Síndrome de Ramsay Hunt: revisión narrativa / Ramsay Hunt Syndrome: Narrative Review

El síndrome de Ramsay Hunt (SRH) corresponde a la asociación de la parálisis facial periférica con una erupción vesicular localizada en el pabellón auricular, causada por el compromiso del ganglio geniculado secundario a una infección por el virus de la varicela-zóster (VVZ). Este síndrome es la segunda causa más común de parálisis facial atraumática y representa aproximadamente el 10 %-12 % de las parálisis faciales agudas, con una incidencia anual de 5 por cada 100 000 habitantes en Estados Unidos. El diagnóstico es principalmente clínico y entre las manifestaciones más destacadas se encuentran síntomas neurológicos como otalgia, tinnitus, hipoacusia asociada con parálisis facial junto a lesiones herpéticas características. Dentro de las complicaciones que se pueden presentar en esta entidad se encuentra, principalmente, la neuralgia posherpética, seguida de otras menos frecuentes como la encefalitis, el herpes zóster oftálmico y la mielitis. El manejo actual del SRH se basa en la aplicación de terapias duales con corticosteroides asociados a terapia antiviral, lo cual ha demostrado que el inicio temprano del tratamiento mejora el pronóstico y disminuye la aparición de complicaciones. El pronóstico de esta patología es inferior en comparación a patologías menos severas que comprometen el nervio facial (como la parálisis de Bell) y se ve impactado por varios factores como el inicio oportuno de tratamiento, el grupo etario y la presencia de comorbilidades.

Ramsay Hunt syndrome corresponds to the association of peripheral facial paralysis with a vesicular eruption located in the pinna, caused by the involvement of the geniculate ganglion secondary to infection by the varicella zoster virus. This syndrome is the second causes of atraumatic facial paralysis, representing approximately 10 %-12 % of acute facial paralysis, with an annual incidence of 5 per 100,000 inhabitants. The diagnosis is mainly clinical and among the most prominent manifestations are neurological symptoms such as otalgia, tinnitus, hypoacusis associated with facial paralysis together with characteristic herpetic lesions. Among the complications that may occur in this entity is mainly postherpetic neuralgia, followed by less frequent ones such as encephalitis, ophthalmic herpes zoster and myelitis. Current management of Ramsay Hunt syndrome is based on the application of dual therapies consisting of corticosteroids associated with antiviral therapy, showing that early initiation of treatment improves prognosis and reduces the appearance of complications. The prognosis of this pathology is inferior compared to less severe pathologies that compromise the facial nerve (Bell's palsy) and is impacted by several factors such as the timely initiation of treatment, the age group, and the presence of comorbidities.

Etiology and therapy of delayed facial paralysis after middle ear surgery.

PURPOSE: This review focuses on the etiology, incidence and therapy of delayed paralysis of the facial nerve (DFP) after different types of middle ear surgery. METHODS: Retrospective review of studies published in English from 1970 until 2019 reporting DFP after tympanoplasty, tympanomastoid surgery, stapedotomy and stapedectomy. The search used the databases of PubMed, Scopus and Cochrane Library. Studies reporting from adult patients and DFP onset after 48 h after surgery were included. Studies dealing with iatrogenic or preexisting facial palsy and case reports were excluded. The initial literature search resulted in 52 studies. The relevance of the publications was verified using title, abstract and full-text analysis. Data were analyzed with descriptive statistics using median, simple sum and statistical significance. RESULTS: Ten studies having 12,161 patients could be included in this review. The incidence of DFP after the middle ear surgeries varies between 0.2 and 1.9%. The surgical stress of the middle ear surgeries is the main trigger for the development of DFP and leads to a virus reactivation and/or neuronal edema. Patients with a dehiscence of the facial canal have a significantly higher probability for a DFP. The recommended therapy of DFP based on the data of the therapy of Bell's palsy, consists of the administration of a steroid. For patients having a case history of previous viral infections, an antiviral prophylaxis is recommended. CONCLUSION: Overall, DFP has a very good prognosis, with mostly complete healing with appropriate therapy. Viral reactivation is the most favored genesis of DFP. Immunization or antiviral prophylaxis is recommended to those patients being at risk for a viral reactivation.

Infant Facial Paralysis Associated with Epstein-Barr Virus Infection.

