Home / Deep Research / Bell's palsy

Bell's palsy

Asta Literature Retrieval: Disease Pathophysiology Research Template Target Disease Disease Name: Bell's palsy MONDO ID: (if available) Category...

2026-03-18
Asta MONDO:0005665 Model: Asta Scientific Corpus Retrieval 20 citations

Asta Literature Retrieval: Disease Pathophysiology Research Template Target Disease Disease Name: Bell's palsy MONDO ID: (if available) Category...

This report is retrieval-only and is generated directly from Asta results.

  • Papers retrieved: 20
  • Snippets retrieved: 20

Relevant Papers

[1] A meta-analysis uncovers the first sequence variant conferring risk of Bell’s palsy

  • Authors: A. Skuladóttir, G. Bjornsdottir, G. Thorleifsson, G. Walters, M. S. Nawaz et al.
  • Year: 2021
  • Venue: Scientific Reports
  • URL: https://www.semanticscholar.org/paper/3f3bee81a0bfc0d39c79f29d7c437b305c42a9fe
  • DOI: 10.1038/s41598-021-82736-w
  • PMID: 33602968
  • PMCID: 7893061
  • Citations: 13
  • Summary: Findings from a meta-analysis of genome-wide association studies uncovering the first unequivocal association with Bell’s palsy are reported, suggesting a common pathogenesis in part or a true pleiotropy.
  • Evidence snippets:
  • Snippet 1 (score: 0.605) > The precise pathophysiology of Bell's palsy is unknown and biologically targeted treatment is lacking. The aim of the study was to search for variations in the human genome affecting risk of Bell's palsy and thus use genetics to uncover biological underpinnings of this somewhat mysterious disease. Here, we report the first unequivocal association between Bell's palsy and a sequence variant, rs9357446-A (P = 6.79 × 10 -23 , OR = 1.23), in a metaanalysis of four study cohorts. While rs9357446-A confers risk of Bell's palsy, it also confers low risk of IDD as well as reduced lung function measured by decreased FVC 16 suggesting shared etiology of these diverse diseases that are all but certain to differ in the pathogenesis. The common variant at 6p21.1 is intergenic. Nearby genes are LOC105375075, CDC5L, MIR4642, SPATS1, AARS2, TCTE1, TMEM151B, and SLC35B2. Our transcript-and proteomics analyses did not pinpoint a Bell's palsy gene at this locus. Although uncorrelated with rs9357446 (r 2 < 0.2), several sequence variants in the closest gene, cell division cycle 5 like (CDC5L), have been found to associate with related phenotypes, including osteoarthritis 17 , bone density 18 , ossification of the spine 19 , and lung function measured by FVC and forced expiratory volume 16 . Another potential candidate at the locus, SLC35B2, is a key component of a protein sulfation pathway where it plays a part in modifying C-C Motif Chemokine Receptor 5 (CCR5), that is one of HIV's host proteins for entry into the cell 20 . Several other studies point to the importance of CCR5 in determining disease severity of other viral infections in animal models 21,22 . In addition, SLC35B2 is involved in proteoglycan synthesis. Cartilage is particularly rich in proteoglycans, and changes in the structure and composition

[2] Comparison of Medical and Surgical Treatment in Severe Bell’s Palsy

  • Authors: Yong Kim, S. Yeo, H. Rim, Jong-Hyup Lee, Dokyoung Kim et al.
  • Year: 2022
  • Venue: Journal of Clinical Medicine
  • URL: https://www.semanticscholar.org/paper/5c75e1e7aa3ff4e5c3b926a7998ef341b6e0a902
  • DOI: 10.3390/jcm11030888
  • PMID: 35160337
  • PMCID: 8836601
  • Citations: 9
  • Summary: (1) Background: The effectiveness of decompression surgery for Bell’s palsy is controversial. This study investigated the effects of facial nerve decompression in patients with severe Bell’s palsy who were expected to have a poor prognosis. (2) Methods: We retrospectively reviewed 1721 patients with Bell’s palsy who visited the Kyung Hee University Hospital between January 2005 and December 2021. Of these, 45 patients with severe Bell’s palsy were divided into two groups; 30 patients were tre...
  • Evidence snippets:
  • Snippet 1 (score: 0.583) > Bell's palsy is an acute, unilateral, peripheral facial nerve paresis or paralysis of unknown cause. It has an annual incidence of 20-30 per 100,000 population [1,2]. The pathophysiology of Bell's palsy includes edematous swelling of the facial nerve within the Fallopian canal, which causes a conduction block and subsequent dysfunction. However, the exact mechanism of impaired nerve function remains unclear. Although most patients with Bell's palsy have a good prognosis, approximately 10-29% of affected patients develop persistent facial nerve dysfunction [3,4]. Facial nerve lesions determine the shape of the face, which can have a significant impact on an individual's social life. It is important to identify and treat patients at high risk of poor long-term outcomes in order to reduce the risk of persistent facial nerve dysfunction and psychological distress [5]. > There is strong evidence supporting the use of steroids as the initial medical treatment in Bell's palsy to reduce facial nerve inflammation [6,7]. Treatment guidelines for Bell's palsy published by the American Academy of Otolaryngology concluded that treatment with oral steroids within 72 h of symptom onset is highly likely to be effective in new-onset Bell's palsy patients with or without concurrent antiviral therapy [8]. However, some patients do not respond to conservative treatment, and suffer sequelae, including facial asymmetry, contracture, and synkinesis [9]. > Electroneuronography (ENoG) and electromyography (EMG) are objective electrical tests that are used to estimate the degree of paralysis and prognosis in Bell's palsy patients. Patients with Bell's palsy are at a high risk of poor recovery if they demonstrate the following clinical findings: a complete lack of facial movement on clinical examination; ENoG findings of >90% degeneration; and EMG findings of no voluntary motor unit potentials [3,[10][11][12]. > For patients at risk of poor recovery, surgical decompression of the facial nerve has been proposed as an additional treatment option to release nerve entrapment in the facial canal and improve outcomes [13][14][15].

