Case Of Peripheral Facial Palsy Research Articles

Clinical case of peripheral facial palsy as first and single COVID-19 symptom in an immunized patient

SARS-CoV-2 virus affects the central as well as the peripheral nervous system. Peripheral facial palsy is possible as the first and single COVID-19 symptom. The author presents own clinical observation of a 58-year-old patient with peripheral facial palsy. It is known that the patient completed the vaccination 8 weeks ago and also had direct contact with the patient SARS-CoV-2 (the patient's son). Facial nerve palsy was the first and only symptom of coronavirus infection. In the blood there was a moderate lymphocytopenia, increased interleukin-6, C-reactive protein, seromukoids. MRI of the brain and CT of the temporal bones did not reveal focal and diffuse pathology. After treatment, there was a complete recovery on the ninth day of treatment. Treatment included antiviral drugs, vitamins, steroids, kinesiotaping of facial muscles. The author substantiates necessity and demonstrates the results of treatment with endothelioprotective therapy (combination of L-arginine and L-carnitine) , which is aimed at elimination of systemic inflammation, oxidative stress caused by SARS-CoV-2 virus. Conclusions. General practitioner need to be alert when examining patients, including those who have been vaccinated and those who have direct contact with patients with coronavirus infection. Pathogenesis of peripheral facial palsy in COVID-19 multidirectional: neuroinvasive and neurotropic effect of the virus on the nerve, hypercoagulation, ischemia of the peripheral nerve on the background of systemic inflammatory reaction, oxidative stress. Timely detection, careful monitoring and adequate treatment of pathology are necessary to prevent complications (persistent facial contractures, synkinesis). Further in-depth studies are needed on a larger sample of patients to identify the incidence of peripheral facial nerve palsy in COVID-19 and the possibility of a link to vaccination.

Facial Palsy, Hypoacusis and Vertigo as Inaugural Symptoms of Neuroborreliosis - Case Report

Introduction: Facial Palsy (FP) is the most common acute mononeuropathy and consists of a decrease in facial muscle strength due to facial nerve damage. Peripheral FP (PFP) can result from a wide variety of disorders and aetiologies, with Lyme Disease (LD) being considered one of the most common causes of FP. LD is an infectious disease that affects the central nervous system, causing Neuroborreliosis (NB) in 15% of cases. Cranial neuropathy is the most common form of presentation of NB, as uni or bilateral PFP. We describe a case of PFP with hypoacusis and vertigo as the inaugural presentation of neuroborreliosis. Case Report: We present a case report of a 75-year-old female patient, referred to ENT consultation due to a 3-day course of a grade 4 right PFP, moderate right sensorineural hearing loss and right vestibular hypofunction. The patient underwent cranioencephalic Computed Tomography (CT-CE) which excluded a central event and was treated with 2 cycles of oral corticosteroids, without any clinical improvement. A Magnetic Resonance Imaging (MRI) was performed, which showed an abnormal inflammatory uptake of the right facial nerve. An analytical positivity for Borrelia IgM was found and the diagnosis of polyneuropathic NB with involvement of the VII and VIII right cranial pairs was assumed. The patient completed 28 days of doxycycline, with FP and vertigo improvement and normalization of hearing acuity. Discussion/Conclusion: In the presented case, the absence of the classical migratory erythema or painful meningopolyneuritis didn’t exclude the diagnosis of NB. FP associated to signs of other cranial nerves involvement raised the hypothesis of a systemic polyneuropathic disease, which motivated the etiological investigation carried out.

Unusual cerebral venous thrombosis presenting with peripheral facial palsy: A case report

Background: Cranial nerve palsy in cerebral venous thrombosis (CVT) is a rare clinical sign resulted from cavernous sinus thrombosis or elevated intracranial pressure. Peripheral facial palsy is extremely rare and individually reported in CVT. Herein, we present a rare case of peripheral facial palsy in transverse sinus thrombosis related to methylenetetrahydrofolate reductase (MTHFR) and factor V Leiden mutations.