BACKGROUND Peripheral facial paralysis is a clinical presentation which, in most cases, is benign. It is relatively frequent, although less so in pediatric patients, where clinical diagnosis is more difficult. This clinical condition can be congenital, neurological, infectious, neoplastic, traumatic, or metabolic in origin. CASE REPORT This report describes the case of a male infant of 23 months of age with peripheral facial paralysis due to Epstein-Barr virus (EBV) upper respiratory infection. A hemogram showed the presence of leukocytosis and lymphocytosis, and a peripheral blood smear indicated the presence of stimulated lymphocytes. Serological tests were compatible with recent EBV infection: IgM anti-VCA (capsid antigen) was positive, while IgG anti-VCA and anti-EBNA (nuclear antigen) were negative. EBV genome was detected in pharyngeal swab and in serum, where viral load was 5.08 log copies/1000 cells and 3.72 log copies/mL, respectively. CONCLUSIONS Whilst the most common cause of facial paralysis is idiopathic paralysis, such problems of the facial nerve may have many origins, including an infectious nature such as infection with viral agents. Rapid determination of the etiology of the problem allows the most appropriate management of the condition and quick follow-up to be implemented, which is essential for the evaluation of treatment response and the avoidance of permanent consequences.

Typical or Atypical Ramsay-Hunt Syndrome in Delayed Facial Palsy After Stapedectomy?

OBJECTIVES: The aim of this study was to define the typical pattern for varicella zoster virus (VZV) reactivation in delayed facial palsy (DFP) after stapedectomy for otosclerosis. MATERIALS AND METHODS: Review of the relevant literature, personal casistics, and case-report. RESULTS: In total, 48 cases of DFP after stapes surgery have been described so far, including the reported case with exclusive manifestation of atypical Ramsay Hunt syndrome (RH); in the personal series of 1253 stapedectomies, DFP occurred in only one case (0.08%). Complete DFP (House-Brackmann grade VI) rapidly developed 12 days after surgery; RH appeared 2 days later, confirming the role of VZV. The DFP started improving after 8 weeks and completely recovered 6 months later. CONCLUSION: Acute otalgia prior to DFP should raise the suspicion of VZV reactivation. Atypical RH is the most frequent pattern that occurs in DFP after stapedectomy.

Peripheral facial paralysis associated with HIV infection: A case series and literature review.

OBJECTIVE: The association between peripheral facial paralysis (PFP) and HIV infection has been scarcely explained. The authors aimed to describe the association between PFP and HIV infection status, along with the related co-morbidities and the outcomes of PFP, as well as the literature review on this topic. PATIENTS AND METHODS: All HIV-infected patients who experienced PFP, both before and after a positive HIV serology test, between January 2002 and June 2015 were retrospectively reviewed. The patients' demographic data, clinical characteristics, HIV co-morbidities and outcomes of PFP were summarized. A literature review of PFP in HIV infection was also performed. Descriptive statistics were used in the data analysis. The Mann-Whitney U test was performed to compare the parameters between the current case series and cases from literature review to determine statistical significant differences (p <  0.05). RESULTS: Sixteen patients (6 males and 10 females) were enrolled. Their median age was significantly higher than that of the cases in the literature review [46 (38, 49.75) vs. 33 (26, 41) years (p =  0.004)]. Nonetheless, a non-significant lower median CD4 count was observed [274 (134.5, 425.5) vs. 373 (265, 718) cells/µL (p =  0.058)]. In our series, unilateral PFP (UFP) was the most frequent, and it typically occurred long after a positive HIV serology test. However, bilateral PFP (BFP) was commonly found in the literature, and a simultaneous positive HIV serology test was reported in almost all cases. Consequently, most of our cases, except for those with HIV-related complications or co-morbidities, experienced a satisfactory recovery from PFP regardless of treatments received. CONCLUSIONS: Most of the cases in our series were UPF with a higher median age and a lower median CD4 count. Moreover, facial paralysis presented later in our series than in the previously reported cases in the literature. Most of our cases experienced satisfactory recovery of facial weakness.