[3] Rehabilitation of a Patient with Bell’s Palsy

  • Authors: Vrushali Athawale, Dushyant Bawiskar, Pratik Phansopkar
  • Year: 2021
  • Venue: Journal of Evolution of Medical and Dental Sciences
  • URL: https://www.semanticscholar.org/paper/590b99acef57798359b4e42aebec24512177ee46
  • DOI: 10.14260/JEMDS/2021/323
  • Citations: 2
  • Summary: This is a diagnosed case of right facial nerve palsy which was treated under physiotherapy department with proper rehabilitation protocol and the aetiology of facial paralysis is not yet thoroughly understood.
  • Evidence snippets:
  • Snippet 1 (score: 0.579) > Facial nerve palsy is the disease of cranial nerve. From the total number of cases, 60 to 75 % of Bell's palsy cases are idiopathic form of facial palsy. Facial nerve palsy results in weakness of facial muscles, atrophy, asymmetry of face and also disturbs the quality of life. Bell’s palsy occurs in every class of population affecting people of all the age groups but the most common age group affected is 15 - 50 years with equal sex prediliction accounting 11 - 40 cases per 100,000. If facial palsy is not treated properly then it may result in variety of complications like motor synkinesis, dysarthria, contractures of facial muscles, and crocodile tear. Currently facial paralysis treatment consists of combination of pharmacological therapy, facial neuromuscular re-entrainment physiotherapy or surgical intervention by static and dynamic facial reanimation techniques. Physiotherapy treatment is effective for treating facial paralysis with minimal complications and can be individualized. Bell's palsy is the idiopathic form of facial nerve palsy which accounts for 60 to 75 % of cases and male to female ratio is 1:3.1 The aetiology of facial paralysis is not yet thoroughly understood. Cases of varicella-zoster, mononucleosis, herpes simplex virus, mumps and measles have demonstrated good serology in several reports for their association but still stands unclear. 2 Peripheral facial nerve palsy may be idiopathic (primary cause) or Bell’s palsy (secondary). Causes of the secondary unilateral facial nerve palsy are diabetes, stroke, Hansen's disease, herpes simplex infection, birth injury, trauma, tumour, Guillain-Barre syndrome, and immune system disorders. Causes of the bilateral facial nerve palsy are leukemia, brainstem encephalitis, leprosy, and meningitis. The most prominent current theories of facial nerve paralysis pathophysiology include the reactivation of herpes simplex virus infection (HSV type 1). Current facial paralysis treatment consists of a combination of pharmacological therapy, facial neuromuscular re-entrainment physiotherapy or surgical intervention by

[4] Emerging Trends in Pathophysiology: Insights from the 9th International Congress of the International Society for Pathophysiology (ISP 2023)

  • Authors: A. Kubyshkin, S. Bolevich, L. Churilov, V. Jakovljevic, E. Kovalenko et al.
  • Year: 2024
  • Venue: Pathophysiology
  • URL: https://www.semanticscholar.org/paper/3ab0c7d37d984c72ca8cba300cb8052c1326e61a
  • DOI: 10.3390/pathophysiology31010011
  • PMID: 38535621
  • PMCID: 10975917
  • Summary: The main trends and the most promising areas of research in current pathophysiology, including investigations of new pathogenic pathways, and the identification of cellular and molecular mechanisms, target molecules, genetic mechanisms, and new therapeutic strategies are described.
  • Evidence snippets:
  • Snippet 1 (score: 0.561) > This article provides a summary of the 9th International Congress of the International Society for Pathophysiology (ISP 2023) which took place in Belgrade, Serbia, from 4 to 6 July 2023. It describes the main trends and the most promising areas of research in current pathophysiology, including investigations of new pathogenic pathways, and the identification of cellular and molecular mechanisms, target molecules, genetic mechanisms, and new therapeutic strategies. The present article also highlights the research conducted by leading scientific teams and national pathophysiological societies from various countries that adds to our understanding of the pathogenesis of diseases and pathological processes.

[5] New onset of Bell’s palsy in a patient with West Nile Encephalitis

  • Authors: Tetyana Vaysman, A. Melkonyan, Antonio Liu
  • Year: 2020
  • Venue: Clinical Case Reports
  • URL: https://www.semanticscholar.org/paper/7f39c432dfee57947bfa6da4682be36e7a2d5966
  • DOI: 10.1002/ccr3.3009
  • PMID: 33088514
  • PMCID: 7562893
  • Citations: 2
  • Summary: A patient who was diagnosed with West Nile virus encephalitis and developed new onset of Bell's palsy within 8 days of diagnosis and it would be beneficial to evaluate WNV‐infected patients for peripheral neuropathy.
  • Evidence snippets:
  • Snippet 1 (score: 0.555) > ess than 1% of affected people develop neuroinvasive disease and mortality rate accounts for <0.1% of all WNVinfected patients. 8 ell's palsy is an idiopathic facial nerve paralysis which often presents with unilateral facial weakness commonly characterized by an inability to close the eye, disappearance of the nasolabial fold, and eyebrow drooping at the affected corner of the mouth. There may also be decreased tearing, hyperacusis, and/or loss of taste sensation on the anterior two thirds of the tongue. 10 The nerve paralysis was named after Scottish physician, surgeon, and neurologist Charles Bell (1774-1842) who first described the lesions of facial nerve (CN VII) and its clinical presentations. 11 It has been widely accepted that herpes simplex virus and herpes zoster virus are the most common etiology of Bell's palsy. Other viral infectious agents such as Epstein-Barr Virus, cytomegalovirus, rubella, mumps virus, adenovirus, influenza B virus, and coxsackievirus have been reported. 12 However, there are no known reports of development of Bell's palsy with WNV encephalitis. The annual incidence of Bell's palsy is 40 000 new cases each year with 8% to 12% recurrence rate. 13 Up to 70% of patients will have complete resolution without treatment. 14 ven though the underlying pathophysiology remains elusive, Bell's palsy is thought to result due to virus-mediated inflammation resulting in swelling of the CN VII and its compression at the geniculate ganglion. 12

