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Bell palsy occurs in different rheumatic diseases, causes hemifacial weakness, and targets the motor branch of the 7th cranial nerve. Severe, persistent, and refractory otalgia having features of neuropathic pain (ie, burning and allodynic) does not characteristically occur with Bell palsy. Whereas aberrant regeneration of the 7th cranial nerve occ...
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Background
An adolescent with recent dengue infection was presented with sudden onset of bilateral facial nerve palsy. It was a rare presentation and posed as a diagnostic challenge to all physicians.
Case presentation
A 13-year-old boy, presented with sudden onset of bilateral facial weakness. His chief complaints were noted drooping of the mouth...
Citations
... One publication has alluded to a novel neurological disorder in three rheumatic disease patients defined by a triad of facial weakness, otalgia with neuropathic features and hemifacial spasm. Intravenous immunoglobulin was successfully used to treat one patient [50]. ...
Objectives of review
To review the literature for the evidence base for the aetiology and management of referred otalgia, looking particularly at non-malignant, neuralgic, structural and functional issues.
Type of review
Systematic review.
Search strategy
A systematic literature search was undertaken from the databases of EMBASE, CINAHL, MEDLINE®, BNI, and Cochrane Library according to predefined inclusion and exclusion criteria.
Evaluation method
All relevant titles, abstracts and full text articles were reviewed by three authors who resolved any differences by discussion and consultation with senior author.
Results
44 articles were included in our review. The overall quality of evidence was low, with the vast majority of the studies being case-series with three cohort and four randomised-controlled trials included. The prime causes and management strategies were focussed on temporomandibular joint dysfunction (TMJD), Eagle syndrome and neuralgia. Our meta-analyses found no difference on the management strategies for the interventions found.
Conclusions
Referred otalgia is common and treatment should be aimed at the underlying pathology. Potential aetiologies are vast given the extensive sensory innervation of the ear. An understanding of this and a structured approach to patient assessment is important for optimal patient management.
... Hadithi et al. describes a patient with facial palsy and concurrent autoimmune hypothyroidism [10], and Rousso et al.'s patient had a concurrent B12 deficiency [11]. Birnbaum et al. found two cases of Sjögren's and facial palsy, both characterized by facial weakness, otalgia, and hemifacial spasm [12]. The author proposes that this constellation of symptoms is unique to rheumatic disease and is separate from Bell palsy, which does not cause hemifacial spasm, otalgia, and severe neuropathic pain. ...
... Our case report is most similar to Birnbaum et al., which describes a similar constellation of features of unilateral facial weakness and otalgia [12]. Our patient's only pre-existing condition was hypertension, treated with olmesartan. ...
... Damage to the nervous system should indicate more intensive treatment. Some patients have shown rapid and almost complete recovery from nerve palsy after therapy with corticosteroids and IVIG [3,12]. This may suggest that lymphocytic infiltrate, rather than a vasculitic process, is likely the cause of cranial neuropathy in SS. ...
Symptoms of dry eyes or dry mouth, otherwise known as sicca symptoms, are not always present in patients with Sjögren's syndrome (SS). Approximately 20% of patients with SS do not have sicca symptoms. An unusual case of a patient presenting with complete left-sided facial hemiparesis, a history of partial bilateral sensorineural hearing loss who was found to have elevated antinuclear antibody (ANA) with high titer positive SSA/Ro antibody, evidence of bilateral parotitis on imaging and absence of sicca symptoms, prompted us to perform a literature review. Twelve case reports relating facial nerve palsy and Sjögren's were found and only one described a similar constellation of features of unilateral facial weakness and otalgia. Management of facial nerve palsy related to Sjögren's is unclear but pharmacological agents have included corticosteroids, intravenous immune globulin (IVIG), cyclophosphamide, and plasmapheresis. This case report describes a patient whose facial nerve palsy is attributed to SS, explores peripheral and central nervous system involvement in SS, and provides some recommended treatments.
... The female gender has been found to be more susceptible to this disease as compared with males [5,6]. The symptoms of RA include fatigue; low-grade fever; malaise; morning stiffness; loss of appetite; loss of weight; otalgia; facial weakness; hemifacial spasm; formation of rheumatoid nodules; swollen, tender, and warm joints; and increased local osteoporosis around the inflamed joints [7][8][9][10][11][12]. ...