Peripheral Facial Nerve Palsy in Severe Systemic Hypertension: A Systematic Review

Signs of nervous system dysfunction such as headache or convulsions often occur in severe systemic hypertension. Less recognized is the association between severe hypertension and peripheral facial nerve palsy. The aim of this study was to systematically review the literature on the association of peripheral facial palsy with severe hypertension. Systematic review of Medline, Embase, Web of Science, and Google Scholar from 1960 through December 2011 and report of two cases. The literature review revealed 24 cases to which we add two cases with severe hypertension and peripheral facial palsy. Twenty-three patients were children. Palsy was unilateral in 25 cases, bilateral in one case, and recurred in nine. The time between the first facial symptoms and diagnosis of hypertension was a median of 45 days (range, 0 days-2 years). In five case series addressing the complications of severe hypertension in children, 41 further cases of peripheral facial palsy were listed out of 860 patients (4.8%). The association between severe hypertension and peripheral facial palsy is mainly described in children. Arterial hypertension is diagnosed with a substantial delay. Outcome is favorable with adequate antihypertensive treatment. The pathophysiology is still debated.

A Case of Breast Cancer Found from Recurrent Facial Palsy

We often come across cases of peripheral facial palsy, most of which can be cured with medication. We report herein on a case of breast cancer, found in a patient with recurrent facial palsy. A seventy-year-old female with facial palsy was cured once, but a few weeks later, facial palsy occurred again. We suspected a tumor as the cause of the recurrent facial palsy. We examined the patient with temporal bone CT and head MRI imaging and found a mass region with bone destruction on images of the temporal bone. When we did an excisional biopsy under general anesthesia, we unexpectedly identified the mass as a locally advanced breast cancer. Finally the patient was diagnosed as having a peripheral facial palsy caused by a metastatic tumor from breast cancer. Breast cancer associated with facial palsy is rare, but when the facial palsy recurs or occurs slowly, with facial spasm or with otitis media with effusion, we should consider the existence of a tumor, especially metastatic tumor from breast or lung cancer.

Presentation of Bilateral Peripheral Seventh Cranial Nerve Palsy in an HIV Patient

Neurological manifestations in patients infected with human immunodeficiency virus can significantly increase overall morbidity and mortality. These complications are neither limited to a specific location in the nervous system nor a focal time period in the disease's progression. A literature review yielded several cases of peripheral facial palsy associated with HIV seropositivity, but few cases have been reported where the patient had bilateral peripheral facial palsy. In this paper, we present a patient with bilateral peripheral facial palsy and aseptic meningitis in the context of newly diagnosed HIV.

