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Association between herpes simplex virus-1 infection and idiopathic unilateral facial paralysis in children and adolescents
Abstract
We studied the association between herpes simplex virus-1 (HSV-1) infection and Bell palsy in children. Thirty-three of 42 affected patients had a positive HSV-1 enzyme-linked immunosorbent assay compared with 16 of 41 controls (P = 0.0003). Ten of 47 affected patients had a positive HSV-1 polymerase chain reaction compared with 4 of 45 of controls (P = 0.08). Our findings support an association between HSV-1 infection and Bell palsy in children.
... These retrospective studies identified duration of headache, presence of cranial neuritis (mainly PFNP), and the proportion of mononuclear cells in cerebrospinal fluid as predictors for Lyme meningitis. 10 -13 A number of other viral infections, mainly herpes simplex virus (HSV), 3,14 and varicella zoster virus (VZV), 2,15 have been discussed as possible causes of PFNP but it still remains controversial what role they play in the pathogenesis of the disease. ...
... 30 In contrast to other studies we found no evidence of HSV infections in tested CSF specimens. 3,14 This may be a result of decreased diagnostic sensitivity in stored specimens. VZV in CSF was detected by PCR in only 2 patients with aseptic meningitis and in one patient with PFNP. ...
A variety of microorganisms have been shown to cause peripheral facial nerve palsy (PFNP) and/or aseptic meningitis in children. Clinical findings and history may help to predict the specific etiology of these entities.
Children > or =12 months old hospitalized at the University Children's Hospital Basel, Switzerland, from 2000 to 2005 with clinical signs of PFNP and/or aseptic meningitis were studied retrospectively. History, clinical, and laboratory findings were evaluated using analysis of variance with Bonferroni (Dunn) correction.
Of 181 patients, 123 (68%) had aseptic meningitis, 28 (15%) had PFNP, and 30 (17%) had a combination of both. PFNP with aseptic meningitis was associated with Borrelia burgdorferi (Bb) infection in the majority of patients (73%) compared with 11% and 9% of patients with PFNP or aseptic meningitis, respectively. The majority of patients with aseptic meningitis without PFNP had enterovirus infection (63%). In patients with aseptic meningitis, mean leukocyte counts in cerebrospinal fluid (CSF) were higher with enterovirus (565/microL) compared with Bb infection (191/microL; P < 0.01) or unknown causes (258/microL; P < 0.01). Further, CSF mean mononuclear cell proportion was higher in patients with Bb (89%) than in those with enterovirus infection (51%; P < 0.01) or unknown causes (60%; P < 0.01). Mean time interval between onset of disease and admission to hospital showed significant differences between Bb (7.6 days) and enterovirus infection (2.8 days; P < 0.01) or unknown causes (2.0 days; P < 0.01).
Time interval between onset of disease and hospital admission and CSF characteristics can contribute to distinguishing the etiology of aseptic meningitis with or without PFNP. As expected, the most common etiology for aseptic meningitis with PFNP was Bb infection whereas enterovirus infection was the predominant cause for aseptic meningitis alone.
... Almost a century later, the management and aetiology of BP is still a subject of controversy. 1 BP leaves more than 8,000 people in the United States each year with permanent, potentially disfiguring facial weakness. 9 Although the actual cause of BP is unknown, but the proposed mechanism thought to be are inflammation of the facial nerve, 5 microcirculatory failure of the vasonervorum, viral infection, ischemic neuropathy, autoimmune reactions [10][11][12][13] surgical procedure such as local anesthesia, 14,15 tooth extraction, [16][17][18] infections, 19,20 pre prosthetic procedures, excision of tumors or cysts, surgery of TMJ, 21,22 surgical treatment of facial fractures and cleft lip/palate 23 are among the proposed etiologies. The literature also reports three mechanisms, in which a dental procedure could damage a nervous structure: direct trauma to nerve from a needle, intraneural hematoma formation or compression and local anaesthetic toxicity. ...
... Although acute facial paralysis can occur during many viral illnesses such as mumps, rubella, herpes simplex, and Epstein-Barr virus infection or as a result of the reactivation of the human herpes virus in the geniculate ganglia. [17][18][19][20] Some patients may be more easily predisposed to facial nerve inflammation by exposure to a preceding pathogen, such as Herpes simplex virus, Epstein-Barr virus and cytomegalovirus. There have been an increasing number of reports on the Herpes simplex virus particle found on facial nerve biopsy in patients with BP 31,32 . ...
