Resolution of anti-LGI1-associated autoimmune encephalitis in a patient after treatment with efgartigimod.

BACKGROUND: Anti leucine-rich, glioma inactivated 1 (LGI1) antibody-associated autoimmune encephalitis (AE) is the second most common AE, where the trafficking and recycling of the pathogenic immunoglobulin (IgG) can be controlled by the neonatal crystallizable fragment receptor (FcRn), making the latter as a candidate therapeutic target. Efgartigimod is an antagonist of FcRn, its ability to increase the degradation of IgGs and improve the health and quality of life of patients. ADAPT trail indicated its rapid efficacy and safety on myasthenia gravis. However, there is currently no case reported using efgartigimod for the treatment of anti-LGI1-associated AE. CASE DESCRIPTION: The patient presented with five episodes of generalized tonic-clonic seizures in the past 2 weeks. The patient had no abnormal signs on magnetic resonance imaging. Electroencephalogram examinations showed an increase in bilateral symmetric or asymmetric slow activity, without any clear epileptic waves. The cerebrospinal fluid (CSF) examination results indicated a slight increase in protein (47 mg/dL). The anti-LGI1 antibody titer in serum was 1:100 and that in CSF was 1:3.2. The treatment with intravenous methylprednisolone 1000 mg once a day combined with levetiracetam tablets failed to completely control the patient's seizures. Thus, 10 mg/kg efgartigimod was administered intravenously once a week for 2 weeks. After 2 weeks of treatment, serum levels of anti-LGI1 antibody and IgG decreased and the patient's epilepsy did not recur in the next 3 months. CONCLUSIONS: This is the first case report of using efgartigimod to treat anti-LGI1-associated AE. The combination of efgartigimod and methylprednisolone resulted in favorable outcomes, indicating that this is an optional treatment plan.

Expression of mGluR5 in Pediatric Hodgkin and Non-Hodgkin lymphoma-A Comparative Analysis of Immunohistochemical and Clinical Findings Regarding the Association between Tumor and Paraneoplastic Neurological Disease.

Autoantibodies targeting the neuronal antigen metabotropic glutamate receptor 5 (mGluR5) have been identified in patients with Ophelia syndrome, which describes a co-occurrence of paraneoplastic limbic encephalitis and Hodgkin lymphoma (HL). Little data exist regarding frequency and function of mGluR5 in HL and its potential role in causing seropositive paraneoplastic disease. We studied a representative cohort of pediatric HL and NHL patients (n = 57) using immunohistochemistry and fluorescence staining to investigate mGluR5 expression. All lymphoma tissues displayed positive mGluR5 staining, with focus on Hodgkin-Reed-Sternberg (H-RS) cells. We did not detect any mGluR5 staining in tumor-free lymph nodes, which is consistent with the absence of GRM5 transcripts in RNA-sequencing data from non-malignant B and T cells. The frequent presence in pediatric lymphoma falls in line with reports of mGluR5 expression and associated tumor progression in other malignancies. We tested for correlation with clinical features, focusing on disease progression and neurological symptoms. Low mGluR5 expression in H-RS cells correlated with young patient age (<15 years) and positive histology for EBV infection. Paraneoplastic or neurological symptoms were found exclusively in HL patients. While an impact of mGluR5 on HL severity remains possible, a prognostic value of mGluR5 expression levels requires further investigation.

Severe Relapsing Autoimmune Encephalitis with GABAA Receptor, Titin, and AchR Antibodies in a Patient with Thymoma: A Case Report.

Introduction: We report a challenging case of autoimmune encephalitis in a patient with a thymoma harboring titin and acetylcholine receptor antibodies, who experienced multiple relapses despite thymectomy and aggressive first-line immunotherapy, and for whom GABAA receptor antibodies were ultimately identified. Case Presentation: This 40-year-old man presented with headaches, weakness, diplopia, hearing loss, and seizures progressing to status epilepticus. Brain MRI showed multifocal cortical and subcortical T2/fluid attenuated inversion recovery hyperintense lesions without enhancement. Initial neural antibody testing identified only acetylcholine receptor and titin antibodies. He presented multiple severe relapses despite complete thymoma resection, intravenous methylprednisolone with immunoglobulins or plasmapheresis, and mycophenolate mofetil. Second-line immunotherapy with rituximab was successful to alleviate symptoms and normalize the EEG and MRI after identification of anti-GABAA receptor antibodies on more comprehensive neural antibody testing for autoimmune encephalitis. Conclusion: This case demonstrates the complexity and importance of identifying pathogenic antibodies and selecting 2nd line treatment accordingly in patients with autoimmune encephalitis when multiple antibodies coexist. Despite tumor resection, aggressive immunotherapy may be needed to prevent further deterioration in anti-GABAA receptor encephalitis.