Parálisis facial neonatal: identificación del virus del herpes simple 1 en el líquido cefalorraquídeo. Caso clínico / Neonatal facial palsy: Identification of herpes simplex virus 1 in cerebrospinal fluid. Case report

En los neonatos, la parálisis facial es muy infrecuente y, por lo general, diagnosticada al nacer. Se presenta el primer caso de parálisis facial neonatal con identificación del virus del herpes simple 1 en el líquido cefalorraquídeo. Un varón de 35 días de vida acudió a Urgencias por la desviación de la comisura bucal hacia la izquierda y la ausencia de cierre del ojo derecho, sin sintomatología infecciosa ni antecedentes relevantes. La exploración física fue compatible con parálisis facial periférica. Las exploraciones complementarias de urgencia (hemograma, bioquímica, coagulación y citoquímica de líquido cefalorraquídeo) fueron normales. Fue ingresado con prednisolona oral y aciclovir intravenoso. La resonancia magnética craneal fue normal. A las 48 horas, se recibió el resultado positivo de la reacción en cadena de la polimerasa para el virus del herpes simple 1 en el líquido cefalorraquídeo. Con evolución favorable, completó 7 días de prednisolona oral y fue dado de alta tras 21 días de aciclovir intravenoso, con exploración neurológica previa normal.

Neonatal facial palsy is very uncommon and is generally diagnosed at birth. We present the first published case of neonatal facial palsy with identification of herpes simplex virus 1 in cerebrospinal fluid. A 35-day-old male was presented at the Emergency Department with mouth deviation to the left and impossibility of full closure of the right eye. There were no symptoms of infection or relevant medical history. Physical examination was compatible with peripheral facial palsy. Studies performed at admission were normal (blood count, biochemical analysis and coagulation blood tests and cerebrospinal fluid analysis). The patient was admitted on oral prednisolone and intravenous aciclovir. Cranial magnetic resonance was normal. Polymerase chain reaction test for herpes simplex virus 1 in cerebrospinal fluid was reported positive after 48 hours of admission. Patient followed good evolution and received prednisolone for 7 days and acyclovir for 21 days. At discharge, neurological examination was normal.

[Bilateral facial nerve palsy associated with Epstein-Barr virus infection in a 3-year-old boy]. / Paralysie faciale bilatérale au cours d'une infection à virus d'Epstein­Barr.

Bilateral facial nerve palsy is a rare and sometimes difficult diagnosis. We describe a case of bilateral simultaneous facial nerve palsy associated with Epstein-Barr virus (EBV) infection in a 3-year-old boy. Several symptoms led to the diagnosis of EBV infection: the clinical situation (fever, stomachache, and throat infection), white blood cell count (5300/mm3 with 70% lymphocyte count), seroconversion with EBV-specific antibodies, lymphocytic meningitis, and a positive blood EBV polymerase chain reaction (9.3×103 copies of EBV-DNA). An MRI brain scan showed bilateral gadolinium enhancement of the facial nerve. A treatment plan with IV antibiotics (ceftriaxone) and corticosteroids was implemented. Antibiotics were stopped after the diagnosis of Lyme disease was ruled out. The patient's facial weakness improved within a few weeks. Bilateral facial nerve palsy is rare and, unlike unilateral facial palsy, it is idiopathic in only 20% of cases. Therefore, it requires further investigation and examination to search for the underlying etiology. Lyme disease is the first infectious disease that should be considered in children, especially in endemic areas. An antibiotic treatment effective against Borrelia burgdorferi should be set up until the diagnosis is negated or confirmed. Further examination should include a blood test (such as immunologic testing, and serologic testing for viruses and bacterium with neurological tropism), a cerebrospinal fluid test, and an MRI brain scan to exclude any serious or curable underlying etiology. Facial bilateral nerve palsy associated with EBV is rarely described in children. Neurological complications have been reported in 7% of all EBV infections. The facial nerve is the most frequently affected of all cranial nerves. Facial palsy described in EBV infections is bilateral in 35% of all cases. The physiopathology is currently unknown. Prognosis is good most of the time.

Facial paralysis due to Ramsay Hunt syndrome - A rare condition / Paralisia facial secundária à síndrome de Ramsay Hunt - Uma condição rara

Summary Ramsay Hunt syndrome (or herpes zoster oticus) is a rare complication of herpes zoster in which reactivation of latent varicella zoster virus infection in the geniculate ganglion occurs. Usually, there are auricular vesicles and symptoms and signs such otalgia and peripheral facial paralysis. In addition, rarely, a rash around the mouth can be seen. Immunodeficient patients are more susceptible to this condition. Diagnosis is essentially based on symptoms. We report the case of a diabetic female patient who sought the emergency department with a complaint of this rare entity.

Resumo A síndrome de Ramsay Hunt (ou zóster auricular) é uma complicação rara do herpes-zóster em que ocorre reativação de uma infecção latente pelo vírus varicela-zóster no gânglio geniculado. Geralmente, estão presentes vesículas auriculares e sintomas como otalgia e paralisia facial periférica. Além disso, mais raramente pode haver rash ao redor da boca. Pacientes com imunodeficiência apresentam maior susceptibilidade para essa condição. O diagnóstico é essencialmente pelo quadro clínico. É apresentado o caso de uma paciente diabética que compareceu ao setor de emergência com essa manifestação rara.