... So, referring to medicines and receiving exercises are effective ways to diminish these adverse effects (8). Fortunately, there is one millimeter per day (10) the axonal regeneration (6,11,12) that initiates 2-3 weeks after beginning of disease (3,6,11,12), but 30 per cent of patients experience incomplete recovery or side effects (3,6,11,13) such as long term spasm, synkinesis, crocodile tear syndrome, Marcus gun and jaw winking phenomena (14), even eye infection and loss of taste in long term (10). ...
Introduction: Bell's palsy is the side effect of peripheral nerve palsy that causes low function of face and quality of life. This study was conducted to assess the effect of two different methods; exercise therapy and biofeedback therapy, accompanied with massage in two groups on facial function and quality of life of these patients. Materials and Methods: In this interventional research with before-after design, 20 patients with acute unilateral peripheral facial palsy participated in two separate programs. Function of face was measured by House Brackman and quality of life was evaluated by SF-36 questionnaire. In each group data were recorded before the intervention and 4 weeks (3 sessions per week) after it. Exercise therapy included receiving massage, doing patterns of Proprioceptive Neuromuscular Facilitation (PNF) and some exercises in front of mirror; besides, biofeedback therapy contained massage and muscular education by biofeedback set. After employing Kolmogorov-Simonov as a Test for normality, Independent T-test was utilized to compare means. Results: After one month doing two different programs in two exercise and biofeedback groups, remarkable increase of quality of life (P≤0.001) and also improvement of function of face (P=0.004) were noticed in each group, but there was not any significant difference between quality of life (P=0.07) and function of face (P=0.85) in two groups. Discussion: This study indicated that with regard to suffering paralysis in Bell's palsy and its bad effects on patients' quality of life, the use of both biofeedback and exercise therapies as treatment is effective. It seems that increasing awareness of patients and training early movements have important role in improvement improve.
... In total, 33 of 42 affected patients had a positive HSV-1 enzyme-linked immunosorbent assay (ELISA) compared with 16 of 41 controls (p = 0.0003). This underlines the potential association between HSV-1 and Bell's palsy in children [18]. ...
Facial nerve palsy (FNP) is a common illness in the paediatric emergency department. Missed or delayed diagnosis can have a serious impact on a patient’s quality of life. The aim of this article is to give a recent overview of this pathology in terms of the causes, diagnosis, red flag symptoms, complementary examinations, treatments and follow-up in the child population. In cases of acquired, acute onset and isolated FNP, Bell’s palsy can be assumed, and no further investigation is required. In any other scenario, complementary examinations are required. Treatment depends on the aetiology. Corticosteroids, in addition to antiviral medication, are recommended to treat Bell’s palsy whenever a viral infection is suspected. However, the lack of randomised control trials in the paediatric population does not allow us to comment on the effectiveness of these treatments. In all cases, treated or not, children have a very good recovery rate. This review emphasises the necessity of randomised control trials concerning this frequent neurological pathology in order to better treat these children.
... Herpes simplex virus infection, which is among the common causes of Bell's palsy in adults, is also included among the causes of Bell's palsy in children [95,96]. On the other hand, reactivation of varicella zoster virus can also lead to the development of facial paralysis without causing the classical skin rash and other otological findings (different from Ramsay Hunt syndrome) [97]. ...
The majority of the tissues and organs that fall into the area of expertise of ear, nose and throat (ENT) specialists are adjacent to the orbit, and therefore to the globe. As a result of this contiguity, ENT diseases can spread to the orbit and present with various orbital complications. While these complications can be mild, they can also manifest as severe morbidities that lead to permanent loss of vision. In addition, ENT diseases can also spread to the cranium as well as the orbit, and lead to severe intracranial complications that may result in mortality. Such intracranial complications may also manifest with findings in an ophthalmological examination, as many cranial nerves (CNs) are also associated with the orbital structures. This is why ENT specialists commonly encounter ophthalmological findings as a result of both the orbital and cranial complications of infectious ENT diseases. In addition, ophthalmological examination findings are useful for diagnosis, as some infectious agents can cause a common infection both in the ocular and head-neck region.
... Все исследования на животных in vivo выявляют острую НЛН после первичной инфекции ВПГ-1. Эти исследования более похожи на НЛН, связанную с ВПГ-1 у детей, у которых развивается НЛН при первичной инфекции ВПГ-1 [21]. ...