Introduction/objectives:
Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in reducing pain and inflammation in rheumatoid arthritis and other joint- and muscle-associated diseases. However, the extensive, long-term, and over the counter administration of NSAIDs may cause various side effects in the patients. In the present study, the chronological effect of NSAIDs on oxidative stress and antioxidant status in patients with rheumatoid arthritis was studied.
Methods:
The study included 100 female individuals categorized in four major groups: (1) control group consisting of age- and gender-matched healthy individuals, (2) NRA-NSAID individuals taking NSAIDs without any history of RA, (3) RA individuals with a history of RA but not taking NSAIDs, and (4) RA-NSAID individuals with chronic RA and taking NSAIDs for a long period. The sera of the participants were analyzed for the oxidative stress and antioxidant status.
Results:
The RA-NSAID group showed the significantly highest oxidative stress, in terms of malondialdehyde content and lipid-reducing ability as determined in thiocyanate and hemoglobin-induced linoleic acid systems. However, the free radical scavenging ability of the RA-NSAID group, against 2,2-diphenyl-1-picrylhydrazyl, hydroxyl, superoxide, and 2,2-azino-bis-tetrazolium sulfate radicals, was found to be lower than those of the other study groups. The regression analysis of the experimental data showed a significant positive relationship between duration of NSAID intake and malondialdehyde production, lipid-reducing ability, and metal chelating ability in the RA-NSAID patients. The free radical scavenging abilities of the RA-NSAID group were negatively correlated with the duration of NSAID intake.
Conclusions:
The prolonged use of NSAIDs significantly increased the oxidative stress and decrease the antioxidant potential of both the RA patients and NRA individuals. The study provides awareness to the public particularly the RA patients regarding the risk of oxidative stress-associated abnormalities caused by the frequent and prolonged use of NSAIDs for temporary relief from pain. Key Points • The study presents the effects of long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) on antioxidant status of patients with rheumatoid arthritis. • The continuous administration of NSAIDs has been found to significantly increase the oxidative stress of the patients with rheumatoid arthritis as well as the individuals with no signs of rheumatoid arthritis. • The prolonged NSAID therapy also decreased the antioxidant potential of the patients with rheumatoid arthritis as well as the individuals with no signs of rheumatoid arthritis. • The study would be a significant and valuable contribution to the literature for the awareness regarding the use of NSAIDs.
... [19] A recent case-series study described Bell's palsy-associated manifestations, including hemifacial weakness, otalgia, and hemifacial spasm, in a patient with rheumatoid arthritis. [20] From a clinical perspective, we have experienced Bell's palsy patients with underlying rheumatoid arthritis. The shared pathogenesis found between rheumatoid arthritis and Bell's palsy is based on a viral infection and a subsequent autoimmune reaction. ...
... However, evidence for this association in support of our hypothesis is limited. When we searched the PubMed and EMBASE databases using the keywords " ( [20,22] Given the rarity of reports of Bell's palsy in rheumatoid arthritis, a large cohort study seems to be mandatory to address the risk of the development of Bell's palsy in rheumatoid arthritis patients. ...
... Previous case studies reported the coexistence of Bell's palsy in patients with rheumatoid arthritis, suggesting a potential mechanism by which immunological mediators elicited facial nerve palsy. [20,22] Furthermore, rheumatoid arthritis medications, including nonsteroidal anti-inflammatory drugs, antimalarial agents, and other disease-modifying antirheumatic drugs, have been shown to alter host immune responses and subsequently induce inflammation. [28,29] Based on this concept, the presence of rheumatoid arthritis might be related to an increased risk of viral infection and a subsequent autoimmune reaction, resulting in Bell's palsy. ...
This study aimed to evaluate the relationship between Bell's palsy and rheumatoid arthritis in a national sample cohort from Korea.
