Transcortical sensory aphasia heralding SARS-Cov-2-induced autoimmune encephalitis with gyral restricted diffusion hyperintensities: a novel case report.

Background: Coronavirus disease 2019 (CoVID-19), primarily thought of as a respiratory system disease is actually a multi-system disease with immunological implications. CNS involvement in COVID has been explained in recent literature mainly for stroke, encephalopathy, encephalitis, acute disseminated encephalomyelitis and myelopathy. There are few studies characterizing clinical spectrum of COVID autoimmune encephalitis. We present a unique case of post-COVID autoimmune encephalitis in a diabetic male presenting with language dysfunction and novel radiologic findings. Case presentation: Patient admitted to inpatient department of a tertiary care hospital of India was evaluated by bedside clinical examination, routine blood tests, CSF study with intrathecal SARS-Cov-2 antibody detection, commercially available tests for autoimmune encephalitis, neuroviral panel with HSV PCR, EEG, 3-Tesla MRI and PET scan. Patient was found to have personality change and transcortical sensory aphasia in the outset of COVID encephalitis. MRI findings like temporal involvement and insular ribboning are also being reported. The patient was treated with IV immunoglobulin and is on an improving course. Conclusions: This case reports dysphasia due to COVID-mediated injury to the language networks, with novel radiologic findings. Role of parainfectious versus immune etiology is also discussed. Further studies are needed to elucidate the mechanism and clinical spectrum of post-COVID autoimmune encephalitis.

The cognitive basis of psychosocial impact in COVID-19 pandemic. Does it encircle the default mode network of the brain? A pragmatic proposal.

Epigenetics, hypothalamic-pituitary axes, environmental and metabolic influences, and transgenerational plasticity govern social behavior. Cognitive research considers the brain's default mode network (DMN) as a central hub that integrates various cognitive and social processing domains responsible for emotion perception, empathy, theory of mind, and morality. Hence, DMN is regarded as the "social brain." Upsurge in social turmoil, social anxiety, panic, depression, post-traumatic stress, hoarding, herd behavior, substance and behavioral addictions, sexual abuse, and violence in the time of the COVID-19 pandemic are intricately related to personality traits resulting in disruptive social cognition and social behavior, conceptualized as the result of unsettling and disruption of the functional nexus of the DMN. Considering overt and conspicuous display of neuroticism during the current pandemic, its impact upon modulation of the DMN functional nexus and the DMN itself, and the potential to presage cognitive impairment in the future, the authors caution that an increase in the global burden of dementia may be one of the long-term ramifications of COVID-19. Social behavior, a functional derivative of the DMN, can strikingly affect the functional nexus of DMN and the DMN itself, in a centripetal way via the phenomenon called "Experience-Dependent Plasticity," with long-term consequences. In this review, we intend to 1) decipher the association between social cognition and social behavior with the DMN, in time of COVID-19; and to 2) discuss the prospective aftermath of disrupted social behavior during the pandemic on modulation/alteration of functional connectomes of DMN or the DMN itself in the time ahead.

Impact of COVID-19 pandemic in natural course of Moyamoya Angiopathy: an experience from tertiary-care-center in India.

BACKGROUND: COVID-19 mediated immune dysregulation and cytokine storm can precipitate and aggravate Moyamoya angiopathy (MMA), influencing its disease course. This index study was undertaken to prospectively evaluate the status of neurological symptoms of MMA in relation to COVID-19 affection. METHODOLOGY AND RESULTS: Follow-up MMA patients of institute's Stroke-clinic were telephonically interview from 24th March to 30th September, 2020. The first call familiarized them with COVID-19 symptoms and neurological manifestations of MMA, followed by monthly-calls with predesigned questionnaire. Patients with suggestion of COVID-19 underwent nasopharyngeal-swab-testing for COVID-19 Reverse transcription-polymerase chain reaction (RT-PCR) positive cases were subjected to antibody levels for COVID-19 Enzyme-linked immunoassay (ELISA) 8-12 weeks after recovery. During symptomatic phase till 14 days of asymptomatic, they were contacted daily/alternate day. Any new onset/worsening of neurological symptoms were noted. The baseline clinico-radiological details were obtained from stroke-clinic registery. Subsequently, all data were analyzed and compared using descriptive statistics. Seventy four of 104 MMA patients could be contacted and enrolled. The mean age, time since last follow-up and compliance to previously prescribed medication were 23.5 ± 16.1 years, 9.2 ± 1.7 months and 90.5% (n = 67), respectively. Aggravation/new onset neurological symptom were seen in 64.3% (n = 9) of COVID-19 positive MMA (n = 14), of which 8 were seen among the 11 pediatric COVID-19 positive MMA [(Transient ischemic attacks) TIA-4, TIA with headache-1, seizure-2, stroke causing mortality-1]. CONCLUSION: COVID-19 infection can potentiate MMA causing significant morbidity and mortality, especially in children. Providing optimal care for severe diseases (such as MMA) in developing countries during pandemic remains a challenge.

COVID-19 associated rhino-orbital-cerebral mucormycosis: An observational study from Eastern India, with special emphasis on neurological spectrum.