... It has been suggested that the pathophysiology usually involves the reactivation of herpes simplex virus within the geniculate ganglion which leads to inflammation and entrapment with facial nerve at the meatal foramen [11]. The use of steroids is said to de- with Bell's palsy. ...
We analyzed the data of using steroid therapy in treating Bell's palsy in pediatrics patients in Bahrain Defense Force hospital, and the aim was to measure and analyze their clinical course, management, and final outcome
... The presence of DNA from HSV-1 or HSV-2 in about 25 percent of patients with ON as clinical entity, not as initial sign of MS, indicates the possible participation of these viruses in the etiology of ON, similar to that reported in another usually ephemeral intracranial neuritis, facial nerve palsy. If further studies confirm these results the etiology of some patients with ON could be similar to the current evidences on the potential participation of herpes simplex virus in the acute, and in many cases ephemeral, demyelination of other cranial nerves [18] as seen frequently in the case of palsy of the facial nerve [8] were the participation of HSV-1 and VZV have long being suspected [19][20][21]. It seems relevant that other investigations have also implicated HSV-1 and VZV in the etiology of ON as potential etiological participant [9,22]. ...
Objective:
Optic Neuritis (ON) might unfold either as a single intracranial neuritis or as multiple sclerosis, a widespread demyelinating disorder. Different herpes viruses have been proposed as potential participants in the etiology of multiple sclerosis (MS). To analyze the potential presence of herpes viruses in blood and subarachnoid area at the time of ON and contrast the findings according to long-term evolution either as intracranial neuritis or as progression to multiple sclerosis.
Patients and methods:
In a prospective investigation we searched the presence of DNA from 5 herpes viruses (HSV-1, HSV-2, VZV, EBV and HHV6) in CSF and blood lymphocytes from 54 patients with ON, patients were followed 62 ± 3 months; those who developed MS were separated from those with ephemeral ON. Long-term prognosis of ON was related to DNA findings.
Results:
As compared with controls, DNA from HSV-1 was significantly more frequent in CSF and blood from cases with ON; VZV and HSV-2 were found only in CSF; EBV was found only in blood samples (p < 0.006).
Conclusions:
Our results point out the potential participation of HSV, VZV and EBV in ON; suggesting the intervention of various herpes viruses as triggering agents of autoimmunity. However, the number of positive cases was minor than negative cases. Also, our results suggest that the etiological mechanisms in ON could be similar to those of neuritis of the facial nerve (Bell's palsy).
... However the causes include microcirculatory failure of the vasonervorum, viral infection, ischemic neuropathy, autoimmune reactions surgical procedure such as local anesthesia tooth extraction, infections osteotomies, preprosthethic procedures, excision of tumors or cysts, surgery of TMJ and surgical treatment of facial fractures and cleft lip/palate. [2][3][4][5][6][7][8][9][10][11][12][13][14][15] Recently, attention has been focused on infection with herpes simplex virus type 1 (HSV-1) as a possible causative since its titers has found to be elevated in affected patients. But studies have failed to isolate viral DNA in biopsy specimens and hence remain a question. ...
Bell’s palsy is a unilateral, lower motor neuron weakness of the facial nerve. Facial dysfunction has a dramatic effect on a patient’s appearance, psychological wellbeing and quality of life. Bell’s palsy has been described in patients of all ages, and is more common in adults than in children.The causes of the paralysis still remain unknown. Establishing the correct diagnosis is imperative and choosing the correct treatment options can optimize the likelihood of recovery. Hence this review deals with etiology, signs and symptoms, diagnosis and treatment management for Bell’s palsy.
... Ten of 47 affected patients had a positive HSV-1 polymerase chain reaction compared with 4 of 45 of controls (P = 0.08). These findings support an association between HSV-1 infection and Bell palsy in 3 children. In recent studies, detection rates of herpes ...
... Patients may receive antibiotic treatment on vague grounds and investigation for other neurotropic agents are seldom performed unless the patient show specific manifestations of viral infection such as skin rash, vesicles, diarrea or distinct signs of viral meningitis/encephalitis. Acute facial nerve palsy or subacute meningitis are major neurological manifestations in LNB [12] [13]. However, facial nerve palsy may also be associated with viral infection, such as an acute or reactivated herpes simplex virus (HSV) infection or a reactivated varicella zoster virus (VZV), even when detectable vesicles or other clinical manifestations of viral infection are absent [14]- [18]. Antiviral therapy and/or corticosteroids have been shown to improve the prognosis in adult patients with idiopathic facial nerve palsy [19], but studies in children are few and not conclusive [20] [21]. ...
