MRI Findings in Two Cases of Acute Facial Paralysis

1989 ◽  
Vol 101 (5) ◽  
pp. 562-565 ◽  
Author(s):  
James Labagnara ◽  
Anthony F. Jahn ◽  
David V. Habif ◽  
Edward M. Solomon
Keyword(s):  
Facial Nerve ◽  
Treatment Options ◽  
Bell’S Palsy ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Mri Findings ◽  
Diagnostic Dilemma ◽  
Nerve Paralysis ◽  
Ramsay Hunt Syndrome ◽  
Hunt Syndrome

This article describes the use of magnetic resonance imaging (MRI) in the evaluation of the facial nerve paralysis of Bell's palsy and herpes zoster oticus. Identification of the nature of inflammatory facial nerve paralysis often presents a diagnostic dilemma. The site of involvement along the course of the nerve may have importance when treatment options are being considered. We have found MRI to be a unique method for localizing the site of nerve injury in both Bell's palsy and Ramsay Hunt syndrome.

Facial Nerve Paralysis Induced by Herpes Simplex Virus in Mice: An Animal Model of Acute and Transient Facial Paralysis

1995 ◽  
Vol 104 (7) ◽  
pp. 574-581 ◽  
Author(s):  
Toshiaki Sugita ◽  
Yasuo Fujiwara ◽  
Shingo Murakami ◽  
Yoshinari Hirata ◽  
Naoaki Yanagihara ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Facial Nerve ◽  
Facial Paralysis ◽  
Bell’S Palsy ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Vacuolar Degeneration ◽  
Nerve Paralysis ◽  
Simplex Virus

We have been the first to succeed in producing an acute and transient facial paralysis simulating Bell's palsy, by inoculating herpes simplex virus into the auricles or tongues of mice. The KOS strain of the virus was injected into the auricle of 104 mice and the anterior two thirds of the tongue in 30 mice. Facial paralysis developed between 6 and 9 days after virus inoculation, continued for 3 to 7 days, and then recovered spontaneously. The animals were painlessly sacrificed between 6 and 20 days after inoculation for histopathologic and immunocytochemical study. Histopathologically, severe nerve swelling, inflammatory cell infiltration, and vacuolar degeneration were manifested in the affected facial nerve and nuclei. Herpes simplex virus antigens were also detected in the facial nerve, geniculate ganglion, and facial nerve nucleus. The pathophysiologic mechanisms of the facial paralysis are discussed in light of the histopathologic findings, in association with the causation of Bell's palsy.

scholarly journals Aetiological Profile of Facial Nerve Palsy Seen in Nigerian Tertiary Hospital

2020 ◽  
Vol 5 (06) ◽  
Author(s):  
Gabriel Toye Olajide ◽  
Waheed Atilade Adegbiji ◽  
Akinwale Olaleye Akinbade ◽  
Anthony Oyebanji Olajuyin ◽  
Paul Olowoyo
Keyword(s):  
Facial Nerve ◽  
Nerve Palsy ◽  
Facial Nerve Palsy ◽  
Road Traffic ◽  
Neck Region ◽  
Bell’S Palsy ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Female Ratio ◽  
Nerve Paralysis

Background/Aim: Facial nerve palsy may cause facial asymmetry, functional and cosmetic impairment, and therefore imposes great psychological and social problems on the individual with the condition. The aim of this paper was to highlight the aetiological profile of facial nerve palsy (FNP) in two tertiary institutions in Ekiti, southwest, Nigeria. Methods: This was a retrospective review of patients with facial nerve palsy seen and treated at Ear, Nose & Throat (ENT) clinic. All folders and registers of patients diagnosed with facial nerve palsy from January 2010 to December 2019 in the central, ENT and Dental medical records departments were retrieved and reviewed. The information extracted included the socio-demographic characteristics of the patients, clinical presentation, type and aetiology of FNP, side affected, diagnosis/impression, nature of impairment, type of lesion, onset of the disease, treatment and outcome. Results: Of 76 patients analysed, 48(63.2%) were males and 28(36.8%) were females given a male to female ratio of 1:1.7. Their age ranged between 5 to 72 years with a mean of 39.83 ± 17.58 SD. The age range 21-40 years was most commonly affected, representing 31 (40.8%). The commonest cause of facial nerve paralysis was Bell’s palsy in 32(42.1%), followed by trauma 28(36.9%). Of the 28 (36.9%) that was caused by trauma, road traffic injury constituted 15(53.6%). Half (50.0 %) of the lesion affected right side of the face. Seventy (92.1%) was treated medically. Majority (37.0%) presented within one week of their symptoms. All the patients presented with deviation of mouth, followed by inability to close eye in 70 (92.1%). Higher proportion (88.2%) of our patients had lower motor neuron lesion. Conclusion: This study found that majority of our patients was young adults. Bell’s palsy was a major cause of facial nerve paralysis followed by trauma. Most of our patient presented early and did well on conservative treatment. High index of suspicion is essential especially when patients present with injuries involving head and neck region.

