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Author

Zufe Rizvi

Other affiliations: Boca Raton Regional Hospital
Bio: Zufe Rizvi is an academic researcher from Florida Atlantic University. The author has contributed to research in topics: Coronavirus & Myasthenia gravis. The author has an hindex of 2, co-authored 3 publications receiving 107 citations. Previous affiliations of Zufe Rizvi include Boca Raton Regional Hospital.

Papers
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Journal ArticleDOI
18 Feb 2021-Cureus
TL;DR: Wang et al. as discussed by the authors reported a case of Guillain-Barre syndrome (GBS) after receiving the first dose of Pfizer - COVID-19 vaccine.
Abstract: Since the first case of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported in Wuhan, China, in December 2019, Coronavirus - 19 (COVID-19) has become a global pandemic with multiple neurological complications. In December 2020, two vaccines have been approved in the United States for the prevention of COVID-19. We report a case of Guillain-Barre Syndrome (GBS) after receiving the first dose of Pfizer - COVID-19 vaccine.

137 citations

Journal ArticleDOI
02 May 2020-Cureus
TL;DR: The neurological complications of coronavirus disease 2019 (COVID-19) are being better understood as the pandemic progresses and CO VID-19 does not seem to cross the blood-brain barrier.
Abstract: The neurological complications of coronavirus disease 2019 (COVID-19) are being better understood as the pandemic progresses. We report a second case of a patient who presented with COVID-19 infection and encephalopathy to our institution. In addition, we report MRI brain and cerebrospinal fluid data. COVID-19 does not seem to cross the blood-brain barrier. The exact mechanisms of encephalopathy and pathological response of COVID-19 are unknown.

67 citations

Journal ArticleDOI
TL;DR: In this article, a basic knowledge of neuromuscular anatomy is needed to identify entrapment neuropathies and initial treatment of mild to moderate cases often is conservative. In severe cases or those refractory to conservative therapy, surgery should be considered.

2 citations

Proceedings ArticleDOI
25 Apr 2023
TL;DR: Zakin et al. as discussed by the authors used efgartigimod to improve myasthenia gravis symptoms in two patients with pembrolizumab-induced myasthens.
Abstract:

Objective:

NA

Background:

Checkpoint inhibitor-induced myasthenia gravis is a life-threatening complication with mortality near 60%.1 Two patients with pembrolizumab-induced myasthenia gravis responded favorably to efgartigimod.

Design/Methods:

NA

Results:

A 68-year-old female with metastatic gallbladder cancer developed ptosis, ophthalmoparesis, and weakness one month after receiving pembrolizumab. She has acetylcholine receptor (binding, blocking) and striated muscle antibodies without thymoma. Her ptosis improved with prednisone 20mg daily. She developed dysphagia, hoarseness, and gait instability which resolved with increased prednisone 60mg. Prednisone was tapered; proximal limb weakness and ptosis returned at 30mg. Efgartigimod improved symptoms after second infusion. Three weeks after cycle one while alternating prednisone 25mg–20mg, she developed exertional dyspnea, hoarseness, and worsening ptosis. Increased prednisone to 25mg. Her symptoms persisted; five weeks after cycle one, the second cycle of efgartigimod started and her symptoms nearly resolved, with intermittent ptosis. She is stable on prednisone 25mg with slow taper. A 78-year-old female with metastatic urothelial carcinoma status post two doses of pembrolizumab presented with dyspnea, leg weakness, and myalgias. She developed ptosis, ophthalmoparesis, and dysphagia. Acetylcholine receptor and MuSK antibodies were negative. Intravenous immunoglobulin was ineffective to prevent worsening. After the second dose, she developed respiratory failure requiring intubation. Prednisone 40mg BID and plasmapheresis (PLEX) were initiated. Her strength improved enough for extubation; subsequently aspirated and required reintubation. Rituximab was infused for long-term immunosuppression while another PLEX cycle was started. She developed thrombocytopenia and gastrointestinal bleeding; PLEX was discontinued after 3 doses. Efgartigimod initiation two days after the final PLEX infusion led to improved strength, ophthalmoparesis, and thrombocytopenia within one week. She died from urosepsis two days after the second dose.

Conclusions:

Current treatments for pembrolizumab-induced myasthenia gravis are corticosteroids, IVIG, and plasmapheresis. Rituximab is effective in refractory cases, although onset of action can take more than 6 weeks.2 Efgartigimod rapidly improved myasthenia gravis symptoms in both patients. Disclosure: Miss Campbell has nothing to disclose. Dr. Rodriguez-Hernandez has nothing to disclose. Dr. Rizvi has nothing to disclose. Dr. Swerdloff has nothing to disclose. The institution of Dr. Zakin has received research support from American Board of Psychiatry and Neurology. Dr. Faktorovich has a non-compensated relationship as a Board of Directors with Brother’s Brother Foundation that is relevant to AAN interests or activities.

Cited by
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Journal ArticleDOI
TL;DR: Research evaluating the direct neuropsychiatric consequences and the indirect effects on mental health is highly needed to improve treatment, mental health care planning and for preventive measures during potential subsequent pandemics.
Abstract: Background During the COVID-19 pandemic general medical complications have received the most attention, whereas only few studies address the potential direct effect on mental health of SARS-CoV-2 and the neurotropic potential. Furthermore, the indirect effects of the pandemic on general mental health are of increasing concern, particularly since the SARS-CoV-1 epidemic (2002–2003) was associated with psychiatric complications.