A Rare Case of Coronavirus Disease 2019 Encephalitis Mimicking Creutzfeldt-Jacob Disease in an Immunocompromised Patient: A Case Report.

Introduction: Coronavirus disease 2019 (COVID-19) encephalitis is characterized by viral entry into the brain, resulting in inflammation and a cascade of neuronal damage. Clinical manifestations include headaches, seizures, and movement disorders. A mortality rate of 20% and infrequent presentation make COVID-19 encephalitis a diagnostic challenge. Case Presentation: We hereby present the case of a 55-year-old man with a history of diabetes mellitus (potential impact on COVID-19 severity discussed in the supplementary material) presenting with altered sensorium, swelling in the left eye, and involuntary jerky limb movements. Neurological examination revealed neck rigidity, myoclonic jerks, and an extensor plantar response. Brain magnetic resonance imaging (MRI) was performed, which revealed cortical enhancement in the bifrontal, temporal, and occipital lobes. Rapid progression of myoclonus, altered sensorium, and cortical enhancement on MRI suggested Creutzfeldt-Jacob disease. After a thorough workup, the diagnosis was COVID-19 encephalitis with rhino-orbital mucormycosis. The treatment regimen consisted of adequate glycemic control, remdesivir injection, intravenous and retroorbital liposomal amphotericin, and levetiracetam. The patient's condition improved, and he was eventually discharged. Conclusion: This case illustrates the uncommon presentation of COVID-19 with neurological involvement and emphasizes the value of history-taking, neuroimaging, and cerebrospinal fluid analysis. A high index of suspicion is critical for a prompt diagnosis and initiating therapy.

West Nile Virus: A Neglected Cause of Bell's Palsy?

The West Nile virus (WNV) is the leading cause of mosquito-borne disease in the United States. Bell's palsy (BP) is a clinical syndrome associated with viral infections, but an association with West Nile virus (WNV) is not well-described, with only two cases reported in the literature. We present a case of a 68-year-old woman presenting with fevers and encephalopathy. Cerebrospinal fluid was positive for WNV. Following improvement, she developed facial weakness and was diagnosed with BP secondary to the WNV infection. Identifying BP associated with WNV infection may have significant clinical implications, but further studies are needed to fully characterize a causative relationship.

Anti-contact protein-associated protein 2 antibody encephalitis in children: A case report.

BACKGROUND: Anti-contactin-associated protein-like 2 (CASPR2) antibody encephalitis is an autoimmune disorder characterized by the presence of antibodies against the voltage-gated potassium channel. This leads to neurological symptoms, such as seizures, cognitive decline, and neuropathic pain, primarily affecting the limbic system. The prognosis of this disorder varies among individuals. CASE SUMMARY: The patient, a girl aged nine years and nine months, underwent treatment for 14 to 21 d. The main clinical manifestations were vomiting and unclear consciousness, positive pathological signs, normal cranial computed tomography and magnetic resonance imaging, and abnormal electroencephalogram. The child was discharged after receiving immunoglobulin and hormone treatment. Subsequent follow-up over a period of 15 months after discharge, conducted through telephone and outpatient visits, showed no recurrence of symptoms. CONCLUSION: Anti-CASPR2 antibody autoimmune encephalitis in children is rare, mainly manifested as convulsions, mental abnormalities, cognitive impairment, and neuropathic pain, among others. Timely evaluation for autoimmune encephalitis antibodies is crucial, especially in cases of recurrent central nervous system involvement in children.

Novel diagnostic and prognostic approach for rapidly progressive dementias: Indicators based on amyloid/tau/neurodegeneration (ATN) framework.