[6] Action Plan for Stroke in Europe 2018–2030

  • Authors: B. Norrving, J. Barrick, A. Dávalos, M. Dichgans, C. Cordonnier et al.
  • Year: 2018
  • Venue: European Stroke Journal
  • URL: https://www.semanticscholar.org/paper/0f21747f78323fb499a020962145d0be1cb425a9
  • DOI: 10.1177/2396987318808719
  • PMID: 31236480
  • PMCID: 6571507
  • Citations: 468
  • Influential citations: 28
  • Summary: The ESAP provides a basic road map and sets targets for the implementation of evidence-based preventive actions and stroke services to 2030 and overall, 30 targets and 72 research priorities were identified for the seven domains.
  • Evidence snippets:
  • Snippet 1 (score: 0.552) > c strokes, and a major cause of intracerebral haemorrhage, vascular cognitive impairment or dementia. Incomplete understanding of SVD pathogenesis and a lack of appropriate animal models are obstacles to progress. Large-scale studies of systems biology can provide insights into the underlying mechanisms of complex diseases and responses to treatment. 109 Key priorities in this area include: better understanding of the pathogenic contribution of endothelial dysfunction or BBB disruption, inflammation and hemodynamic factors; understanding the role of proteins and pathways involved in monogenic forms of SVD and (multifactorial) sporadic SVD; 110 understanding the mechanisms leading to cognitive impairment and deciphering the intricate relationship with Alzheimer's disease; designing protective approaches to reduce progression of white matter damage; expanding the identification of genetic and other molecular biomarkers and translating the new putative targets discovered through genetic, molecular and cellular biology data into diseasemodifying therapies. > Functional recovery and rehabilitation. A key objective is to expand our knowledge on functional recovery mechanisms and potential therapeutic targets to enhance the effects of physical rehabilitation in the chronic phase after stroke. Research is needed on neuronal plasticity and network recovery, and their interaction with delayed pathophysiological mechanisms such as neuroinflammation, apoptosis, neurogenesis and angiogenesis. This will require the adoption of methodology from stem cell research, gene therapy, optogenetics, non-invasive brain stimulation and other fields. The methodology for evaluating functional recovery in experimental stroke models should be improved.

[7] Psychosocial functioning in patients with altered facial expression: a scoping review in five neurological diseases

  • Authors: N. Rasing, W. van de Geest-Buit, On Ying A Chan, K. Mul, A. Lanser et al.
  • Year: 2023
  • Venue: Disability and Rehabilitation
  • URL: https://www.semanticscholar.org/paper/df39d3d69ccc1115843457a6070c199396eca110
  • DOI: 10.1080/09638288.2023.2259310
  • PMID: 37752723
  • Citations: 10
  • Summary: Patients with altered facial expression in four of five included neurological diseases had reduced psychosocial functioning, and learning of compensatory strategies could be a beneficial therapy for patients with psychosocial distress.
  • Evidence snippets:
  • Snippet 1 (score: 0.551) > A systematic review on psychosocial distress in facial palsy patients has recently been performed, but other neurological diseases were not included [12]. Our review has a different starting point by including five neurological disorders (i.e., neuromuscular and movement disorders) and also including smaller studies (case reports) to maximize existing knowledge to give insight on the common themes of having an altered facial expression on psychosocial functioning. > We included five neurological diseases: Bell's palsy, FSHD, Moebius syndrome, myotonic dystrophy type 1, and Parkinson's disease. These diseases have a very different pathophysiology, but can all cause an altered facial expression. This selection of diseases was chosen carefully to ensure a diverse overview of possible causes of altered facial expression: acute versus gradual onset, congenital versus acquired disease, and different aetiologies. Figure 2 highlights the similarities and differences between the diseases. The psychosocial study outcomes in these diseases are expected to create an understanding of the possible psychosocial impairments of having an altered facial expression and to help identify future research directions for improving verbal and non-verbal communication, and thus psychosocial functioning.

[8] Treatment Approaches for Altered Facial Expression: A Systematic Review in Facioscapulohumeral Muscular Dystrophy and Other Neurological Diseases

  • Authors: N. Rasing, W. van de Geest-Buit, On Ying A Chan, K. Mul, A. Lanser et al.
  • Year: 2024
  • Venue: Journal of Neuromuscular Diseases
  • URL: https://www.semanticscholar.org/paper/8a055850bd49d4c16be74241b5086c5e4a2a7406
  • DOI: 10.3233/JND-230213
  • PMID: 38517799
  • PMCID: 11091602
  • Citations: 3
  • Summary: A systematic search for symptomatic treatment approaches that target facial muscle function and psychosocial interventions in various neurological diseases with altered facial expression in order to discuss the applicability to FSHD found forty studies met the inclusion criteria.
  • Evidence snippets:
  • Snippet 1 (score: 0.542) > Multiple neurological diseases were included, because of the expected scarcity of literature about treatment options for improving facial weakness in FSHD patients and of the expected wide applicability of certain symptomatic treatments.However, the anatomical location of the defect and the pathophysiology is different in these diseases (Fig. 2), therefore some recommended treatments are not applicable to FSHD. > When comparing the included diseases on altered facial expression, especially Parkinson's disease has a different underlying mechanism.As bradykinesia causes the altered facial expression, whereas in the other included disease this is caused by facial weakness or facial paresis.Additionally, medication and associated on-off phenomenon can effect the degree of bradykinesia, potentially affecting the outcomes of symptomatic treatments.However, the included studies did provide valuable insights into current symptomatic therapies, which could be discussed for their potential applicability in FSHD. > Bell's palsy patients have a high spontaneous recovery rate, as about seventy percent has a spontaneous recovery within three to six months [93].Therefore, in studies with Bell's palsy patients a high number of patients recovering after treatment, would also recover without treatment.Treatment effectivity could therefore be overestimated in this disease, this applies especially for studies performed in the acute phase of Bell's palsy. > Of the included studies, 12 consisted of case reports.Level of evidence is low, and conclusions must be taken with caution.Nevertheless, these studies were included because they could point out treatment options that would otherwise not be identified and might be interesting for future research. > Studies performed before 1990 were excluded, because of the expected outdated treatment usage before 1990, especially for surgery techniques.Despite we could have missed important references.