2,018 citations

Journal ArticleDOI
29 Sep 2020
TL;DR: A six-criterion additive scale for hyperinflammation in COVID-19, based on a framework of conserved clinical characteristics, might be helpful in defining target populations for trials and immunomodulatory therapies.
Abstract: Summary Background A subset of patients with COVID-19 develops a hyperinflammatory syndrome that has similarities with other hyperinflammatory disorders. However, clinical criteria specifically to define COVID-19-associated hyperinflammatory syndrome (cHIS) have not been established. We aimed to develop and validate diagnostic criteria for cHIS in a cohort of inpatients with COVID-19. Methods We searched for clinical research articles published between Jan 1, 1990, and Aug 20, 2020, on features and diagnostic criteria for secondary haemophagocytic lymphohistiocytosis, macrophage activation syndrome, macrophage activation-like syndrome of sepsis, cytokine release syndrome, and COVID-19. We compared published clinical data for COVID-19 with clinical features of other hyperinflammatory or cytokine storm syndromes. Based on a framework of conserved clinical characteristics, we developed a six-criterion additive scale for cHIS: fever, macrophage activation (hyperferritinaemia), haematological dysfunction (neutrophil to lymphocyte ratio), hepatic injury (lactate dehydrogenase or asparate aminotransferase), coagulopathy (D-dimer), and cytokinaemia (C-reactive protein, interleukin-6, or triglycerides). We then validated the association of the cHIS scale with in-hospital mortality and need for mechanical ventilation in consecutive patients in the Intermountain Prospective Observational COVID-19 (IPOC) registry who were admitted to hospital with PCR-confirmed COVID-19. We used a multistate model to estimate the temporal implications of cHIS. Findings We included 299 patients admitted to hospital with COVID-19 between March 13 and May 5, 2020, in analyses. Unadjusted discrimination of the maximum daily cHIS score was 0·81 (95% CI 0·74–0·88) for in-hospital mortality and 0·92 (0·88–0·96) for mechanical ventilation; these results remained significant in multivariable analysis (odds ratio 1·6 [95% CI 1·2–2·1], p=0·0020, for mortality and 4·3 [3·0–6·0], p Interpretation We proposed and validated criteria for hyperinflammation in COVID-19. This hyperinflammatory state, cHIS, is commonly associated with progression to mechanical ventilation and death. External validation is needed. The cHIS scale might be helpful in defining target populations for trials and immunomodulatory therapies. Funding Intermountain Research and Medical Foundation.

235 citations

Journal ArticleDOI
TL;DR: The most common neurological complaints in COVID-19 were anosmia, ageusia, and headache, but more serious complications, such as stroke, impairment of consciousness, seizures, and encephalopathy, have also been reported.

166 citations

Journal ArticleDOI
19 Jan 2021-Viruses
TL;DR: In this article, the authors demonstrate that SARS-CoV-2 neuroinvasion and encephalitis is associated with mortality in K18-hACE2 mice with 105 plaque-forming units.
Abstract: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can cause neurological disease in humans, but little is known about the pathogenesis of SARS-CoV-2 infection in the central nervous system (CNS). Herein, using K18-hACE2 mice, we demonstrate that SARS-CoV-2 neuroinvasion and encephalitis is associated with mortality in these mice. Intranasal infection of K18-hACE2 mice with 105 plaque-forming units of SARS-CoV-2 resulted in 100% mortality by day 6 after infection. The highest virus titers in the lungs were observed on day 3 and declined on days 5 and 6 after infection. By contrast, very high levels of infectious virus were uniformly detected in the brains of all the animals on days 5 and 6. Onset of severe disease in infected mice correlated with peak viral levels in the brain. SARS-CoV-2-infected mice exhibited encephalitis hallmarks characterized by production of cytokines and chemokines, leukocyte infiltration, hemorrhage and neuronal cell death. SARS-CoV-2 was also found to productively infect cells within the nasal turbinate, eye and olfactory bulb, suggesting SARS-CoV-2 entry into the brain by this route after intranasal infection. Our data indicate that direct infection of CNS cells together with the induced inflammatory response in the brain resulted in the severe disease observed in SARS-CoV-2-infected K18-hACE2 mice.

156 citations

Journal ArticleDOI
TL;DR: Encephalopathy is common in older patients, the majority are more than 50 years of age, and the patients having encephalopathy/encephalitis are either severely or critically ill, many patients were already on mechanical ventilation.
Abstract: Encephalopathy and encephalitis are major and devastating severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus-associated central nervous system complications Hypoxic/metabolic changes produced by intense inflammatory response against the virus triggers cytokine storm and subsequently acute respiratory distress syndrome and multiple organ failure Hypoxic/metabolic changes result in encephalopathy The presence of comorbidities predisposes to hypoxic/metabolic changes responsible for encephalopathy Altered consciousness, ranging from mild confusion, delirium, to deep coma, is hallmark clinical features Cortical and subcortical T2/FLAIR signal changes are common neuroimaging abnormalities In a few isolated case reports of SARS-CoV-2 encephalitis, the virus has been demonstrated in cerebrospinal fluid The presence of anosmia and ageusia can help in differentiation from other encephalopathies We analyzed published reports on coronavirus disease 2019-associated encephalopathy Encephalopathy is common in older patients, the majority are more than 50 years of age The patients having encephalopathy/encephalitis are either severely or critically ill Many patients were already on mechanical ventilation Lung abnormalities are noted in almost all of the patients, presenting with encephalopathy Encephalopathy is always preceded by commoner clinical features, like, fever, cough, dyspnoea, and headache In majority, patients are already in the intensive care unit, when encephalopathy develops

150 citations