Data were collected for individuals ≥20 years old from 2002 to 2013 in the Korean National Health Insurance Service-National Sample Cohort. We extracted data for patients with rheumatoid arthritis (n = 7628) and 1:4-matched controls (n = 30,512) and analyzed the occurrence of Bell's palsy in both groups. Matching was performed based on age, sex, income, and region of residence. Rheumatoid arthritis was diagnosed according to International Classification of Disease-10 (ICD-10) codes (M05-M06) and the prescription of biological agents and/or disease-modifying antirheumatic drugs. Bell's palsy patients were diagnosed according to ICD-10 code H912 and treatment ≥2 times with steroids. Adjusted hazard ratios (HRs) were calculated using stratified Cox proportional hazard models for the Charlson comorbidity index and 95% confidence intervals (CIs). Subgroup analyses based on age and sex were also performed.
The rates of Bell's palsy were similar between the rheumatoid arthritis group (0.5% [38/7628]) and the control group, with no significant difference (0.4% [124/30,512], P = .270). The adjusted HR for Bell's palsy was 1.12 (95% CI, 0.78–1.62) in the rheumatoid arthritis group (P = .540). In the subgroup analyses according to age and sex, the relationship between Bell's palsy and rheumatoid arthritis did not reach statistical significance.
The risk of Bell's palsy was not increased in patients with rheumatoid arthritis.
... Very few cases of peripheral facial nerve paralysis associated with pSS have been described previously [5,[8][9][10][11]. Most of them were unilaterally affected and facial palsy was often accompanied by other cranial nerve damage [5,11,12]. ...
... In other cases, facial paralysis presenting as multiple cranial neuropathy were generally responsive to steroid treatment [11]. Recurrent episodes of facial weakness and subsequent facial spasm can be seen occasionally [9]. Our patient received methotrexate treatment for 2 months and the facial weakness did not recover, which did not support the diagnosis of Bell's palsy. ...
Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disorder associated with a variety of systemic presentations. Varied neurological dysfunctions of newly diagnosed adult patients with pSS have been observed in recent years. We aimed to describe a rare case of acute bilateral facial paralysis diagnosed with pSS for the first time and review the previous studies including similar cases. A 69-year-old female, who had experienced ocular and oral dryness for more than 10 years, presented with bilateral facial palsy. Her laboratory test results showed positive anti-Ro (SSA) and anti-Ro-52 antibodies. Ophthalmic examination and test of saliva secretion verified xerophthalmia and xerostomia, respectively. Other possibilities of Lyme disease, Möbius syndrome, tumor, bilateral temporal bone fracture, Guillain–Barré syndrome, central nervous system lymphoma and HIV infection were ruled out. A diagnosis of pSS associated with bilateral facial paralysis was made. The literature review revealed one article describing a similar patient. Our case was the only one suffering from acute bilateral facial palsy without other nerve involvement. The presence of such patients reveals that pSS is an underlying cause of acute bilateral facial paralysis.
... The two possible mechanisms, vascular origin with damage to the vasa nervorum, and an immunologic cause inducing lymphocytic infiltration of the nerve have been suggested in nerve palsies related to SS. Vasculitis in peripheral neuropathy and ganglionopathy in trigeminal or ataxic neuropathies have been reported as the main pathogenic etiology. The rapid and almost complete recovery from nerve palsy after therapy with corticosteroids and azathioprine suggests that lymphocytic infiltrate, rather than a vasculitic process, was the cause of cranial neuropathy in SS [33][34][35][36][37][38][39][40]. ...