AIMS: Apply established cerebrospinal fluid (CSF) and serum biomarkers and novel combined indicators based on the amyloid/tau/neurodegeneration (ATN) framework to improve diagnostic and prognostic power in patients with rapidly progressive dementias (RPDs). METHODS: CSF and serum biomarkers of Alzheimer's disease (AD) common neuropathology including Aß42, Aß40, p-Tau, and t-Tau were measured in cognitively normal (CN) controls (n = 33) and three RPD groups with rapidly progressive AD (rpAD, n = 23), autoimmune encephalitis (AE, n = 25), and Creutzfeldt-Jakob disease (CJD, n = 28). Logistic regression and multiple linear regression were used for producing combined indicators and prognostic assessment, respectively, including A&T, A&N, T&N, A&T&N, etc. RESULTS: Combined diagnostic indicator with A&T&N had the potential for differentiating AE from other types of RPDs, identifying 62.51% and 75% of AE subjects based on CSF and serum samples, respectively, compared to 39.13% and 37.5% when using autoantibodies. CSF t-Tau was associated with survival in the CJD group (adjusted R-Square = 0.16, p = 0.02), and its prognosis value improved when using combined predictors based on the ATN framework (adjusted R-Square = 0.273, p = 0.014). CONCLUSION: Combined indicators based on the ATN framework provide a novel perspective for establishing biomarkers for early recognition of RPDs due to treatment-responsive causes.

Neuropsychiatric manifestations of anti-N-methyl-D-aspartate receptor encephalitis in a 14-year-old female: A case report.

Key Clinical Message: This case underscores the critical importance of timely recognition and management of NMDAR encephalitis in adolescents to mitigate potential long-term sequelae. If a pediatric patient presents with suspected viral encephalitis, autoimmune etiology must be excluded via cerebrospinal fluid antibody assay to guide appropriate immunosuppressive therapy, and improve patient outcomes. Abstract: Autoimmune encephalitis particularly involving the n-methyl-d-aspartate receptor (NMDAR) is recognized as a rare cause of acute encephalopathy in pediatric patients. The following case is of a 14-year-old female diagnosed with anti-NMDAR encephalitis who initially presented with fever, episodic convulsions, and loss of consciousness. She subsequently developed right-sided body weakness, expressive aphasia, and visual hallucinations. Clinical examination revealed prominent neuropsychiatric manifestations such as altered sensorium, motor deficits, hallucinations, and visual disturbances. Cerebello-bulbar signs were not appreciable in this particular case. She was treated for viral encephalitis but showed no improvement. Laboratory investigations revealed the presence of NMDAR antibodies in the cerebrospinal fluid confirming the diagnosis of autoimmune etiology. The patient demonstrated notable improvement following immunosuppressive treatment.

Recurrent COVID-19-related psychotic disorder with neuro-immuno-endocrine dysfunction as a possible underlying mechanism: A case report from China.

Background: SARS-CoV-2, first identified in Wuhan, China, in December 2019, has been gradually spreading worldwide since 2020. The relationship between SARS-CoV-2 infection and psychotic disorders has received much attention, and several studies have described the direct/indirect mechanisms of its effects on the brain, but no mechanism has been found to explain recurrent episodes of COVID-19-related psychotic symptoms. Case: We report the case of an 18-year-old female patient with no family or personal psychotic disorder history with multiple hospital admissions with symptoms such as disorganized speech and behavior, hyperactivity, restlessness, and impulsive aggression during the COVID-19 recovery period. Relevant tests revealed longitudinal changes such as persistent IL-6 and IL-10 elevation, abnormal discharges on EEG, and brain and hippocampal MRI abnormal signals. The patient was treated with antipsychotics, MECT, combination therapy of hormones and antivirals, then discharged after multiple treatment rounds. Conclusion: The case presented here outlines the possibility that the COVID-19 recovery period may be a critical period for acute psychotic episodes and that the patient's recurrent psychotic symptoms may be associated with neuro-immuno-endocrine dysfunction mediated by sustained cytokine synthesis, further causing structural and functional brain damage. Routine psychiatric evaluation and related screening should be performed at all stages of the illness to better identify, prevent, and effectively intervene in psychiatric disorders following COVID-19. Because many outcomes require long-term assessment, a clearer understanding of the impact of the COVID-19 epidemic on mental health is likely to emerge in the future.

Clinical analysis of Bornavirus Encephalitis cases demonstrates a small time window for Etiological Diagnostics and treatment attempts, a large case series from Germany 1996-2022.