Inaccuracies and useless debats associated with the use of secondary references

We are really disappointed by the saga born after the publication of “Peripheral facial palsy in the past: contri­ butions from Avicenna, Nicolaus Friedrich and Charles Bell”, written by Resende and Weber. The controversy be­ gan with the statement that “Charles Bell [...] himself had right peripheral facial paralysis”. This hypothesis generat­ ed a letter to the editor by Korteweg et al. which clearly demonstrates that this affirmation was not based on origi­ nal documents, but on interpretation of secondary sourc­ es, and that it was erroneous. The authors’ reply intro­ duced new doubtful pictorial arguments not mentioned in the first publication. Once again, Korteweg et al. re­ plied in proving that these new arguments were based on invalid suppositions and that they can’t be used to support the fact that Bell had himself a facial paralysis. This time, the authors’ reply added some inadequate “per­ sonal” comments, which have nothing to do with a con­ structive and scholarly discussion. Such kind of saga is no more acceptable in a well educated exchange of knowl­ edge. The historian’s task is to assemble a sufficient num­ ber of facts, based on valid original documents; history takes shape from these and can then be discussed and in­ terpreted. Theoretical reflection is sometimes harmful, because it can introduce erroneous speculation. Original Bell’s publications demonstrate that Bell never describes that he was suffering himself of a facial palsy and no ex­ isting portraits confirm this hypothesis. Resende and Weber support the affirmation of Kor­ teweg et al. that “we should always check the primary sources concerned”, but they do not apply it in their writ­ ings. How can they discuss the contributions of Avicenna, Nicolaus Friedreich and Charles Bell without mentioning their original contributions? Their article contains inaccu­ racies such as the following sentence concerning Charles Bell: “His first case of peripheral facial palsy was pub­ lished in 1821, and his most important paper was pub­ lished in 1828”. Two debatable points are found here: the text published in 1821 effectively contains a case of a man which “had the trunk of the respiratory nerve of the face injured by suppuration”, but not a case of idiopathic pe­ ripheral facial palsy later named after Bell. Its major con­ cerns is the description of the anatomy of the “respirato­ ry nerve of the face”, i.e. the facial nerve, and the results obtained after sectioning the nerve in animals. It is not in 1828 but in 1827 that Bell published his main text deal­ ing with the description of a case of peripheral facial pal­ sy which bears his name. Thus the first case of a Bell’s pal­ sy was described by Bell in 1827 and not in 1821. These are typical examples of inaccuracies generated with the use of secondary references as often found in the med­ ical literature. Further, Resende and Weber used main­ ly Jongkees’s publication as indisputable reference. Once again this publication contains inaccuracies, the first dis­ puted one being the interpretation of the original text of Bell. The German translation made by Jongkees is incom­ plete, because Jongkees did not mention the first part of the original Bell’s text which clearly explains that it was a professor named Roux who was suffering from a right facial palsy and not Bell himself, thus leading Jongkees to wrongly think that Bell had himself a facial paralysis. If we closer look Jongkees’ text we can find other inaccura­ cies, for example when he wrote that Falloppio: “schrieb nur ein Buch” “Observationes anatomicae” (wrote only one book)”. This is wrong: Falloppio also wrote at least two other books: Lectiones de partibus similaribus corporis humani. His accessere diversorum animalium sceletorum explicationes iconibus illustratae. Norimberg: Ger­ lachius, 1575, and Opera, quae adhuc extant, omnia. Ve­ netiis: Valgrisius, 1584. Even more, Jongkees mentions in reference three Bell’s articles published in the Philosophical Transactions of the Royal Society of London. The first one has wrong pages, the second one does not exist and the third one has also wrong pages! Jonckees also did not mention the exact reference of 1827 Bell’s text. How

Sequelae of peripheral facial palsy

Introduction and objectivesOur purpose was to study functional sequelae after peripheral facial palsy (PFP) and to analyse its impact and relationship with the degree of facial nerve dysfunction, from the neurophysiological point of view. Material and methodsWe present a retrospective study that covers a total of 150 cases of peripheral facial palsy. All patients underwent electroneurography and electromyography to establish the degree of axonal damage and to evaluate the existence of signs of reinnervation in the muscles explored or possible innervation errors. ResultsOf the patients studied, 31.9% (46) had sequelae; 67.4% (31) were women, a statistically significant result (P=.031). Of all the sequelae, the most frequent was myokymia, which appeared in 24% (36) of the cases. Patients with left side involvement presented a higher number of sequelae (40.3%, 27 cases) with a statistically significant difference (P=.05). The average rate of axonal injury on first visit by patients who subsequently developed sequelae was 75.26%; worse results on electroneurography were statistically associated with the onset of sequelae (P=.007). Electromyography of patients with sequelae shows that a greater degree of denervation could be considered a risk factor for the occurrence of sequelae (P=.039). Discussion/conclusionsIn our study, we found that sequelae are more frequent after facial palsy when there is significant axonal loss. This study shows other risk factors not mentioned in the literature as yet, such as female gender and left-side involvement