Facial palsy after dental procedures - Is viral reactivation responsible?

OBJECTIVES: Herpes labialis viral reactivation has been reported following dental procedures, but the incidence, characteristics and outcomes of delayed peripheral facial nerve palsy following dental work is poorly understood. Herein we describe the unique features of delayed facial paresis following dental procedures. MATERIALS AND METHODS: An institutional retrospective review was performed to identify patients diagnosed with delayed facial nerve palsy within 30 days of dental manipulation. Demographics, prodromal signs and symptoms, initial medical treatment and outcomes were assessed. RESULTS: Of 2471 patients with facial palsy, 16 (0.7%) had delayed facial paresis following ipsilateral dental procedures. Average age at presentation was 44 yrs and 56% (9/16) were female. Clinical evaluation was consistent with Bell's palsy in 14 (88%) and Ramsay-Hunt syndrome in 2 patients (12%). Patients developed facial paresis an average of 3.9 days after the dental procedure, with all individuals developing a flaccid paralysis (House Brackmann (HB) grade VI) during the acute stage. 50% of patients developed persistent facial palsy in the form of non-flaccid facial paralysis (HBIII-IV). CONCLUSION: Facial palsy, like herpes labialis, can occur in the days following dental procedures and may also be related to viral reactivation. In this small cohort, long-term facial outcomes appear worse than for spontaneous Bell's palsy.

Pretreatment Hematologic Findings as Novel Predictive Markers for Facial Palsy Prognosis.

OBJECTIVE: To examine the relationship between prognosis of 2 different facial palsies and pretreatment hematologic laboratory values. STUDY DESIGN: Multicenter case series with chart review. SETTING: Three tertiary care hospitals. SUBJECTS AND METHODS: We examined the clinical records of 468 facial palsy patients who were treated with an antiviral drug in combination with either oral or intravenous corticosteroids in participating hospitals between 2010 and 2014. Patients were divided into a Bell's palsy group or a Hunt's palsy group. We used the Yanagihara facial nerve grading system to grade the severity of facial palsy. "Recovery" from facial palsy was defined as achieving a Yanagihara score ≥36 points within 6 months of onset and having no accompanying facial contracture or synkinesis. We collected information about pretreatment hematologic findings, demographic data, and electrophysiologic test results of the Bell and Hunt group patients who recovered and those who did not. We then compared these data across the 2 palsy groups. RESULTS: In the Bell's palsy group, recovered and unrecovered patients differed significantly in age, sex, electroneuronography score, stapedial muscle reflex, neutrophil rate, lymphocyte rate, neutrophil-to-lymphocyte ratio, and initial Yanagihara score. In the Hunt's palsy group, recovered and unrecovered patients differed in age, electroneuronography score, stapedial muscle reflex, monocyte rate, platelet count, mean corpuscular volume, and initial Yanagihara score. CONCLUSIONS: Pretreatment hematologic findings, which reflect the severity of inflammation and bone marrow dysfunction caused by a virus infection, are useful for predicting the prognosis of facial palsy.

Clinical manifestations in patients with herpes zoster oticus.

Patients with herpes zoster oticus (HZO) may exhibit diverse symptoms regarding cochleovestibular dysfunction. This study investigated the clinical manifestations of HZO by comparing symptoms associated with dysfunctions of the 7th and 8th cranial nerves (CN VII and VIII, respectively). This study is a retrospective case series. Eighty-one patients with HZO who had dysfunction of CN VII or VIII were included in this study. Electroneuronography (ENoG) values were compared among patient groups with facial weakness. Patients with ipsilateral facial weakness (62 of 81) were more common than those without. Among 81 patients, those with facial weakness, hearing loss, and vertigo were most common, and only 1 patient had vertigo without hearing loss or facial weakness. Most patients with vertigo also had hearing loss (28 of 30), and patients without hearing loss did not have vertigo (19 of 21). While patients with vertigo had worse ENoG values than those without vertigo, ENoG values were not significantly different between patients with and without hearing loss. In conclusion, various clinical manifestations of CN VII and VIII dysfunction are possible in patients with HZO. Patients with vertigo had worse ENoG values than those without, which may indicate that vertigo reflects more severe facial nerve degeneration in HZO patients with facial weakness.