... Histopathologic studies of temporal bone obtained from patients with recent episodes of Bell's palsy have revealed an inflammatory process surrounding the nerve fibers, with infiltration of lymphocytes and associated demyelination or axonal degeneration [6]. Many viral infections have been reported to cause acute peripheral facial paralysis (APFP) in children, for example, reactivation of Varicella-zoster virus (VZV), Herpes simplex virus type 1 (HSV-1), Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpes virus 6 (HHV-6), mumps virus, human immunodeficiency virus (HIV) and hepatitis B virus [5][6][7][8][9][10][11][12][13]. However, in the majority of patients the cause remains unknown and a diagnosis of ''idiopathic'' peripheral facial paralysis or Bell's palsy is made. ...
Objectives:
Bell's palsy is considered the most common cause of facial nerve paralysis in children. Although different theories have been postulated for its diagnosis, reactivation of the Varicella zoster virus (VZV) has been implicated as one of the causes of Bell's palsy. The aim of the study was to evaluate the association of Varicella-zoster virus infection with Bell's palsy and its outcome in children.
Methods:
A total of 30 children with Bell's palsy were recruited and were assayed for evidence of VZV infection. The severity of facial nerve dysfunction and the recovery rate were evaluated according to House-Brackmann Facial Nerve Grading Scale (HB FGS). Paired whole blood samples from all patients were obtained at their initial visit and 3 weeks later, and serum samples were analyzed for VZV IgG and IgM antibodies using ELISA.
Results:
A significantly higher percentage of Bell's palsy patients were seropositive for VZV IgM antibodies than controls (36.6% of patients vs 10% of controls) while for VZV IgG antibodies the difference was statistically nonsignificant. HB FGS in Bell's palsy patients with serologic evidence of VZV recent infection or reactivation showed a statistiacally significant less cure rate than other patients.
Conclusions:
VZV reactivation may be an important cause of acute peripheral facial paralysis in children. The appropriate diagnosis of VZV reactivation should be done to improve the outcome and the cure rate by the early use of antiviral treatment.
... All of the in vivo animal studies elicit an acute facial palsy following lytic (primary) HSV1 infection. These studies more closely resemble HSV1-related BP in pediatric patients, who develop their facial palsy in the setting of a primary HSV1 infection (39,40). However, they are less relevant to cases of BP and DFP in adults, who have experienced primary HSV1 infection many years prior to onset of facial palsy (17). ...
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.
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.
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.
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.
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.
... Although the actual cause of Bell's palsy is unknown, the widely accepted mechanism is inflammation of the facial nerve during its course through the bony labyrinthine part of the facial canal, which leads to compression and demyelination of the axons, and disruption of blood supply to the nerve itself [3]. Previous studies have suggested viral infection as the etiology of the disease based on serological evidence; [4,5] for example, positive serology for Herpes Simplex virus (HSV) has been reported in 20-79% of patients. ...
Previous meta-analyses of treatments for Bell's palsy are still inconclusive due to different comparators, insufficient data, and lack of power. We therefore conducted a network meta-analysis combining direct and indirect comparisons for assessing efficacy of steroids and antiviral treatment (AVT) at 3 and 6 months.
We searched Medline and EMBASE until September 2010 using PubMed and Elsviere search engines. A network meta-analysis was performed to assess disease recovery using a mixed effects hierarchical model. Goodness of fit of the model was assessed, and the pooled odds ratio (OR) and 95% confidence interval (CI) were estimated.
Six studies (total n = 1805)were eligible and contributed to the network meta-analysis. The pooled ORs for resolution at 3 months were 1.24 (95% CI: 0.79 - 1.94) for Acyclovir plus Prednisolone and 1.02 (95% CI: 0.73 - 1.42) for Valacyclovir plus Prednisolone, versus Prednisolone alone. Either Acyclovir or Valacyclovir singly had significantly lower efficacy than Prednisolone alone, i.e., ORs were 0·44 (95% CI: 0·28 - 0·68) and 0·60 (95% CI: 0·42 - 0·87), respectively. Neither of the antiviral agents was significantly different compared with placebo, with a pooled OR of 1·25 (95% CI: 0·78 - 1·98) for Acyclovir and 0·91 (95% CI: 0·63 - 1·31) for Valacyclovir. Overall, Prednisolone-based treatment increased the chance of recovery 2-fold (95% CI: 1·55 - 2·42) compared to non-Prednisolone-based treatment. To gain 1 extra recovery, 6 and 26 patients need to be treated with Acyclovir and prednisolone compared to placebo and prednisolone alone, respectively.
