ABSTRACT
Intro: Coronavirus disease (COVID-19) is currently a global health crisis and is caused by a new strain of coronavirus. However, emerging literature of case reports noted possible extrapulmonary manifestations of the disease. Because COVID 19 is a relatively new disease, at present, little existing literature tackles the diagnosis and therapeutic management of COVID-19-related conditions outside the pulmonary system. Method(s): This is a case of a 24-year-old male presented with the chief complaint of sudden stiffening of all extremities. Non-contrast computed tomography (CT) scan was unremarkable. Chest X-ray revealed interstitial pneumonia and SARS-CoV-2 RT-PCR (OPS/NPS) was positive. Electrocardiogram (ECG) findings showed supraventricular tachycardia and had elevated Troponin I levels. Pertinent physical findings noted were slurring of speech, dysmetria, and vertical nystagmus. Finding(s): The patient was initially treated as a case of Bacterial Abscess versus Viral encephalitis. Pericardial ultrasound revealed small pericardial effusion and was started on Colchicine. Repeat cranial CT scan noted unremarkable results but due to persistence of symptoms, the patient was started with Dexamethasone. On Day 16 of illness, the patient was noted to have full resolution of symptoms. Rapid antibody testing was done which revealed positive for both IgG and IgM hence the patient was discharged with the final diagnosis of Viral Myopericarditis resolved, Viral encephalitis resolved, COVID-19 pneumonia recovered. Conclusion(s): Extrapulmonary manifestations have been reported increasingly as an atypical presentation of COVID 19 infection. Early recognition of viral myopericarditis and viral encephalitis as a manifestation of COVID 19 can lead to the initiation of proper treatment and management. More reports on these cases can aid future studies on diagnostics and therapeutic approaches during the COVID-19 pandemic.Copyright © 2023
ABSTRACT
Increasingly prevalent acute and chronic human brain diseases are scourges for the elderly. Besides the lack of therapies, these ailments share a neuroinflammation that is triggered/sustained by different innate immunity-related protein oligomers called inflammasomes. Relevant neuroinflammation players such as microglia/monocytes typically exhibit a strong NLRP3 inflammasome activation. Hence the idea that NLRP3 suppression might solve neurodegenerative ailments. Here we review the recent Literature about this topic. First, we update conditions and mechanisms, including RNAs, extracellular vesicles/exosomes, endogenous compounds, and ethnic/pharmacological agents/extracts regulating NLRP3 function. Second, we pinpoint NLRP3-activating mechanisms and known NLRP3 inhibition effects in acute (ischemia, stroke, hemorrhage), chronic (Alzheimer's disease, Parkinson's disease, Huntington's disease, MS, ALS), and virus-induced (Zika, SARS-CoV-2, and others) human brain diseases. The available data show that (i) disease-specific divergent mechanisms activate the (mainly animal) brains NLRP3; (ii) no evidence proves that NLRP3 inhibition modifies human brain diseases (yet ad hoc trials are ongoing); and (iii) no findings exclude that concurrently activated other-than-NLRP3 inflammasomes might functionally replace the inhibited NLRP3. Finally, we highlight that among the causes of the persistent lack of therapies are the species difference problem in disease models and a preference for symptomatic over etiologic therapeutic approaches. Therefore, we posit that human neural cell-based disease models could drive etiological, pathogenetic, and therapeutic advances, including NLRP3's and other inflammasomes' regulation, while minimizing failure risks in candidate drug trials.
ABSTRACT
Background/Purpose: The coronavirus disease 2019 (COVID-19) pandemic has led to the emergence of a severe associated condition, multisystem inflammatory syndrome in adults (MIS-A). Initially identified in children as MIS-C, literature regarding the clinical manifestations, illness progression, and treatment of MIS-A are limited. Method(s): This study describes a case of MIS-A presenting as fever and seizures. She was initially given steroids and IVIG, and due to recurrence of fever, she was later treated with tocilizumab. Result(s): The patient was a 55-year- old Filipino female presenting to the emergency department with five days of fever, headache, and disorientation. Lumbar tap was done, which showed elevated opening pressure, normal leukocyte count, normal glucose, slightly elevated protein, and no microorganisms. She was admitted and managed as a case of viral encephalitis. On hospital day 6, she had sudden onset of head-jerking and further decrease in sensorium, hence she was transferred to the intensive care unit. Brain MRI was unremarkable, and subsequent immune-mediated encephalitis was considered. The patient underwent methylprednisolone pulse therapy and IVIG infusion, which provided immediate improvement of sensorium and resolution of fever episodes. Her condition stabilized, and she was transferred out of intensive care. She underwent physical and occupational rehabilitation as preparation for discharge. Two weeks after infusion therapy, on hospital day 26, patient had recurrence of fever episodes and persistence of elevated inflammatory markers. The patient had reported a previous COVID-19 infection 10 weeks prior to admission and received a booster dose of Moderna (Spikevax) COVID-19 vaccine three weeks prior. She tested positive for ANA (1:640, nuclear speckled), while the rest of the autoimmune antibody tests were negative. She was diagnosed as MIS-A based on the following: documented fever (>=38 degrees centigrade) for >=24 hours prior to hospitalization;new-onset neurologic signs and symptoms including seizures and encephalopathy in a patient without prior cognitive impairment;elevated CRP, ferritin, IL-6, and ESR;and a positive SARS-CoV- 2 test for recent infection by RT-PCR. Patient was treated with a locally available monoclonal antibody, tocilizumab, which was given on hospital day 43. Following infusion, she had lysis of fever and marked decrease in CRP, ferritin, IL-6, and ESR. Patient was discharged improved and without end-stage organ damage. Conclusion(s): Immunomodulators target hyperinflammation seen in MIS-A. There may be a role for the use of tocilizumab via blockage of IL-6. MIS-A remains a topic for research, particularly its disease characteristics, management, and relation to a dysregulated immune system.