PURPOSE: The emerging zoonotic Borna disease virus 1 (BoDV-1) and the variegated squirrel bornavirus 1 (VSBV-1) cause severe and fatal human encephalitis in Germany. We conducted the first systematic clinical analysis of acute, molecularly confirmed fatal bornavirus encephalitis cases comprising 21 BoDV-1 and four VSBV-1 patients to identify options for better diagnosis and timely treatment. METHODS: Analyses were based on medical records and, for BoDV-1, on additional medical interviews with patients' relatives. RESULTS: Disease onset was unspecific, often with fever and headache, inconsistently mixed with early fluctuating neurological symptoms, all rapidly leading to severe encephalopathy and progressive vigilance decline. Very shortly after seeking the first medical advice (median time interval 2 and 0 days for BoDV-1 and VSBV-1, respectively), all except one patient were hospitalised upon manifest neurological symptoms (median 10 and 16 days respectively after general symptom onset). Neurological symptoms varied, always progressing to coma and death. BoDV-1 and VSBV-1 patients required ventilation a median of three and five days, and died a median of 32 and 72 days, after hospitalisation. Death occurred mostly after supportive treatment cessation at different points in time based on poor prognosis. Disease duration therefore showed a wide, incomparable range. CONCLUSION: The extremely rapid progression is the most obvious clinical characteristic of bornavirus encephalitis and the timeframe for diagnosis and targeted therapy is very short. Therefore, our results demand an early clinical suspicion based on symptomatology, epidemiology, imaging, and laboratory findings, followed by prompt virological testing as a prerequisite for any potentially effective treatment.

Anti-CRMP2 antibody induces anxiety-like behavior and increases pyramidal neuron excitability in mice.

BACKGROUND: We have previously identified auto-antibody (Ab) to collapsin response mediator protein 2 (CRMP2) in patients with encephalitis. The present study aims to evaluate the pathogenic effects of anti-CRMP2 Ab. METHODS: Recombinant CRMP2 protein was injected subcutaneously into mice to establish an active immune mouse model with anti-CRMP2 Ab. Behavioral assessments, histopathological staining, and electrophysiological testing were performed to identify any pathogenic changes. RESULTS: The mice exhibited signs of impaired motor coordination four weeks post-immunization of CRMP2 protein. Moreover, CRMP2 immunized mice for eight weeks showed anxiety-like behaviors indicating by tests of open field and the elevated plus maze. After incubating the CA1 region of hippocampal brain section with the sera from CRMP2 immunized mice, the whole-cell path-clamp recordings showed increased excitability of pyramidal neurons. However, no obvious inflammation and infiltration of immune cells were observed by histopathological analysis. Western blot showed that the phosphorylation levels of CRMP2-Thr514 and -Ser522 were not affected. CONCLUSION: In an active immunization model with CRMP2 protein, impaired coordination and anxiety-like behaviors were observed. Also, anti-CRMP2 Abs containing sera heightened the excitability of hippocampal pyramidal neurons in vitro, which imply the pathogenic effects of anti-CRMP2 Ab.

The clinical and predictive value of 18F-FDG PET/CT metabolic patterns in a clinical Chinese cohort with autoimmune encephalitis.

AIMS: To investigate the diagnostic and predictive role of 18F-FDG PET/CT in patients with autoimmune encephalitis (AE) as a whole group. METHODS: Thrty-five patients (20 females and 15 males) with AE were recruited. A voxel-to-voxel semi-quantitative analysis based on SPM12 was used to analyze 18F-FDG PET/CT imaging data compared to healthy controls. Further comparison was made in different prognostic groups categorized by modified Rankin Scale (mRS). RESULTS: In total, 24 patients (68.6%) were tested positive neuronal antibodies in serum and/or CSF. Psychiatric symptoms and seizure attacks were major clinical symptoms. In the acute stage, 13 patients (37.1%) demonstrated abnormal brain MRI results, while 33 (94.3%) presented abnormal metabolism patterns. 18F-FDG PET/CT was more sensitive than MRI (p < 0.05). Patients with AE mainly presented mixed metabolism patterns compared to the matched controls, demonstrating hypermetabolism mainly in the cerebellum, BG, MTL, brainstem, insula, middle frontal gyrus, and relatively hypometabolism in the frontal cortex, occipital cortex, temporal gyrus, right parietal gyrus, left cingulate gyrus (p < 0.05, FWE corrected). After a median follow-up of 26 months, the multivariable analysis identified a decreased level of consciousness as an independent risk factor associated with poor outcome of AE (HR = 3.591, p = 0.016). Meanwhile, decreased metabolism of right superior frontal gyrus along with increased metabolism of the middle and upper brainstem was more evident in patients with poor outcome (p < 0.001, uncorrected). CONCLUSION: 18F-FDG PET/CT was more sensitive than MRI to detect neuroimaging abnormalities of AE. A mixed metabolic pattern, characterized by large areas of cortical hypometabolism with focal hypermetabolism was a general metabolic pattern. Decreased metabolism of right superior frontal gyrus with increased metabolism of the middle and upper brainstem may predict poor long-term prognosis of AE.