Our evidence suggests that the current practice of treating Bell's palsy with AVT plus corticosteroid may lead to slightly higher recovery rates compared to treating with prednisone alone but this does not quite reach statistical significance; prednisone remains the best evidence-based treatment.
Background: Bell’s Palsy is an idiopathic non-progressive neuropathy of the facial nerve occurring in a lower motor neuron pattern. The treatment conventionally consists of steroids, but the effectiveness of the addition of antivirals such as acyclovir, valacyclovir, and famciclovir, is not established. Our study aims to assess the effectiveness of antiviral drugs for the treatment of Bell’s Palsy patients. Methods: A systematic search was performed on PubMed, Cochrane Library, and ClinicalTrials.gov, from January 1992 to December 2022, to collect randomized controlled trials (RCTs) considering the addition of antivirals in treating Bell’s palsy. The bibliographies of the identified trials and Google Scholar were reviewed to identify additional data. A meta-analysis was launched to assess the overall facial recovery, measured in terms of the odds ratios (ORs) and a corresponding 95% confidence interval (CI). Secondary outcomes are adverse effects attributable to the use of antivirals. Results: A total of 18 studies were included in the qualitative synthesis of this systematic review. Among the included studies, 15 studies representing 2,563 patients contributed to the meta-analysis. There were statistically significant differences in complete facial recovery between the antiviral group and the comparison group, with a pooled odds ratio of 1.79 (95% CI: 1.24-2.60, P= 0.002), indicating higher recovery outcomes in the antiviral group. Conclusion: Overall, adding antivirals to the therapy provided a significant additional benefit in facial recovery from Bell’s Palsy. Adding antiviral drugs such as acyclovir, valacyclovir, and famciclovir to the conventional therapy consisting of steroids achieves a better treatment for Bell’s palsy patients.
The aim: to characterize the clinical and etiological features of facial palsy (FP) in children of different ages at the present stage and their correlation with the outcome and duration of the disease.
Materials and methods: the data of 68 children with FP were obtained. The neurological examination with an assessment of the level of facial nerve damage and the severity of FP using the House-Brackmann scale (HB), the concomitant symptoms and the etiological verification of a possible infectious agent were performed to all children. Also, their correlation with the outcomes and duration of the disease were assessed.
Results: in the etiological structure infectious FP are more common in children under 12 years of age, with a predominance of herpesviruses and enteroviruses, whereas, more than half of the cases in children over the age of 12 years are idiopathic (Bell’s palsy), less often herpesviruses. A longer course and the probability of an unfavorable are significantly more often observed in the group of children under 12 years of age. There was also a significant correlation between the severity of FP according to HB with the outcomes and duration of the disease.
Conclusion: The results confirm the importance and necessity of laboratory confirmation of a possible etiological agent associated with the development of FP. The severity of FP doesn’t depend on the age of the child, but correlates with the outcome and duration of the disease, more less with the synkinesia. A promising direction for further research is to clarify the climatic factors affecting the incidence of FP.
Facial paralysis in children is a condition that requires urgent intervention in otorhinolaryngology practice and appropriate treatment should be initiated as soon as possible. The incidence of acquired peripheral facial paralysis in children is between 5 and 21 per 100,000 per year [1]. Facial paralysis is divided into peripheral and central according to the nerve damage regions [2]. Facial paralysis in children can occur due to congenital or acquired causes and may be a sign of a serious underlying disease. The quality of life of the child is generally negatively affected by its aesthetic and functional effects.
Bell's Palsy is the most frequent acute neuropathy of cranial nerves; it has been associated in various reports to herpes viruses. In a prospective study we searched the presence of DNA from five herpes viruses (HSV-1 and 2, VZV, EBV and HHV-6) in 79 patients at the acute phase of Bell's Palsy. Results were related with various parameters; age, gender and clinical outcome. We found the significant presence (p˂0.001) of HSV-1 and VZV in 39% and 42% of patients. However, a large percentage of cases were negative. When comparisons were made between subgroups according to gender and age no differences were found with viral findings nor with clinical outcome of palsy, which was of clinical remission in most cases (78%). Our results suggest that herpes viruses might participate in the complex mechanisms of autoimmunity of Bell's Palsy but not as determinant etiological element.
