and nystagmus. The intensity of the signs varied greatly with duration of the disease, and in 3 cases facial paralysis was also present. Tympanosclerosis was demonstrable in all cases subject to radiology. Trauma was the causative factor in most cases. The causes of, and relationships between, vestibular dysfunction and concomitant facial paralysis are discussed. The exact etiology of the tympanosclerosis is unknown.

Animals↗