Pathophysiology of Facial Nerve Paralysis Induced by Herpes Simplex Virus Type 1 Infection

2002 ◽  
Vol 111 (7) ◽  
pp. 616-622 ◽  
Author(s):  
Naohito Hato ◽  
Hisanobu Kisaki ◽  
Nobumitu Honda ◽  
Hirotaka Takahashi ◽  
Shingo Murakami ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Facial Nerve ◽  
Time Course ◽  
Bell’S Palsy ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Nerve Paralysis ◽  
Simplex Virus

Herpes simplex virus type 1 (HSV-1) has been proven to be a cause of Bell's palsy; however, the underlying pathophysiology of the facial nerve paralysis is not fully understood. We established a mouse model with facial nerve paralysis induced by HSV-1 infection simulating Bell's palsy and investigated the pathophysiology of the facial nerve paralysis. The time course of the R1 latency in the blink reflex tests paralleled the recovery of the facial nerve paralysis well, whereas electroneurographic recovery tended to be delayed, compared to that of the paralysis; these responses are usually seen in Bell's palsy. On histopathologic analysis, intact, demyelinated, and degenerated nerves were intermingled in the facial nerve in the model. The similarity of the time course of facial nerve paralysis and the electrophysiological results in Bell's palsy and the model strongly suggest that the pathophysiological basis of Bell's palsy is a mixed lesion of various nerve injuries.

Recurrent Bell's palsy in pregnancy

1990 ◽  
Vol 104 (9) ◽  
pp. 713-714 ◽  
Author(s):  
Anand D. Deshpande
Keyword(s):  
Side Effects ◽  
Facial Nerve ◽  
Bell’S Palsy ◽  
Motor Neurone ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Nerve Paralysis ◽  
In Pregnancy

AbstractA case of recurrent Bell's palsy occurring in two successive pregnancies in a 37-year-old woman is presented. The causes of facial nerve paralysis of the lower motor neurone type are discussed. The rate of recurrence of Bell's palsy during pregnancy is unknown. Treatment with corticosteroids of Bell's palsy during pregnancy poses the threat of possible side effects on the fetus.

scholarly journals Intratemporal Facial Nerve Paralysis- A Three Year Study

2016 ◽  
Vol 24 (2) ◽  
pp. 94-99
Author(s):  
Anirban Ghosh ◽  
Sankar Prasad Bera ◽  
Somnath Saha
Keyword(s):  
Facial Nerve ◽  
Facial Palsy ◽  
Bell’S Palsy ◽  
Facial Nerve Paralysis ◽  
Bell's Palsy ◽  
Prospective Longitudinal Study ◽  
Nerve Paralysis ◽  
Excellent Outcome ◽  
Stapedial Reflex ◽  
Prospective Longitudinal

Introduction This study on intratemporal facial paralysis is an attempt to understand the aetiology of facial nerve paralysis, effect of different management protocols and the outcome after long-term follow-up. Materials and Methods A prospective longitudinal study was conducted from September 2005 to August 2008 at the Department of Otorhinolaryngology of a medical college in Kolkata comprising 50 patients of intratemporal facial palsy. All cases were periodically followed up for at least 6 months and their prognostic outcome along with different treatment options were analyzed. Result Among different causes of facial palsy, Bell’s palsy is the commonest cause; whereas cholesteatoma and granulation were common findings in otogenic facial palsy. Traumatic facial palsies were exclusively due to longitudinal fracture of temporal bone running through geniculate ganglion. Herpes zoster oticus and neoplasia related facial palsies had significantly poorer outcome. Discussion Otogenic facial palsy showed excellent outcome after mastoid exploration and facial decompression. Transcanal decompression was performed in traumatic facial palsies showing inadequate recovery. Complete removal of cholesteatoma over dehiscent facial nerve gave better postoperative recovery. Conclusion The stapedial reflex test is the most objective and reproducible of all topodiagnostic tests. Return of the stapedial reflex within 3 weeks of injury indicates good prognosis. Bell’s palsy responded well to conservative measures. All traumatic facial palsies were due to longitudinal fracture and 2/3rd of these patients showed favourable outcome with medical therapy.

Tofacitinib-induced Ramsay- Hunt Syndrome in a Patient with Rheumatoid Arthritis

2020 ◽  
Vol 15 ◽  
Author(s):  
Senol Kobak
Keyword(s):  
Rheumatoid Arthritis ◽  
Hearing Loss ◽  
Facial Nerve ◽  
Varicella Zoster Virus ◽  
Facial Nerve Paralysis ◽  
Nerve Paralysis ◽  
Varicella Zoster ◽  
Ramsay Hunt Syndrome ◽  
Hunt Syndrome ◽  
Intravenous Acyclovir

Background: Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint and systemic involvement. Tofacitinib is a JAK- inhibitor that is an effective agent in the treatment of active RA. Varicella zoster virus (VZV) reactivation is among the most important advers effects of tofacitinib. Ramsay-Hunt syndrome (RHS) is a rare clinical condition that develop as a result of VZV reactivation and progresses with hearing loss, dizziness and facial nerve paralysis. Objective: To present a case with Ramsay-Hunt syndrome due to varicella zoster reactivation in RA patient using tofacitinib Case report: A 63-year-old female RA patient under tofacitinib treatment was admitted to the rheumatology outpatient clinic due to widespread skin rashes on her face and ear, and hearing loss. On inspection widespread erythematous, vesicular rashes on the left side of the face, lips, around the eye and in the ear, and mild facial paralysis on the left side were detected. On laboratory investigations acute phase reactants were increased. Serological study for specific antibodies against varicella zoster virus showed higher titers. Dermatology and ear nose throat specialist consultations was performed, varicella zoster lesions on the left inner ear, face and mild facial paresis were considered. According to clinical and laboratory findings the patient was diagnosed with RHS triggered by tofacitinib. Tofacitinib and methotrexate was discontinued, and intravenous acyclovir was started. On the control examination the patient's skin lesions and facial nerve paralysis regressed. Conclusion: Herein we reported the fırst case of tofacitinib-induced RHS in a patient with RA. This is may be the another side effect of biologic treatment. New studies are needed in this subject.

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