Bell palsy (BP) is the most common neuropathy and accounts for 11.5–53.3 cases per 100,000 people a year. Diagnosis and early identification of the cause of the disease are crucial for successful treatment. The article provides a literature review on the main hypotheses of the main BP causes: anatomical factors, viral infection and immunological factor.
Aim
To report the causes and clinical evaluation of children with facial nerve palsy (FNP) admitted to an affiliated university hospital during a 5‐year period (2011–2015).
Methods
A total of 124 children were retrospectively categorised into two groups: idiopathic Bell's palsy (109 patients) and the second group into other FNP aetiologies (15 patients). All children received a standardised work‐up and follow‐up. Therapy consisted of steroid administration associated with antiviral treatment when a viral infection was suspected.
Results
All children of the first group had a full recovery under oral steroids within 2 months of treatment. From the second group, seven children (46%) had a viral infection based on serological findings, two of them were positive for neurotropic herpes viruses, and one had Ramsay Hunt syndrome; six children with infectious FNP had recurrent FNP on the ipsilateral or contralateral side. Five patients had FNP as a complication of acute otitis media; three of them (60%) had partial or full recovery postoperatively. One child developed FNP following temporal bone trauma that had an uneventful recovery with conservative treatment. One child suffered from Melkersson–Rosenthal syndrome, and another child presented with FNP associated with unilateral hemiparesis following an ischaemic cerebral infarct.
Conclusions
Facial palsy in children is a manifestation of a heterogeneous group of causes. The most common aetiology of FNP in children in our study was idiopathic (Bell's palsy), followed by infective causes, such as acute otitis media and neurotropic herpes viruses. Therefore, treatment should be adapted to each patient depending on the underlying disease and severity of FNP.
Peripheral facial nerve paralysis in children might be an alarming sign of serious disease such as malignancy, systemic disease, congenital anomalies, trauma, infection, middle ear surgery, and hypertension. The cases of 40 consecutive children and adolescents who were diagnosed with peripheral facial nerve paralysis at Baskent University Adana Hospital Pediatrics and Pediatric Neurology Unit between January 2010 and January 2013 were retrospectively evaluated. We determined that the most common cause was Bell palsy, followed by infection, tumor lesion, and suspected chemotherapy toxicity. We noted that younger patients had generally poorer outcome than older patients regardless of disease etiology. Peripheral facial nerve paralysis has been reported in many countries in America and Europe; however, knowledge about its clinical features, microbiology, neuroimaging, and treatment in Turkey is incomplete. The present study demonstrated that Bell palsy and infection were the most common etiologies of peripheral facial nerve paralysis.
Facial nerve palsy has a broad differential diagnosis and possible psychological and anatomical consequences. A thorough investigation must be performed to determine the cause of the palsy and to direct treatment. If no cause can be found, therapy with prednisone with or without an antiviral medication can be considered and begun as early as possible after onset of symptoms. Resolution and time to recovery vary with etiology, but overall prognosis is good.
To determine the association of the Herpes Simplex virus Type-1 infection and Bell's palsy in patients treated at the outpatient department of a tertiary care center.
A prospective, observational study was carried out at the outpatient department of Medical and ENT units of Abbasi Shaheed Hospital, Karachi. Fifty patients were enrolled in the study with their informed and written consent, between 2006-2007. All were >12 years of age. They were diagnosed as having Bell's palsy and were investigated for serologic evidence of Herpes simplex virus (HSV). The IgG and IgM antibodies for HSV were identified in the blood samples at the Aga Khan University hospitals laboratory.
Of the 50 patients enrolled, 35 (70%) patients were IgG/IgM positive for the HSV stressing the etiological association of HSV with Bell's palsy.
The study suggests that a relationship exists between HSV infection and Bell's palsy. The information might prove helpful in hastening the recovery by modifying management guidelines in view of the results of this study.
The use of eponyms has long been contentious, but many remain in common use, as discussed elsewhere (Editorial: Oral Diseases. 2009: 15; 185-186). The use of eponyms in diseases of the head and neck is found mainly in specialties dealing with medically compromised individuals (paediatric dentistry, special care dentistry, oral and maxillofacial medicine, oral and maxillofacial pathology, oral and maxillofacial radiology and oral and maxillofacial surgery) and particularly by hospital-centred practitioners. This series has selected some of the more recognised relevant eponymous conditions and presents them alphabetically. The information is based largely on data available from MEDLINE and a number of internet websites as noted below: the authors would welcome any corrections. This document summarises data about Bell paralysis.