Anterior opercular syndrome induced by Epstein-Barr virus encephalitis.

We report a 19-year-old female presenting with fever, drooling, anarthria, and voluntary facial movement disruption, characteristic of anterior opercular syndrome (AOS). Serological examination revealed Epstein-Barr virus (EBV) infection following acute encephalitis with severe ataxia. A single-photon emission computerized tomography (SPECT) examination indicated hypoperfusion in the left perisylvian region, bilateral thalamus, occipital lobe, and cerebellum. This is the first report of AOS related to EBV encephalitis. SPECT was a useful method for detecting the damaged region of the operculum. In addition, AOS is a clinically distinct entity that may help us understand the mechanisms of language circuits within the operculum.

Acupuncture: a potential modality for the treatment of auricular pruritus in Ramsay Hunt Syndrome with multiple cranial nerve lesions.

Auricular pruritus coexisted with multiple cranial nerve lesions in Ramsay Hunt syndrome has been rarely reported in the literature especially its treatment. However, auricular pruritus cannot be better improved along with the improvement of multiple cranial nerve lesions. We tried to solve the problem with acupuncture and got experience from it. The following 2 cases of Ramsay Hunt syndrome show a potential modality for the treatment of auricular pruritus with acupuncture.

Contralateral facial nerve palsy following mandibular second molar removal: is there co-relation or just coincidence?

Peripheral facial nerve palsy (FNP) is the most common cranial nerves neuropathy. It is very rare during dental treatment. Classically, it begins immediately after the injection of local anaesthetic into the region of inferior dental foramen and it's homolateral to the injection. Recovery takes a few hours, normally as long the anaesthetic lasts. The authors present a 44-year-old patient who presented a contralateral delayed-onset facial paralysis arising from dental procedure and discuss the plausible pathogenesis mechanism of happen and a possible relationship between dental procedure and contralateral FNP.

Role of nitric oxide in the onset of facial nerve palsy by HSV-1 infection.

IMPORTANCE: Although herpes simplex virus type 1 (HSV-1) is a causative agent of Bell palsy, the precise mechanism of the paralysis remains unknown. It is necessary to investigate the pathogenesis and treatment of Bell palsy due to HSV-1 infection. OBJECTIVE: This study elucidated the role of nitric oxide (NO) in the incidence of facial nerve paralysis caused by HSV-1 in mice and to evaluate the possible role of edaravone, a free radical scavenger, in preventing the paralysis. DESIGN, SETTING, PARTICIPANTS: Sixty-two mice served as animal models of Bell palsy in this laboratory study conducted at an academic institution. INTERVENTIONS: Levels of NO in the facial nerve were measured using high-performance liquid chromatography and absorption photometry. The incidence of facial palsy was assessed following administration of edaravone immediately after HSV-1 inoculation and daily for 11 days thereafter. MAIN OUTCOMES AND MEASURES: The ratio of NO (inoculated side to control side) and incidence of facial palsy. RESULTS Before the onset of facial palsy, no substantial difference in the NO level was noted between the HSV-1-inoculated side and the control side. When facial palsy occurred, usually at 7 days after inoculation, the NO level was significantly higher on the inoculated side than on the control side. Following recovery from the palsy, the high NO level of the inoculated side decreased. No increase in the NO level was observed in animals without transient facial palsy. When edaravone was administered, the incidence of facial palsy decreased significantly. CONCLUSIONS AND RELEVANCE: These findings suggest that NO produced by inducible NO synthase in the facial nerve plays an important role in the onset of facial palsy caused by HSV-1 infection, which is considered a causative virus of Bell palsy. Hato and colleagues elucidate the role of nitric oxide in HSV-1­related facial nerve paralysis in mice and evaluate the role of edaravone, a free radical scavenger, in preventing the paralysis.

A cell culture model of facial palsy resulting from reactivation of latent herpes simplex type 1.