Secuelas de las parálisis faciales periféricas

Introduction and objectivesThe purpose of this work is to study the functional sequelae after peripheral facial palsy (PFP) to analyze its impact and relationship with the degree of facial nerve dysfunction, from the neurophysiological point of view. MethodsWe present a retrospective study which includes a total of 150 cases of peripheral facial palsy. All patients underwent electroneurography and electromyography to see the degree of axonal damage and to evaluate the existence of signs of reinervation in the muscles explored or possible innervation errors. ResultsOf the patients studied, 31.9% (46) had sequelae; 67.4% (31) were women, a statistically significant result (P=.031).Of all the sequelae, the most frequent was miochymia which appeared in 24% of cases (36).Patients with left side involvement presented a higher number of sequelae (40.3%, 27 cases) with a statistically significant difference (P=.05).The average rate of axonal injury on first visit by patients who subsequently developed sequelae was 75.26%; worse results on electroneurography were statistically associated with the onset of sequelae (P=.007).Electromyography of patients with sequelae shows that a greater degree of denervation could be considered a risk factor for the occurrence of sequelae (P=.039). Discussion/conclusionsIn our study we found that sequelae are more frequent after facial palsy when there is significant axonal loss.This work shows other risk factors so far not mentioned in the literature, such as female gender and left-side involvement.

Observation on the therapeutic effect of the comprehensive therapy in the treatment of peripheral facial palsy

Thirty cases of peripheral facial palsy were treated with the comprehensive therapy, and 30 cases of peripheral facial palsy were treated with shallow electro-acupuncture as control. The results showed that the cure rate in treatment group was higher than that in the control group (P<0.05), and no significant difference was found in effective rate between two groups.

顔面神経麻痺に対する低出力レーザー治療の効果

Seven cases of peripheral facial palsy, who were patients of our hospital's dermatological clinic, were treated with diode low power laser therapy while another seven cases, who were patients of our hospital's otolaryngological clinic, were treated with a combination therapy consisting of low power laser and corticosteroid therapy, over the past one and half years. The clinical efficacy of the two regimens were analysed so that the comparison could be made utilizing a separate corticosteroid therapy group as the control.Those patients who had received laser therapy showed a very similar overall recovery from the palsy when compared to those treated with corticosteroid, however those patients who had received the combination therapy showed the best recovery in the shortest period. No clinically significant adverse effect resulting from the low power laser therapy was noted. Our results suggest that low power laser therapy would be a suitable alternative treatment for those facial palsy patients for whom corticosteroid is not manageable, and furthermore that low power laser therapy would be an adjunctive treatment for those facial palsy patients for whom corticosteroid is manageable.

Peripheral facial palsy and herpes zoster infection

A clinical and virological study of 133 consecutive cases of peripheral facial palsy has provided evidence for simultaneous infection with the varicella-zoster virus in 9 patients (6-8 per cent). Seven of these presented differing but typical manifestations of the Ramsay Hunt syndrome, and the diagnosis was therefore strongly suspected on the basis of the clinical findings alone. The remaining two patients had neither herpetiform rash nor involvement of the eighth cranial nerve, and had been diagnosed in the clinic as typical cases of Bell's palsy. In this series the incidence of zoster infection in apparent idiopathic facial palsy was 1-8 per cent.

GENICULATE GANGLION FACIAL PALSY.

EVER since Ramsay Hunt's (1907)2description of the syndrome of facial palsy, herpetic rash in and around the ear on the same side often accompanied by a constitutional disturbance and sometimes by deafness and giddiness, there has been a tendency to think of a lesion of the nerve trunk at or near the geniculate ganglion only when the Ramsay Hunt syndrome is present. For some years now, however, I have been aware of a group of cases of peripheral facial palsy in which the onset of the paralysis is unaccompanied by any herpetic vesicles around the pinna or by any constitutional disturbance or eighth nerve disorder, but in which there is loss of lachrymal secretion on the paralyzed side, Cawthorne ( 1963).1Before I included a test of lachrymation as part of the routine examination of eighth nerve function in a case of facial palsy, I used to regard