In 45 patients with Bell's palsy of recent onset, the neutralization antibody titers to herpes simplex virus type 1 (HSV-1) were assayed by a microtiter technique. As a control, the neutralization antibody titers of 50 normal subject were assayed. Complement fixation tests also were performed. The geometric means of the neutralization antibody titers of the patients appeared higher at all times than those of the normal subjects. Significant change in the neutralization antibody titer suggesting a recent infection of HSV-1 was seen in seven patients (15.6%), while the complement fixation test demonstrated significant change in only one patient (2.2%). The higher geometric means of the neutralization antibody titers in the patients was thought to indicate that reactivation of the HSV-1 infection was responsible for the onset of Bell's palsy.
Reactivation of herpes simplex virus type 1 (HSV-1) has been implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study used the polymerase chain reaction (PCR) to analyze the saliva of patients with Bell's palsy for the presence of shed HSV-1. The study involved 47 patients with Bell's palsy, 24 patients with Ramsay Hunt syndrome, and 16 healthy HSV-seropositive volunteers. HSV-1 DNA was not detected in the saliva samples from HSV-seronegative patients. The prevalence of shed HSV-1 in patients with Bell's palsy (50%) was significantly higher than that in healthy volunteers (19%, p<0.05). When saliva samples were tested within 7 days after the onset of palsy, the prevalence of shed HSV-1 in patients with Bell's palsy (40%) was significantly higher than that in patients with Ramsay Hunt syndrome (7%, p<0.05). Furthermore, HSV-1 usually became undetectable by the second week after the onset of Bell's palsy when HSV-1 was detected during the acute phase of the disease. These findings strongly suggest that reactivation of HSV-1 is involved in the pathogenesis Bell's palsy, and indicate that PCR is a useful tool for early diagnosis of HSV-1 reactivation in patients with Bell's palsy.
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.
To ascertain if there is an association between Bell's palsy and infection by viruses of the herpes group, 78 patients and 59 controls were investigated. The specific antiviral IgG subclass pattern in serum against cytomegalovirus (CMV), herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) was analysed using an enzyme-linked immunosorbent assay (ELISA) combined with monoclonal antibodies directed against the four subclasses of human IgG. Additional ELISA assays of IgG and IgM antibodies were also used. The mean titres of IgG antibodies against HSV-1 were higher in the acute and convalescent stages compared with controls. The frequency of values greater than 0.2 for all subclasses was raised in the patients, but not significantly so. The mean values for the subclasses were alike in patients and controls. The mean titres of IgG antibodies against CMV and VZV were similar throughout the palsy and also in controls. In the patients, the pattern of IgG subclasses was different from the controls, but not statistically so. The patients and controls were not seropositive for IgM against CMV and VZV. Four patients in the acute phase, 4 in the convalescent phase and 3 controls were positive for IgM against HSV-1. While the subclass pattern of IgG antibodies against HSV-1 is not diagnostic of reactivation of the virus, the raised IgG antibodies may suggest reactivation of a disease process and/or a superadded infection.
Recent studies provide compelling data for the hypothesis that herpes simplex virus type I (HSV-1) is implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study analyzed the severity of facial palsy in patients with HSV-1 reactivation and sought to determine the efficacy of acyclovir-prednisone therapy for these patients.
In total, 176 patients, clinically diagnosed with Bell's palsy. were divided into three groups by polymerase chain reaction (PCR) and serological tests--31 patients with HSV-1 reactivation, 45 patients with VZV reactivation (zoster sine herpete) and 100 patients without HSV-1 or VZV reactivation (Bell's palsy).
The difference in the worst grade of facial palsy between patients with zoster sine herpete and Bell's palsy was significant (P = 0.01 10, Mann-Whitney U-test). In contrast, no difference in the severity of palsy was observed between patients with HSV-1 reactivation and Bell's palsy. Twelve patients received acyclovir-prednisone treatment within 7 days of onset based on positive PCR results and ten of the 12 (83%) recovered completely. In contrast, 14 patients with HSV-1 reactivation received prednisone treatment because their PCR tests were performed at a later date; ten of these 14 (71%) recovered completely. The difference in the cure rate between the two treatment groups was not significant (P > 0.05, Fisher exact test).