[9] Lower motor neuron facial palsy in a postnatal mother with COVID-19

  • Authors: Vignesh Kumar, P. Narayanan, Seema Shetty, Afsal P Mohammed
  • Year: 2021
  • Venue: BMJ Case Reports
  • URL: https://www.semanticscholar.org/paper/b69d9ac169040035e4f502469c82c94be2374938
  • DOI: 10.1136/bcr-2020-240267
  • PMID: 33649026
  • PMCID: 7929834
  • Citations: 17
  • Influential citations: 2
  • Summary: The authors present a case of Bell’s palsy associated with COVID-19 in a term primigravida.
  • Evidence snippets:
  • Snippet 1 (score: 0.538) > Bell's palsy is the most common cause of acute unilateral lower motor neuron facial nerve palsy. The worldwide incidence of Bell's palsy varies between 11.5 and 40.2 cases per 100 000 population. 9 Bell's palsy has been associated with viral infections like Epstein-Barr virus, mumps, rubella, and most commonly, HSV. A cell-mediated autoimmune response against myelin basic protein has been linked with Bell's palsy. 10 Risk factors for Bell's palsy include pregnancy, severe preeclampsia, obesity, upper respiratory diseases, hypertension and diabetes. The pathophysiology of Bell's palsy has been a topic of intense debate. Some authors describe it as an acute demyelinating disease similar to Guillain-Barré disease. 11 Murakami et al successfully isolated Herpes simplex-1 DNA from the endoneurial fluid of the facial nerve by PCR during the acute phase of Bell's palsy. 12 Autoimmune or virus-mediated damage to facial nerve leads to oedema of the nerve and causes lower motor neuron palsy. > COVID-19 has a deleterious effect on the nervous system ranging from anosmia, dysgeusia to acute stroke. Autopsy reports in patient's with COVID-19 has shown brain tissue oedema and partial neuronal degeneration in deceased patients. 13 Moriguchi et al reported a case of COVID-19 where the patient had a loss of consciousness, seizures, neck stiffness. SARS-CoV-2 RNA was isolated from the cerebrospinal fluid (CSF) though it was absent in the nasopharyngeal swab, providing further evidence that SARS-CoV-2 is a neurotropic virus. 14 Viral encephalitis, meningitis, encephalopathy, demyelination and acute cerebrovascular accidents have been reported in COVID-19 patients. 15 The mechanism of neuroinvasion by SARS-CoV-2 could be a direct invasion of the nervous system or entry through the blood circulation. Coronaviruses have been known to infect sensory or motor nerve endings achieving anterograde

[10] Comprehensive review on the pathogenesis of hypertriglyceridaemia-associated acute pancreatitis

  • Authors: Minhao Qiu, Xiaoying Zhou, M. Zippi, Hemant Goyal, Zarrin Basharat et al.
  • Year: 2023
  • Venue: Annals of Medicine
  • URL: https://www.semanticscholar.org/paper/45eb6adcd7600f6a642f6adcf51182e2de45ba30
  • DOI: 10.1080/07853890.2023.2265939
  • PMID: 37813108
  • PMCID: 10563627
  • Citations: 44
  • Influential citations: 1
  • Summary: An overview of triglyceride metabolism and the potential mechanisms that may contribute to developing or exacerbating hypertriglyceridaemia appears promising, with ongoing research focused on developing more specific and effective treatment strategies.
  • Evidence snippets:
  • Snippet 1 (score: 0.537) > HTAP is a complex disease with a multifactorial aetiology, and not fully understood pathophysiology.As our knowledge regarding the disease evolves, we are likely to develop more effective and targeted treatments, which can reduce the occurrence of more severe disease outcomes or prevent the disease altogether.Future research will need to focus on elucidating the underlying genetic and molecular mechanisms of the disease, as well as identifying specific pathways and targets that can be used to develop more effective treatments.This will require a multidisciplinary approach that combines genetics, molecular biology, and clinical research and will likely involve collaborations between basic and clinical scientists across multiple disciplines.Ultimately, developing more effective treatments for HTAP will require a deep understanding of the underlying pathophysiology of the disease, as well as the development of more targeted and personalized approaches to diagnosis and treatment.