Sjögren’s syndrome (SS) affects numerous different areas, and many specialists may be involved in the diagnosis and treatment of SS. Otolaryngological and dental manifestations, neurological impairment, and hearing loss may be the initial symptoms of SS. This chapter describes the most common otolaryngological and oral manifestations of SS, its pathomechanism and possible etiology. Dryness accompanying SS is associated with many clinical implications. The rate of dry mouth in SS ranged from 41% at initial diagnosis to 84% 10 years after diagnosis. An unstimulated salivary flow rate of 0.1 ml/min in sialometry gives a score of 1 to the weighted sum of 5 items according to the current EULAR/ACR criteria. The presence of mononuclear cell aggregates around the ducts and acini of salivary glands results in functional and structural alterations at the level of these glands and impairs their secretory function. The most common oral signs and symptoms are dental caries, tooth decay, fungal infections, traumatic oral lesions, dysphagia, dysgeusia, and inflammation of the salivary glands. Saliva in SS is characterized by the increased concentration of lactoferrin, potassium and cystatin C and the decreased concentration of amylase, carbonic anhydrase, mucins, histatines, IgA, statherins, proline-rich proteins, and the loss of salivary buffer properties. The lack of these physiological defense mechanisms increases the risk of opportunistic infections, mainly fungal infections by Candida albicans. Candidiasis accompanies angular cheilitis, simple cheilitis, and exfoliative cheilitis. The salivary glands of SS patients are characterized by chronic inflammation with the presence of lymphocytic infiltrates located around the striated ducts. These periductal foci may lead to the development of organized ectopic lymphoid structures resembling secondary lymphoid organs with segregated T- and B-cell areas, and high endothelial venules. These structures become an active center of immune response. The presence of foci in labial salivary glands is a hallmark of SS, and their histopathologic analysis is an important item in the diagnosis and classification. A biopsy can be taken from either the labial or the parotid salivary gland, but currently according to the diagnostic criteria, only labial salivary gland biopsy (LSGB) is recommended to confirm the diagnosis of SS. The authors present their own experience and recommendations in taking labial salivary gland biopsy, the main surgical approaches, and the main limitations for this diagnostic method and describe the possibilities and principles of histopathological examination in SS. The authors present the main ultrasonic signs of SS major salivary glands and perspectives of the usage of salivary gland ultrasonic examination in the diagnosis and monitoring of SS. The presented chapter also includes the most common laryngological manifestations associated with SS: nose dryness, crusting, or atrophy of the nasal mucosa, dryness of the throat, dysphagia, hoarseness, otalgia and tinnitus, gastro-esophageal reflux, and chronic cough. Patients with SS tend to have a higher prevalence of sensorineural hearing impairment compared with the general population. Idiopathic hearing loss may represent the initial manifestation of SS. Furthermore, authors present and discuss the main neurological symptoms of SS. Neurological manifestations are reported in about 20% of patients with SS. In patients with SS, neurological manifestations may occur, such as peripheral neuropathy and other forms of neuropathies, including sensory ataxia, painful sensory neuropathy without sensory ataxia, multiple mononeuropathy, multiple cranial neuropathy, autonomic neuropathy, radiculoneuropathy and intra- and extraoral paresthesias, facial hypaesthesia, and trigeminal nerve neuropathy.
... The rapid and almost complete recovery from nerve palsy after therapy with corticosteroids and azathioprine suggests that lymphocytic infiltrate, rather than a vasculitic process, was the cause of cranial neuropathy in SS [41][42][43]. Birnbaum [44] reported a new, previously unrecognized neurological disorder in rheumatic diseases, characterized by facial weakness, otalgia with neuropathic features, hemifacial spasm, and with both otalgia and hemifacial spasm persisting after the extinction of mild facial weakness. ...
Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration of exocrine glands and a range of extra-glandular features. The most common and earliest symptoms are oral and ocular dryness. The aim of this study is to present the most common otolaryn-gological manifestations of SS, their pathomechanism and possible aetiology. The most common oral signs and symptoms are xerostomia, tooth decay, fungal infections, traumatic oral lesions, dys-phagia, dysgeusia, and inflammation of the salivary glands. The salivary glands of SS patients are characterised by chronic inflammation. The presence of foci is thus a hallmark of SS. A biopsy can be taken from either the labial or the parotid salivary gland. The most significant complication of SS is the development of lymphoproliferative malignancy, which occurs in about 5% of SS patients. The ultrasonic greyscale scoring system, glandular volume measurement, and intraglandular power Doppler ultrasonography are specific ultrasound parameters of SS.
... En todos los casos de PFR, los estudios radiológicos están indicados con el fin de descartar una lesión del nervio facial (32,(56)(57)(58)(59). Estos estudios radiológicos incluyen una tomografía computarizada de hueso temporal de alta resolución y una resonancia magnética cerebral con énfasis en pares craneanos (9,32,60,61). Otros estudios como pruebas de química sanguínea, endoscopia nasal, evaluación audiológica, biopsias o cultivos, están indicados sólo en caso de una sospecha diagnóstica específica y no se recomiendan de rutina en todos los pacientes (12,15,38,40,47,(62)(63)(64). ...