Current Mycoplasma pneumoniae outbreak: Don't forget its role in Bickerstaff encephalitis.

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia in children and young adults. It is responsible of a broad array of extrapulmonary manifestations, the most severe affecting the central nervous system. We report a challenging diagnosis of macrolide-resistant M. pneumoniae-induced Bickerstaff encephalitis in a 16-year-old man.

Focal Seizures Induced by Paraneoplastic Syndrome Leading to a Diagnosis of Small Cell Lung Carcinoma.

Paraneoplastic neurological disorders are a rare complication of multiple neoplasms, such as lung, testis, and breast, and can be associated with positive antibody anti-Hu (anti-neuronal nuclear antibody type 1 or ANNA-1), anti-Ta, anti-Ma, and uncharacterized antibody, or be antibody-negative. Early treatment of the underlying tumor is the most likely modality that will lead to regression of the paraneoplastic neurological symptoms. Here, we present a case of a 73-year-old female with new-onset seizure activity from ANNA-1 encephalitis found to have undiagnosed small cell lung cancer to highlight the need for further workup for malignancy.

A Changed Man: A Rare Case of Behcet's Disease Autoimmune Encephalitis.

Behcet's disease (BD) is characterized by recurrent oral ulcers with concomitant systemic multi-organ involvement, which may include neurological disease, ocular disease, vascular disease, genital ulcers, skin lesions, and arthritis. The clinical symptoms arise from vasculitis that involves small, medium, and large blood vessels. We present the case of a young male who presented with atypical Behcet's autoimmune encephalitis with recurrent oral ulcers, neurological manifestations, HLA-B51 positivity, abnormal EEG findings, and improvement following multiple plasma exchange treatments.

A devastating case of a Balamuthia mandrillaris pediatric brain infection.

Balamuthia mandrillaris is an amoeba that causes an uncommon but deadly encephalitis, referred to as granulomatous amoebic encephalitis (GAE). The highest incidence reported worldwide has occurred in America, and within the United States, it has been highest in the Southwest affecting predominantly children and young men of Hispanic ethnicity. Clinical presentation of GAE includes fever, headache, nausea, vomiting, lethargy, irritability, stiff neck, hallucinations, photophobia, and seizures. Our patient was a Hispanic male child living in Arizona. The patient presented at 3 years of age for severe encephalitis. Symptoms included difficulty with balance, gait, and sitting up and seizure-like activity. Initial CT showed an area of decreased density consistent with edema in the right frontal and left frontoparietal lobes. Rapid progression was seen on further imaging over the length of the patient's hospital stay revealing diffusion restriction, necrosis/blood products, edema, and hemorrhage. The patient expired three weeks after onset of symptoms and one week after admission to our institution. While there are multiple biochemical techniques that can test for B. mandrillaris, they are rarely employed for multiple reasons stemming from the rare occurrence of this infection. Because of the fatal nature of this infection, we propose (1) testing should be considered if a patient presents with progressing encephalitis on imaging and other pathogenic etiologies are ruled out and (2) the threshold to treat empirically should be low due to the fatal nature of the infection.

Acute Encephalitis During a SARS-CoV-2 Infection: A Case Report.

It was in December 2019 that the coronavirus causing COVID-19 was first detected in Wuhan, China. Although the primary clinical presentation is respiratory disease, an increasing number of reports worldwide have noted various neurological manifestations, such as acute encephalitis. We present a case of a 49-year-old female admitted with afebrile impaired consciousness, diagnosed with acute encephalitis and a severe infection of COVID-19. Clinical and radiological improvement was observed following treatment with corticosteroids.

Anti-LGI1 Autoimmune Encephalitis in a Patient with Rheumatoid Arthritis and MGUS.