[11] Increased risk of Bell palsy in patient with migraine

  • Authors: So Young Kim, C. Lee, Jae-Sung Lim, I. Kong, Songyong Sim et al.
  • Year: 2019
  • Venue: Medicine
  • URL: https://www.semanticscholar.org/paper/63ff6044765415b3c757a54ffc245b1d3ce880b3
  • DOI: 10.1097/MD.0000000000015764
  • PMID: 31124964
  • PMCID: 6571209
  • Citations: 10
  • Influential citations: 2
  • Summary: Migraine increased the risk of Bell palsy in the total population and among age subgroups, migraine patients ≥30 and <60 years old had an increased risk ofBell palsy.
  • Evidence snippets:
  • Snippet 1 (score: 0.536) > In the present study, migraine was found to increase the risk of Bell palsy. This increased risk in migraine patients was evident in the ≥30 and <60-year-old population. Few previous studies have reported a relationship between migraine headaches and Bell palsy. The details of the pathophysiology of Bell palsy have not been completely unraveled. Vascular ischemia, immunologic disorders, infectious diseases, and psychological disorders have all been suggested to be associated with Bell palsy. [1] Thus, migraine headaches could also contribute to various aspects of the pathophysiologic mechanism(s) leading to Bell palsy. > The direct neural effects from the trigeminal nerve to the facial nerve could contribute to the risk of facial palsy in migraine patients. A case was reported of a 32-year-old woman with migraine who suffered from recurrent facial paralysis. [11] That study proposed that a reciprocal connection between the trigeminal nerve and the facial nerve could explain the concurrent trigeminal neuralgia and facial palsy. Specifically, the sensory pain afferents of the nervus intermedius, which branches from the maxillary nerve, innervate the facial nerve. [12] However, the concurrent peripheral neural dysfunction of both the trigeminal and facial nerves is rare. In addition to concurrent trigeminal and facial nerve dysfunction, the facial nerve could be gradually weakened leading to paralysis in migraine patients. Repetitive nociceptive neural stimuli in these patients may increase the susceptibility of the facial nerve to injury. > Common pathophysiologic mechanisms exist that could underlie both migraine and Bell palsy. For instance, cardiovascular ischemia is a risk factor for both conditions. [13] lthough the pathophysiologic mechanism of migraines is not completely understood, alteration of the trigeminovascular function has been suggested to trigger migraines. [14,15] Aura migraines are thought to result from a cortical spreading depression induced by cerebral ischemia and inhibition of neural activity. [15,16] Prior studies have demonstrated a 2-fold increase in the risk of stroke and cardiovascular diseases in migraine patients. [17]

[12] Unilateral Facial Paralysis in an Infant Post-vaccination: Insights Into Bell’s Palsy

  • Authors: Sonal Kumar, Adnan A Islam, Patricia Ward, Taylor E Collignon, A. Castro
  • Year: 2025
  • Venue: Cureus
  • URL: https://www.semanticscholar.org/paper/c15f53d1f9da48f89eccd7c914ddefb4de595984
  • DOI: 10.7759/cureus.79971
  • PMID: 40182388
  • PMCID: 11966339
  • Summary: The story of a unique instance of Bell’s palsy in a two-month-old infant with unilateral facial paralysis one day following standard immunizations is shared, highlighting the need for further investigation into the risk of post-vaccination neurological complications, particularly in the pediatric population.
  • Evidence snippets:
  • Snippet 1 (score: 0.525) > Bell's palsy is an acute FNP associated mostly with viral infections, autoimmune conditions, and inflammatory processes. It commonly presents in adults. Pediatric presentations are, therefore, uncommon. While the pathophysiology of Bell's palsy is unclear, reactivation of HSV in the geniculate ganglion is a leading hypothesis [5]. Triggers such as EBV, VZV, and immune-mediated mechanisms may also contribute [6]. > Our case presentation is an important addition to the literature because we discuss the temporal relationship between the onset of Bell's palsy and the administration of the infant's routine two-month vaccinations. Bell's palsy occurring following vaccination is reported in the literature, though it remains an uncommon event [7]. Literature has described cases of FNP following the administration of vaccines such as the COVID-19 vaccination [8], hepatitis B vaccine [9], and HPV vaccine [10]. These associations may suggest that an immune-mediated response is responsible. Still, however, more epidemiological studies are warranted as a causal link between vaccination and Bell's palsy has not been established [11]. > One proposed mechanism for post-vaccination Bell's palsy includes an immune-mediated inflammatory reaction leading to facial nerve edema and compression in the facial canal [12]. Molecular mimicry where vaccine antigens trigger an immune response that cross-reacts with host neural tissues has also been proposed as another mechanism [12]. However, given the overall rarity of Bell's palsy following immunization, the risk remains low compared to the benefits of vaccination in preventing serious infectious diseases. > Future studies such as large-scale surveillance data and population-based cohort studies are necessary to clarify such proposed associations. Clinicians must remain vigilant for post-vaccination neurological events yet still advocate for routine immunization given the overall public health benefits.

[13] A Multi-omics Exploration Revealing SLIT2 as a Prime Therapeutic Target for Peripheral Facial Paralysis: Integrating Single-Cell Transcriptomics and Plasma Proteome Data