Introducción: La parálisis facial tiene una incidencia anual de 13-52 casos por cada 100.000 habitantes. 7% de los episodios corresponden a Parálisis Facial Recurrente (PFR). Estudios electrofisiológicos han evidenciado mayor degeneración del nervio facial tras recurrencias repetitivas, y el pronóstico parece ser peor comparado con un único episodio.Objetivo: Revisar sistemáticamente la literatura existente y presentar un algoritmo clínico actualizado sobre el diagnóstico y manejo de la PFR, basado en una compilación y síntesis metodológica de la literatura disponible.Diseño: Revisión sistemática de la literatura. Materiales y métodos: Se realizó una búsqueda en las bases de datos MEDLINE/Pubmed, Cochrane, Scopus, Scielo y LILACS, con los términos Mesh “Nervio Facial, Parálisis Facial Recurrente, TécnicasResultados: Se encontraron 84 artículos. Después de una lectura cuidadosa y filtro basado en los criterios, 63 artículos fueron seleccionados.Discusión: El abordaje diagnóstico de la PFR sin excepción debe incluir una detallada historia clínica, examen físico completo, tomografía de hueso temporal de alta resolución y resonancia magnética del nervio facial. Los estudios adicionales deben basarse en una sospecha diagnóstica y su uso rutinario no está recomendado.Conclusiones: El manejo oportuno de la inflamación y el edema, independientemente de la etiología de la PFR, tendrá un impacto positivo en el pronóstico funcional del nervio.
... Otaljinin 7 ve 8. ci siniri etkileyen nöropatik ağrıya bağlı olduğunu be- lirtmiştir. [8] Olgu 1'de izole 12. sinir etkilenimi bulgusu (dilde deviasyon), Olgu 2'de yukarı bakış kısıtlılığı ve Olgu 3'te sağ hemiparezi saptanmıştır. Ancak hiçbir hastada beyin görün- tüleme bulgusu ile klinik bulgu arasında net bağlantı kurula- mamıştır. ...
Sjögren's syndrome (SS) is a chronic autoimmune vasculitic disease
involving the lacrimal and salivary glands. The central and peripheral
nervous system can be affected by the ratio of 1.5–20% and 10%, in
SS, respectively. In this study, clinical-neuroradiological findings and
response to treatment of five female patients with SS who were
affected by different parts of the central nervous system were pre-
sented in the context of current literature.
Keywords: Pain; connective tissue; gabapentin; Sjögren’s, vasculitis.
... Otaljinin 7 ve 8. ci siniri etkileyen nöropatik ağrıya bağlı olduğunu be- lirtmiştir. [8] Olgu 1'de izole 12. sinir etkilenimi bulgusu (dilde deviasyon), Olgu 2'de yukarı bakış kısıtlılığı ve Olgu 3'te sağ hemiparezi saptanmıştır. Ancak hiçbir hastada beyin görün- tüleme bulgusu ile klinik bulgu arasında net bağlantı kurula- mamıştır. ...
Sjögren sendromu (SS), gözyaşı ve tükürük bezlerini tutan kronik otoimmün vaskülitik bir hastalıktır. SS’de santral sinir sistemi %1.5-20, periferik sinir sistemi ise %10 oranında etkilenebilmektedir. Bu çalışmada santral sinir sisteminin farklı bölümlerinin etkilendiği SS tanılı beş kadın olgunun klinik -nöroradyolojik bulguları ile tedaviye yanıtları güncel literatür bilgileri eşliğinde sunulmuştur. Sjögren
sendromu (SS), gözyaşı ve tükürük bezlerini tutan kronik otoimmün vaskülitik
bir hastalıktır. SS’de santral sinir sistemi %1.5-20, periferik sinir sistemi
ise %10 oranında etkilenebilmektedir. Bu
çalışmada santral sinir sisteminin farklı bölümlerinin etkilendiği SS tanılı
beş kadın olgunun klinik -nöroradyolojik bulguları ile tedaviye yanıtları
güncel literatür bilgileri eşliğinde sunulmuştur.