AIMS: 1: Describe the epidemiology and determine risk factors for COVID-19 associated mucormycosis. 2: Elaborate the clinical spectrum of Rhino-Orbital-Cerebral Mucormycosis (ROCM), pattern of neuroaxis involvement and it's radiological correlates. METHODS: Observational study. Consecutive, confirmed cases of mucormycosis (N = 55) were included. A case of mucormycosis was defined as one who had clinical and radiological features consistent with mucormycosis along with demonstration of the fungus in tissue via KOH mount/culture/histopathological examination (HPE). Data pertaining to epidemiology, risk factors, clinico-radiological features were analysed using percentage of total cases. RESULTS: Middle aged, diabetic males with recent COVID-19 infection were most affected. New onset upper jaw toothache was a striking observation in several cases. Among neurological manifestations headache, proptosis, vision loss, extraocular movement restriction; cavernous sinus, meningeal and parenchymal involvement were common. Stroke in ROCM followed a definitive pattern with watershed infarction. CONCLUSIONS: New onset upper jaw toothache and loosening of teeth should prompt an immediate search for mucormycosis in backdrop of diabetic patients with recent COVID-19 disease, aiding earlier diagnosis and treatment initiation. Neuroaxis involvement was characterized by a multitude of features pertaining to involvement of optic nerve, extraocular muscles, meninges, brain parenchyma and internal carotid artery.

Treatment related fluctuation and response to intravenous immunoglobulin therapy in post COVID-19 Guillain-Barre syndrome.

Treatment related fluctuation (TRF) poses a special challenge in the treatment of Guillain-Barre syndrome (GBS). Many cases of GBS following COVID-19 infection have been reported in literature till date, but treatment related fluctuation (TRF) in post COVID-19 GBS has not been reported till date. We report a 35-year-old male patient who developed GBS following COVID-19 infection and had TRF after intravenous immunoglobulin (IV-IG) therapy. He required ventilator support but repeat IV-IG therapy led to complete recovery. Significant proximal muscle involvement, cranial nerve palsy, no antecedent diarrhea and absence of anti-GM1 antibodies are important predictors of TRF in GBS and need to be recognized early in the course of this illness. Early recognition of TRF and differentiating it from other forms of immune mediated neuropathy such as acute onset chronic inflammatory demyelinating polyradiculoneuropathy (A-CIDP) are important for prognostication and management.

Cerebral venous thrombosis in COVID-19.

BACKGROUND AND AIMS: Initially, novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) was considered primarily a respiratory pathogen. However, with time it has behaved as a virus with the potential to cause multi-system involvement, including neurological manifestations. Cerebral venous sinus thrombosis (CVT) has increasingly been reported in association with coronavirus infectious disease of 2019 (COVID-19). Here, we have shed light upon CVT and its possible mechanisms in the backdrop of the ongoing COVID-19 pandemic. METHODS: In this review, data were collected from PubMed, EMBASE and Web of Science, until March 30, 2021, using pre-specified searching strategies. The search strategy consisted of a variation of keywords of relevant medical subject headings and keywords, including "COVID-19", "SARS-CoV-2", "coronavirus", and "cerebral venous sinus thrombosis". RESULTS: COVID-19 has a causal association with a plethora of neurological, neuropsychiatric and psychological effects. CVT has gained particular importance in this regard. The known hypercoagulable state in SARS-CoV-2 infection is thought to be the main mechanism in COVID-19 related CVT. Other plausible mechanisms may include vascular endothelial dysfunction and altered flow dynamics. CONCLUSIONS: Although there are no specific clinical characteristics, insidious or acute onset headache, seizures, stroke-like, or encephalopathy symptoms in a patient with, or who has suffered COVID-19, should prompt the attending physician to investigate for CVT. The treatment of COVID-19 associated CVT does not differ radically from the therapy of CVT without the infection, i.e. urgent initiation of parenteral unfractionated heparin or low molecular weight heparin followed by conventional or mostly newer oral anticoagulants.

COVID-19 Induced Miller Fisher Syndrome Presenting With Autonomic Dysfunction: A Unique Case Report and Review of Literature.

A plethora of neurological manifestations are associated with the 2019 coronavirus infectious disease (COVID-19). We hereby report the first case of a patient infected with SARS-CoV-2 who acutely presented with autonomic dysfunction preceding the onset of complete clinical picture of Miller Fisher syndrome. She was finally diagnosed to be a case of anti-ganglioside antibody positive post-COVID-19 Miller Fisher syndrome with dysautonomia and treated with intravenous immunoglobulin with an excellent response. We also discuss the plausible pathogenic mechanisms of COVID-19 induced Miller Fisher syndrome and furnish a review of the post-COVID-19 Miller Fisher syndrome cases reported.

De Novo Movement Disorders and COVID-19: Exploring the Interface.

Background: Neurological manifestations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are being widely documented. However, movement disorders in the setting of 2019 coronavirus infectious disease (COVID-19) have been a strikingly less discussed topic. Objectives: To summarize available pieces of evidence documenting de novo movement disorders in COVID-19. Methods: We used the existing PRISMA consensus statement. Data were collected from PubMed, EMBASE, Web of Science, and Scopus databases up to the 29th January, 2021, using pre-specified searching strategies. Results: Twenty-two articles were selected for the qualitative synthesis. Among these, a total of 52 patients with de novo movement disorders were reported. Most of these had myoclonus, ataxia, tremor or a combination of these, while three had parkinsonism and one a functional disorder. In general, they were managed successfully by intravenous immunoglobulin or steroids. Some cases, primarily with myoclonus, could be ascribed to medication exposures, metabolic disturbances or severe hypoxia, meanwhile others to a post-or para-infectious immune-mediated mechanism. SARS-CoV-2 could also invade the central nervous system, through vascular or retrograde axonal pathways, and cause movement disorders by two primary mechanisms. Firstly, through the downregulation of angiotensin-converting enzyme 2 receptors, resulting in the imbalance of dopamine and norepinephrine; and secondly, the virus could cause cellular vacuolation, demyelination and gliosis, leading to encephalitis and associated movement disorders. Conclusion: De novo movement disorders are scantly reported in COVID-19. The links between SARS-CoV-2 and movement disorders are not yet established. However, we should closely monitor COVID-19 survivors for the possibility of post-COVID movement disorders.