  • Authors: Yuchao Liu, Chunli Li, Linli Yao, Miao Tian, Yuan Tan et al.
  • Year: 2025
  • Venue: Cellular and Molecular Neurobiology
  • URL: https://www.semanticscholar.org/paper/a2ebd0eb0eb2a2b91933d7493d52a120cc1e03df
  • DOI: 10.1007/s10571-025-01607-4
  • PMID: 41099890
  • PMCID: 12532790
  • Citations: 1
  • Summary: This study successfully identified SLIT2 as potential therapeutic targets for PFP and detected SLIT2 alteration after facial-nerve injury, a role that has been previously well-documented in many central nervous system diseases.
  • Evidence snippets:
  • Snippet 1 (score: 0.518) > Peripheral facial paralysis (PFP) is a common neurological disorder characterized by facial-nerve dysfunction. Identifying therapeutic targets and understanding the molecular and cellular mechanisms underlying PFP are crucial for developing effective treatment strategies. This study combined Mendelian randomization (MR) analysis and single-cell RNA sequencing (scRNA-seq) to explore potential therapeutic candidates and their roles in PFP pathophysiology. The MR analysis included 1925 publicly available plasma protein cis-heritability instruments. Instrumental variables were selected for MR analysis to identify plasma proteins associated with PFP, followed by colocalization analysis to evaluate shared genetic variants between the identified proteins and PFP. After the initial identification of plasma proteins associated with Bell’s palsy using MR analysis, a rat model of facial-nerve injury was established to further dissect underlying mechanisms at cellular and molecular levels. Using scRNA-seq technology, we delved deeply into cellular Heterogeneity and dynamic changes in gene expression in the facial-nerve nucleus tissues under both injured and control conditions, thereby achieving a systematic study ranging from macroscopic genetic associations to microscopic cellular functions. Finally, expression patterns were preliminarily validated by performing in vitro immunofluorescence analysis on the facial-nerve nucleus samples of SD rats. The MR analysis results identified 30 plasma proteins significantly associated with PFP, with nine target genes showing differential expression in the scRNA-seq data. Colocalization analysis demonstrated that slit guidance Ligand 2 (SLIT2), semaphorin 4D (SEMA4D), EGF containing fibulin extracellular matrix protein 1 (EFEMP1), and sprouty related EVH1 domain containing 2 (SPRED2) shared causal variants with PFP. SLIT2 was highly expressed in the microglia and inhibitory neurons in the experimental group, whereas SEMA4D showed elevated expression across multiple glial cell types in the same group. In contrast, EFEMP1 and SPRED2 showed distinct expression patterns in fibroblasts and oligodendrocytes. The role of SLIT2 has been previously well-documented in many central nervous system diseases. However, for the first time, this study detected SLIT2 alteration after facial-nerve injury. Altered intercellular signaling, particularly enhanced SLIT2-ROBO signaling between neurons and

[14] Of Mice and Men: Comparative Analysis of Neuro-Inflammatory Mechanisms in Human and Mouse Using Cause-and-Effect Models

  • Authors: A. Kodamullil, Anandhi Iyappan, Reagon Karki, S. Madan, E. Younesi et al.
  • Year: 2017
  • Venue: Journal of Alzheimer's Disease
  • URL: https://www.semanticscholar.org/paper/55820fd5fc6231bc4bf3c0330cb6cbfea9a4827c
  • DOI: 10.3233/JAD-170255
  • PMID: 28731442
  • PMCID: 5545904
  • Citations: 27
  • Summary: This paper investigates the failure of a neuroinflammation targeted drug in the late phases of clinical trials based on the comparative analyses between the two species and assesses to what extend a mouse can mimic the cellular and molecular interactions in humans at a mechanism level.
  • Evidence snippets:
  • Snippet 1 (score: 0.518) > Mouse models are extensively used in biomedical research mainly to understand the etiology of the disease. Complex diseases like AD may involve several simultaneous alterations in molecular and processual activities, including neuroinflammation, aggregation of A␤ peptides, or tau phosphorylation, which are likely to contribute to pathophysiology. In this paper, we have compared the mouse and human at molecular, cellular, and pathway levels to shed light on mechanistic differences with important implications for translation outcomes. Mechanistic modelling specific to species allows us to "embed" and "represent" similarities and differences in innate immunity which can lead to the development of "conflictious information detection engine". It is important to note that our analysis is purely based on the research and publication bias in mouse and human experiments as many mouse experiments are mainly focused on particular explorative areas, and experiments with human tissues are also concentrated on limited areas of disease mechanism. We found that mouse experiments often reveal new molecular interactions between different entities that are not observed or reported in human experiments. Differential analysis of mouse and human model for neuroinflammation shows that mouse and human differ at the molecular and cellular levels, but have more similarities at the pathway levels as numbers indicate. More explicitly, the underlying molecular patterns which lead to a particular bioprocess differ between the two species. This finding implies that although the two species share some similarities at the cellular or pathway level, the pattern of molecular interactions that form, govern, and regulate those pathways is substantially different between mouse and human. > It is notable that mouse models have provided significant insights into many disease areas like cancer; acute promyelocytic leukemia. However, recent drug failures in the area of neurodegeneration have put a question mark behind the extent to which mouse models have been used in preclinical drug discovery and to what extent transgenic mice mimic human brain pathophysiology mechanisms. Pathophysiology mechanisms are likely to act together and they seem to be organized in a temporal cascade of events that ultimately result in a severe disease phenotype. Experiments with single gene knock-out in mice can reveal only minor aspects of the disease perturbations and do not usually allow us to decipher the full complexity of the mechanisms underlying the disease.

[15] Exploring the Role of Inflammation and Metabolites in Bell’s Palsy and Potential Treatment Strategies

  • Authors: Jiaye Lu, Ziqian Yin, Youjia Qiu, Yayi Yang, Zhouqing Chen et al.
  • Year: 2025
  • Venue: Biomedicines
  • URL: https://www.semanticscholar.org/paper/4ce13514569cb37f6aab52f4f13df3e4578cae50
  • DOI: 10.3390/biomedicines13040957
  • PMID: 40299566
  • PMCID: 12024589
  • Citations: 2
  • Summary: This study identifies causal relationships between inflammatory proteins, metabolites, immune cells, and Bell’s palsy, highlighting that the JAK/STAT signaling pathway may be a potentially critical target for intervention in Bell’s palsy and that its modulation may provide new directions and opportunities for therapeutic strategies and drug discovery for the disease.
  • Evidence snippets:
  • Snippet 1 (score: 0.514) > Further KEGG pathway analyses highlighted the potential role of cytokine-cytokine receptor interactions and rheumatoid arthritis pathways in the pathogenesis of Bell's palsy, further supporting the association of the disease with neuroinflammation, immune imbalance and infection. > To further elucidate the potential role of inflammatory immune-related proteins in Bell palsy, we constructed a PPI network and screened 31 high-confidence interacting proteins, among which IL-6 showed a high degree of connectivity. Further analysis showed that VCAM-1, CCL19, IL27RA and IL-6 play important roles in immunomodulation, cell adhesion, inflammatory response and immune cell migration. In addition, based on the MCODE plugin, we identified six core proteins, including VCAM-1, CCL19, IL27RA, OSM, SELL and JAK2, of which VCAM-1, CCL19, OSM and IL27RA passed co-localization analysis. > Our research suggests that CCL19, SELL and VCAM-1 may promote inflammatory cell infiltration and nerve injury through synergistic effects in the pathology of Bell's palsy, and although there is no clear signaling axis linking the three indirect crosstalk, their joint role in immune cell recruitment and vascular endothelial activation may be key to the onset and progression of the disease [25][26][27]. CCL19 acts as a chemokine that attracts T cells and dendritic cells to migrate toward inflammatory sites, whereas SELL, as an adhesion molecule, plays an important role in leukocyte rolling and adhesion, facilitating the penetration of immune cells through the vascular wall and into diseased tissues, which synergistically enhances local inflammatory responses with CCL19 [25,28]. In addition, this process may be further amplified by the up-regulation of VCAM-1 expression, which promotes strong binding of immune cells to endothelial cells by binding to VLA-4 and increases the permeability of the blood-nerve barrier, allowing more immune cells to penetrate into peripheral tissues of the facial nerve, thereby exacerbating local inflammation and nerve injury [26,29].