Background: Anti-leucine-rich glioma inactivated 1 limbic encephalitis (anti-LGI1 LE) is one of the most frequent autoimmune encephalitis, commonly coexisting with other autoimmune diseases. Rheumatoid arthritis (RA) and monoclonal gammopathy of unknown significance (MGUS) are commonly associated with autoimmune phenomena. However, neither RA nor MGUS have been described in the literature to date as coexisting with anti-LGI1 LE. Case description: We present the case of anti-LGI1 LE in a male patient with rheumatoid arthritis, who was also found to have an MGUS. The patient was initially treated with corticosteroids and IV immunoglobulin. After a mild relapse, his treatment was complemented with rituximab, resulting in complete regression of the disease symptoms. Conclusions: Our report provides evidence for the coexistence of anti-LGI1 LE with RA and/or MGUS, thus extending the differential diagnosis of patients suffering with these disease entities that present with neuropsychiatric symptoms suggestive of encephalitis. Moreover, this case raises challenges on the management of the coexistence of these diseases, given the lack of therapeutic guidelines and their potential interaction on a pathophysiological and a clinical level. LEARNING POINTS: In a patient with known autoimmune or malignant background who presents with neuropsychiatric symptoms, after excluding infectious encephalitis or central nervous system involvement in the primary disease condition, autoimmune limbic encephalitis (LE) should also be considered.In a patient diagnosed with anti-LGI1 LE there should be an extensive check for coexisting occult pre-malignant conditions, even for months after disease presentation.Clinical management and treatment options of anti-LGI1 LE when coexisting with other autoimmune or pre-malignant conditions can be challenging; thus, more research is needed towards that direction.

The spectrum of anti-GQ1B antibody syndrome: beyond Miller Fisher syndrome and Bickerstaff brainstem encephalitis.

INTRODUCTION: Since the initial identification of Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE),significant milestones have been achieved in understanding these diseases.Discoveries of common serum antibodies (IgG anti-GQ1b), antecedent infections, neurophysiological data, andneuroimaging suggested a shared autoimmune pathogenetic mechanism rather than distinct pathogenesis, leadingto the hypothesis that both diseases are part of a unified syndrome, termed "Fisher-Bickerstaff syndrome". The subsequent identification of atypical anti-GQ1b-positive forms expanded the classification to a broader condition known as "Anti-GQ1b-Antibody syndrome". METHODS: An exhaustive literature review was conducted, analyzing a substantial body of research spanning from the initialdescriptions of the syndrome's components to recent developments in diagnostic classification and researchperspectives. RESULTS: Anti-GQ1b syndrome encompasses a continuous spectrum of conditions defined by a common serological profilewith varying degrees of peripheral (PNS) and central nervous system (CNS) involvement. MFS and BBE represent theopposite ends of this spectrum, with MFS primarily affecting the PNS and BBE predominantly involving the CNS.Recently identified atypical forms, such as acute ophthalmoparesis, acute ataxic neuropathy withoutophthalmoparesis, Guillain-Barré syndrome (GBS) with ophthalmoparesis, MFS-GBS and BBE-GBS overlap syndromes,have broadened this spectrum. CONCLUSION: This work aims to provide an extensive, detailed, and updated overview of all aspects of the anti-GQ1b syndromewith the intention of serving as a stepping stone for further shaping thereof. Special attention was given to therecently identified atypical forms, underscoring their significance in redefining the boundaries of the syndrome.

Mild Encephalopathy/Encephalitis With Reversible Splenial Lesion Associated With Meningitis Related to Mumps Disease: An Unusual Presentation in a Male Adult.

Mild encephalitis/encephalopathy with reversible splenial lesion (MERS) is characterized by mild neurological manifestations associated with spontaneously reversible lesions of the splenium of the corpus callosum. While various conditions and diseases can trigger MERS, infectious causes predominate, with mumps being notably linked to MERS in the pediatric population. Although rare in adults, there are sporadic case reports associating mumps with MERS. Here we report a 23-year-old male patient with a typical presentation of mumps who presented with meningeal syndrome, dizziness, seizures, and right orchitis. Brain MRI showed classic findings of MERS syndrome while cerebrospinal fluid analysis demonstrated lymphocytic pleocytosis. Our patient had a confirmed diagnosis of mumps disease with multiple complications, including MERS, meningitis, and orchitis, and was managed with symptomatic medications and antiviral therapy. Subsequently, there was a gradual resolution of these manifestations and the outcome was favorable, with no residual sequelae.