ABSTRACT
Objective: The objective of this study is to determine the frequency of seizures in adult hospitalized patients with COVID-19 without a prior history of epilepsy. Background: Infection with COVID-19 has been associated with neurological complications such as headache, dizziness, peripheral neuropathy, and acute vascular events. Acute onset seizures have been reported as a rare neurological complication in patients with COVID-19 infection. Design/Methods: PUBMED and EMBASE were searched from 12/01/2019 - 3/31/2021 in accordance with PRISMA guidelines, using the MESH terms ((Seizure) OR (Electroencephalography) OR (Status Epilepticus)) AND (COVID-19). The primary outcome was frequency of new onset seizure in hospitalized COVID-19 patients. Secondary outcomes were frequency of seizure in patients who had Electroencephalography (EEG) completed, risk of abnormal CerebroSpinal Fluid (CSF) results, and risk of abnormal imaging in patients with COVID-19. An inverse variance meta-analysis of single proportions was performed using the double arcsine method. A random effects model was used due to high inconsistency within the studies. Results: Ninety-four studies identifying 333 patients with COVID-19 and new onset seizures were included. Frequency of new onset seizures in adult hospitalized patients with COVID-19 was 0.71% ([95% confidential interval]: [0.16-1.65], I2=89%, 147/28242 patients). Frequency of seizures in hospitalized COVID-19 patients who had EEG completed was 8.49% ([95% confidential interval]: [0.62-24.07], I2=14%, 44/535 patients). The risk of abnormal imaging by either CT head, MRI or vessel imaging was 43.85% ([95% confidential interval]: [17.47-72.27%], I2=58%, 58/128 patients). The risk of abnormal CSF results was 43.03% ([95% confidential interval]: [4.28-88.35], I2=41%, 28/58 patients). Conclusions: The frequency of new onset seizures in patients with COVID-19 was 0.71% ([95% confidential interval]: [0.16-1.65], I2=89%, 147/28242 patients). Slightly less than half of COVID-19 patients with seizures had evidence of structural abnormalities on head imaging as a complication from infection. A small percentage of patients with COVID-19 and seizures were diagnosed with acute viral encephalitis.
ABSTRACT
Objective: NA Background: Previous case reports have described 3 cases of autoimmune encephalitis and 1 case of new-onset refractory status epilepticus (NORSE) following COVID-19 viral vector vaccinations. However, no cases have been documented in association with COVID-19 mRNA vaccinations. We describe a case of NORSE after vaccination with Pfizer-BioNTech COVID-19 vaccine. Design/Methods: Case report. Results: A 56 year old healthy man presented with three days of fever, fatigue, and aphasia beginning 2 weeks after he received his first dose of the Pfizer-BioNTech COVID-19 vaccine. Video EEG showed temporally predominant seizures occurring independently bilaterally (right greater than left). Clinical seizures were characterized by head turn to the left and right hand movements. He then developed sustained right frontotemporal spike and slow wave activity consistent with non-convulsive status epilepticus. CSF demonstrated mild lymphocytic pleocytosis with WBC 16 cells/mm3, protein 24, glucose 76, and an opening pressure of 47. CSF bacterial and viral encephalitis panels, HSV, lyme, West Nile virus, and VDRL were all negative. Oligoclonal bands, paraneoplastic panel, and encephalopathy panel were negative. Systemic malignancy workup was negative. Initial MRI brain was unremarkable, but 1 week after symptom onset he developed bilateral hippocampal edema. The patient was empirically treated with broad spectrum antibiotics and antivirals which were later discontinued. Due to presumed diagnosis of autoimmune encephalitis, he was treated with high dose steroids, plasmapheresis, IVIG, and rituximab. He was treated with progressively escalating anti-seizure medications including midazolam, propofol, and ketamine continuous infusions and eventually stabilized on levetiracetam, lacosamide, phenobarbital, clobazam, zonisamide, oxcarbazepine, and perampanel. At the time of discharge, mental status had improved and aphasia resolved. Conclusions: To our knowledge, this is the first case of NORSE reported after Pfizer COVID-19 vaccination. While no test exists to definitively establish causality, these findings warrant further investigation of the possible association between COVID-19 vaccination and autoimmune encephalitis.
ABSTRACT
The pathophysiological underpinnings of central nervous system (CNS) involvement in SARS-CoV-2 infection, as well as the profile of adverse neuropsychiatric effects of pharmacological agents employed in the management of COVID-19, are yet to be elucidated. Here, we report a 43-year-old female patient who suffered from COVID-19 and who developed new-onset psychotic agitated behavior which may be related to either the COVID-19 infection itself or to the drugs that were used in the treatment. On her third day of treatment with oseltamivir, hydroxychloroquine, and azithromycin, the patient, who had no previous background of neurological or psychiatric diagnosis, presented with a new-onset psychomotor agitation with auditory hallucinations and insomnia. Her psychiatric symptoms have improved with oral olanzapine 5 mg/d. This report underscores the importance of neuropsychiatric monitoring in patients with COVID-19. Clinicians should be aware of the limited knowledge on the neuropsychiatric safety profile of the medication used for COVID-19 treatment, while they have focused on the neuropsychiatric outcomes of COVID-19 itself.