[16] The use of intra-cellular signaling pathways in anesthesiology and pain medicine field.

  • Authors: J. Joo
  • Year: 2009
  • Venue: Korean journal of anesthesiology
  • URL: https://www.semanticscholar.org/paper/d20f7ea110adebeb95be021611d90522a87a42c1
  • DOI: 10.4097/kjae.2009.57.3.277
  • PMID: 30625873
  • Citations: 1
  • Summary: If efforts are focused on applying the new cellular and molecular biologic research, these efforts could identify the mechanism of diseases and help develop new drugs in the field of anesthesiology and pain medicine.
  • Evidence snippets:
  • Snippet 1 (score: 0.503) > At the level of individual cells, signaling is crucial in cell division, differentiation, metabolic control and death. Reception of the signals depends on receptor proteins that are usually at the cell surface, and these receptor proteins bind the signal molecule. The binding activates the receptor, which in turn activates one or more of the intra-cellular signaling pathways. These relay chains of molecules, mainly intra-cellular signaling proteins, process the signal inside the receiving cell and distribute it to the appropriate intra-cellular targets. Cell signaling pathways are involved in the pathophysiology of many diseases and also in the mechanisms of action of many drugs, including local and general anesthetics. Knowledge of the basic cell signaling mechanisms is essential for understanding many of the pathophysiologic and pharmacologic mechanisms. Therefore, if we focus on applying the new cellular and molecular biologic research, these efforts could identify the mechanism of diseases and help develop new drugs in the field of anesthesiology and pain medicine.

[17] Clinical Prognostic Factors Associated with Good Outcomes in Pediatric Bell’s Palsy

  • Authors: M. Yoo, D. Park, J. Byun, S. Yeo
  • Year: 2021
  • Venue: Journal of Clinical Medicine
  • URL: https://www.semanticscholar.org/paper/2c0e8d61a7ba5cc7f717091b0dde0ecd37b8d825
  • DOI: 10.3390/jcm10194368
  • PMID: 34640384
  • PMCID: 8509832
  • Citations: 13
  • Summary: The results showed that the most important factor influencing the complete recovery of Bell’s palsy in children was the lower initial H–B grade at initial presentation.
  • Evidence snippets:
  • Snippet 1 (score: 0.500) > Acute peripheral facial palsy is uncommon in children, with an annual incidence ranging from 5 to 21 per 100,000 children [1,2]. Idiopathic facial paralysis, known as Bell's palsy, is a disease characterized by acute, unilateral, idiopathic peripheral facial palsy [3]. Unilateral facial weakness of unknown cause develops rapidly, with Bell's palsy considered the most common cause of facial paralysis in children compared with other etiologies, including traumatic, congenital, infectious and neoplastic causes [4][5][6]. The etiology and pathophysiology of Bell's palsy in children are not completely understood. It can be caused by inflammation and edema of the facial nerve fibers, with infiltration of lymphocytes and associated demyelination or axonal degeneration [7,8]. Moreover, infections with many viruses have been reported to cause acute peripheral facial paralysis in children. These findings have suggested that treatment with corticosteroids and/or antiviral agents may be effective in patients with Bell's palsy. Corticosteroid treatment of adults was shown to improve their chances of recovery, especially if treatment is started within 72 h of symptom onset [9]. In contrast to adults, the clinical prognosis of Bell's palsy in children is not well documented. To date, there has been a relative lack of research on the prevalence, treatment, and outcomes of Bell's palsy in children and no standardized treatment guidelines have yet been developed. Therefore, the treatment of children, including the types and dosages of corticosteroids and antiviral agents, is empirical, based on each physician's experience. > The natural progression of Bell's palsy in children is thought to be good, with many children tending to show favorable recovery within two months and most by six months, with spontaneous recovery occurring in up to 90% of children under the age of 14 years [10,11]. > However, the degree of paralysis at onset can affect the degree of recovery and, in the case of severe paralysis, patients are rarely known to achieve a complete recovery of the nerve function [12,13].