HYPOTHESIS: Reactivation of herpes simplex virus type 1 (HSV-1) in geniculate ganglion neurons (GGNs) is an etiologic mechanism of Bell's palsy (BP) and delayed facial palsy (DFP) after otologic surgery. BACKGROUND: Several clinical studies, including temporal bone studies, antibody, titers, and intraoperative studies, suggest that reactivation of HSV-1 from latently infected GGNs may lead to both BP and DFP. However, it is difficult to study these processes in humans or live animals. METHODS: Primary cultures of GGNs were latently infected with Patton strain HSV-1 expressing a green fluorescent protein-late lytic gene chimera. Four days later, these cultures were treated with trichostatin A (TSA), a known chemical reactivator of HSV-1 in other neurons. Cultures were monitored daily by fluorescent microscopy. Titers of media from lytic, latent, and latent/TSA treated GGN cultures were obtained using plaque assays on Vero cells. RNA was harvested from latently infected GGN cultures and examined for the presence of viral transcripts using reverse transcription-polymerase chain reaction. RESULTS: Latently infected GGN cultures displayed latency-associated transcripts only, whereas lytically infected and reactivated latent cultures produced other viral transcripts, as well. The GGN cultures displayed a reactivation rate of 65% after treatment with TSA. Media from latently infected cultures contained no detectable infectious HSV-1, whereas infectious virus was observed in both lytically and latently infected/TSA-treated culture media. CONCLUSION: We have shown that cultured GGNs can be latently infected with HSV-1, and HSV-1 in these latently infected neurons can be reactivated using TSA, yielding infectious virus. These results have implications for the cause of both BP and DFP.

[Facial paralysis induced by herpes simplex virus type 1 and the study of facial neurons apoptosis in mice].

OBJECTIVE: To study the apoptosis of facial motor neurons and the expression of apoptosis-related genes, Bcl-2 and Bax, in the animal model of viral facial paralysis. METHODS: Total of 84 Balb/c mice were divided into viral inoculation group and nerve transaction group. The animals were executed 1, 3, 7, 10, 15, 20 and 30 days after being operated respectively. The histopathological features of facial neurons in brain stem were observed by HE and Nissl stain. The changes of facial neuronal apoptosis were observed by TUNEL. The changes of expression of Bcl-2 and Bax genes in facial neurons were observed by immunohistochemistry staining. RESULTS: After nerve transection, increased apoptotic cells were found in homolateral facial motor nucleus and the peak appeared at 10 and 15 days. The level of Bcl-2 expression in neurons declined while the expression of Bax increased gradually. Correspondingly, the ratio of Bcl-2/Bax declined. In the viral inoculation group, no visible change of apoptosis and Bax expression, but the level of Bcl-2 and the ratio of Bcl-2/Bax increased gradually. CONCLUSIONS: Comparing to axotomy, facial motor nucleus in HSV-1 infective animal model are free of apoptosis. Both the mild form of lesion and the ability to block apoptosis of HSV-1 are likely to be involved into the phenomenon. Bcl-2 and Bax might interfere with the apoptotic response.

Unilateral facial paralysis caused by Ramsay Hunt syndrome.

The Ramsay Hunt syndrome is a rare disease caused by an infection of the geniculate ganglion by the varicella-zoster virus. The main clinical features of the syndrome are as follows: Bell palsy unilateral or bilateral, vesicular eruptions on the ears, ear pain, dizziness, preauricular swelling, tingling, tearing, loss of taste sensation, and nystagmus. We describe a 23-year-old white woman, who presented with facial paralysis on the left side of the face, pain, fever, ear pain, and swelling in the neck and auricular region on the left side. She received appropriate treatment with acyclovir, vitamin B complex, and CMP nucleus. After 30 days after presentation, the patient did not show any signs or symptoms of the syndrome. At follow-up at 1 year, she showed no relapse of the syndrome.

Intratemporal facial nerve ultrastructure in patients with idiopathic facial paralysis: viral infection evidence study.

UNLABELLED: The etiology of idiopathic peripheral facial palsy (IPFP) is still uncertain; however, some authors suggest the possibility of a viral infection. AIM: to analyze the ultrastructure of the facial nerve seeking viral evidences that might provide etiological data. MATERIAL AND METHODS: We studied 20 patients with peripheral facial palsy (PFP), with moderate to severe FP, of both genders, between 18-60 years of age, from the Clinic of Facial Nerve Disorders. The patients were broken down into two groups - Study: eleven patients with IPFP and Control: nine patients with trauma or tumor-related PFP. The fragments were obtained from the facial nerve sheath or from fragments of its stumps - which would be discarded or sent to pathology exam during the facial nerve repair surgery. The removed tissue was fixed in 2% glutaraldehyde, and studied under Electronic Transmission Microscopy. RESULTS: In the study group we observed an intense repair cellular activity by increased collagen fibers, fibroblasts containing developed organelles, free of viral particles. In the control group this repair activity was not evident, but no viral particles were observed. CONCLUSION: There were no viral particles, and there were evidences of intense activity of repair or viral infection.