The results indicate that the severity of palsy in patients with HSV-1 reactivation is similar to that in patients with Bell's palsy and suggest that early diagnosis of HSV-1 reactivation by PCR and subsequent acyclovir-prednisone therapy do not improve recovery from facial palsy.
The majority of the human population has been infected with herpes simplex virus type 1 (HSV-1). During a typical primary episode, HSV-1 spreads from the oral pharynx to the trigeminal ganglia, where a latent HSV-1 infection is established. Cold sores at the mucocutaneous junction of the lip are the typical manifestation of recurrent HSV-1. We investigated whether HSV-1 also infects the brain during the primary infection. We used HSV-1 infected BALB/c mice and inbred cotton rats as models. While both species were susceptible to HSV-1 infection, the time course of lesion formation and healing in the cotton rat more closely reflected that seen in humans. In both species, HSV-1 replicated in the brainstem and cerebellum, as well as the trigeminal ganglia during a primary infection of the lip. The brain infection was produced by a low inoculation dose, and did not cause observable neurologic signs or mortality. Using PCR and RT-PCR techniques, we demonstrated HSV-1 thymidine kinase in the absence of infectivity in the brains of both species 30-40 days after primary infection.
For clarification of the direct relationship between the reactivation of herpes simplex virus and the development of Bell's Palsy, a detection of the virus genome by deoxyribonucleic acid diagnostics and a quantitative analysis of its time-course change are both needed. The authors detected the HSV genome in specimens from patients with Bell's Palsy, quantified its number of copies, and examined time-course changes.
The subjects were 16 patients with Bell's Palsy. The tear fluid and saliva from the submandibular gland and the parotid gland were separately collected from the affected and unaffected sides twice or more. A total of 244 specimens were subjected to extraction of deoxyribonucleic acid, polymerase chain reaction, and microplate hybridization.
Herpes simplex virus-1 deoxyribonucleic acid was detected in 38 specimens (11.8%) from 5 patients (31%). The high detection (28.5%) was obtained within 2 weeks after onset. Detection at 3 weeks and later (2.8%) was significantly lower ( < 0.05). In three cases, deoxyribonucleic acid was also found on the unaffected side in the initial phase of the disease, but detection on that side (18.9%) was significantly lower than on the affected side (83.8%) ( < 0.01). The number of copies of the herpes simplex virus-1 genome was large on the affected side and early after the onset of the disease.
The reactivation of herpes simplex virus-1 on the affected side is involved as a pathogenic factor of Bell's Palsy. A reactivation of herpes simplex virus-1 may be generated even on the unaffected side in the early phase of the disease. Herpes simplex virus deoxyribonucleic acid was not detected in any of the examined specimens collected from the remaining 11 cases. The need for constant study to clarify other causative factors of Bell's Palsy remains.
To investigate the effects of valacyclovir and prednisolone in comparison with those of placebo and prednisolone for the treatment of Bell's palsy, excluding zoster sine herpete.
Prospective, multicenter, randomized placebo-controlled study.
Six academic tertiary referral centers.
Ultimately, 221 patients with Bell's palsy who were treated within 7 days of the onset. Serological and polymerase chain reaction examinations were performed to distinguish Bell's palsy from zoster sine herpete.
The patients were treated with either valacyclovir (dosage, 1,000 mg/d for 5 days) plus prednisolone (VP [n = 114]) or placebo plus prednisolone (PP [n = 107]) administered orally.
Recovery from the palsy was defined as a score higher than 36 using Yanagihara 40-point scoring system without facial contracture or synkinesis. The patients were followed up until complete recovery occurred or for more than 6 months in cases with a poor prognosis.
The overall rate of patient recovery among those treated with VP (96.5%) was significantly better (p < 0.05) than the rate among those treated with PP (89.7%). The rate of patient recovery was also analyzed by classifying the initial severity of facial palsy. In cases of complete or severe palsy, the rates of patients treated with VP and PP who recovered were 95.7% (n = 92) and 86.6% (n = 82), respectively; the recovery rate for treatment with VP was significantly better than that with PP (p < 0.05).
The valacyclovir and prednisolone therapy was more effective in treating Bell's palsy, excluding zoster sine herpete, than the conventional prednisolone therapy. To our knowledge, this is the first controlled study of an antiviral agent in the treatment of a sufficient number of Bell's palsy cases based on an etiologic background.
Acute facial palsy. Some clinical and virological observations.
- Berg