[18] Construction of neural system disease models from the perspective of cellular biomechanics and their application in teaching practice

  • Authors: Hong Xue, Qiong Zhao, Zhilan Zhao, Ruozhao Li, Guangyu Li
  • Year: 2025
  • Venue: Frontiers in Bioengineering and Biotechnology
  • URL: https://www.semanticscholar.org/paper/d9021c44bd3dca261a0cc5378c6fdd99e89d7127
  • DOI: 10.3389/fbioe.2025.1715222
  • PMID: 41480584
  • PMCID: 12754723
  • Summary: This approach prepares future healthcare professionals to address complex neurological disorders more effectively by bridging biomechanical insights with clinical and teaching applications, and enriches both research and educational practices.
  • Evidence snippets:
  • Snippet 1 (score: 0.500) > Neurological diseases, including Parkinson's disease, Alzheimer's disease, and stroke, pose a substantial global health burden, impacting millions of individuals and their families worldwide. The World Health Organization has recognized these conditions as critical public health challenges, necessitating urgent attention and innovative approaches to treatment and education. In this context, Maryam (2023) provides a comprehensive overview of the molecular genetic perspective on neurological diseases, emphasizing the complex interplay between genetic predispositions and environmental influences that contribute to the pathogenesis of these disorders. This multifaceted understanding is crucial for developing targeted therapeutic strategies that address the underlying mechanisms of disease progression (Maryam, 2023). > Moreover, Sharma (2022) highlights the emerging interrelationship between the gut microbiome and cellular senescence, suggesting that these factors may significantly influence the onset and progression of neurological diseases. This perspective underscores the importance of considering not only the central nervous system but also peripheral factors that may impact neurological health. The intricate connections between cellular mechanisms and biomechanical processes are vital for elucidating the pathophysiology of neurodegenerative conditions and motor dysfunctions, which often manifest as debilitating symptoms in affected individuals (Sharm, 2022). > The construction of accurate and representative disease models is essential for advancing our understanding of these complex disorders. Such models facilitate the analysis of pathological mechanisms, allowing researchers to investigate the effects of various interventions and treatments. Furthermore, the implications of these models extend beyond research; they hold significant value for educational practices. By integrating cellular biomechanics and disease modeling into the curriculum, educators can provide students with a more comprehensive understanding of neurological diseases, fostering critical thinking and problemsolving skills. This dual significance of model construction-both for elucidating pathological mechanisms and enhancing educational practices-highlights the necessity of incorporating biomechanical perspectives into the study of neurological disorders (Jnana Therapeutics, 2020).

[19] Understanding the Pathophysiology of Atopic Dermatitis – insights into Immune Dysregulation and Skin Barrier Dysfunction

  • Authors: Maja Kucharska, Kacper Kwiliński, Barbara Wawrzyńska, Marlena Cąkała, Adrian Kruszewski et al.
  • Year: 2024
  • Venue: Quality in Sport
  • URL: https://www.semanticscholar.org/paper/9ba8ec050f511e04ecb6b80a72906f5c9323e629
  • DOI: 10.12775/qs.2024.19.54073
  • Summary: Atopic dermatitis is a complex, chronic inflammatory skin disease with a multifaceted pathophysiology involving genetic, immunological, and environmental factors including filaggrin mutations, Th2 cytokine-mediated inflammation, and the skin microbiome.
  • Evidence snippets:
  • Snippet 1 (score: 0.498) > Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a disrupted skin barrier and immune dysregulation. The exact pathophysiology of atopic dermatitis despite extensive research remains complex. It includes genetic disorders, a defect in the epidermal barrier, an altered immune response, and disruption of the skin’s microbial balance. Recent advances in research have provided deeper insights into the molecular mechanisms including the role of filaggrin mutations, Th2 cytokine-mediated inflammation, and the skin microbiome. Understanding the intricate interplay between these components is crucial for developing targeted therapeutic strategies. > Aim of the study: This review provides a comprehensive overview of the current knowledge on the pathophysiological mechanisms underlying AD, highlighting recent advances and areas for future research. > Material and methods: Comprehensive literature searches were performed across the main electronic databases of PubMed and GoogleScholar using the keywords: “atopic dermatitis”, “eczema pathophysiology”, “skin barrier”. > Conclusions: Atopic dermatitis (AD) is a complex, chronic inflammatory skin disease with a multifaceted pathophysiology involving genetic, immunological, and environmental factors. Recent advances in understanding the molecular mechanisms underlying AD have highlighted the importance of skin barrier dysfunction, immune system dysregulation, and microbial interactions in the disease's progression.

[20] Skin Development and Disease: A Molecular Perspective

  • Authors: Iasonas Dermitzakis, Despoina Chatzi, Stella Aikaterini Kyriakoudi, Nikolaos Evangelidis, E. Vakirlis et al.
  • Year: 2024
  • Venue: Current Issues in Molecular Biology
  • URL: https://www.semanticscholar.org/paper/3b0d602b335c265102e2a9f169bab20f51343212
  • DOI: 10.3390/cimb46080487
  • PMID: 39194704
  • PMCID: 11353016
  • Citations: 15
  • Influential citations: 1
  • Summary: By delving into the molecular mechanisms implicated in developmental processes, as well as in the pathogenesis of diseases, a comprehensive understanding of these aspects paves the way for developing innovative targeted therapies and personalised treatment approaches for various skin conditions.
  • Evidence snippets:
  • Snippet 1 (score: 0.497) > Understanding the molecular mechanisms underlying congenital skin diseases and cancer has significantly advanced in recent years, providing crucial insights into the pathogenesis of these conditions. Researchers have uncovered key genetic mutations, signalling cascades, and cellular interactions that drive the development and progression of these disorders by unravelling the intricate molecular pathways affected. This section emphasises that the various molecular signals involved in embryonic development are also implicated in the pathophysiology of certain congenital skin diseases and types of cancer. Analysing these connections provides valuable insights into the molecular mechanisms underlying both skin development and the pathogenesis of skin cancers, such as basal cell and squamous cell carcinoma. Skin cancers often stem from disruptions in essential biological pathways that are also involved in normal skin development. Therefore, identifying these specific molecules can pave the way for developing new targeted therapies through laboratory-based interventions.

Notes

  • This provider combines search_papers_by_relevance with snippet_search.
  • No synthesis or second-stage model call is performed.