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1.
Neurologist ; 26(6): 268-270, 2021 Nov 04.
Article in English | MEDLINE | ID: covidwho-1501226

ABSTRACT

INTRODUCTION: Neurological problems may be part of severe and early course of coronavirus disease 2019 (COVID-19). COVID-19 associated encephalitis as an evident etiology of altered consciousness has been rarely reported in the literature. CASE REPORT: A case of 66-year-old female presented with classic COVID-19 symptoms and associated diabetic ketoacidosis. Although diabetic ketoacidosis was managed, the patient had persistent impaired level of consciousness with recurrent attacks of left focal fits because of COVID-19-associated encephalitis. However, the patient has markedly improved after recovering from COVID-19. CONCLUSION: Neurologists should be involved in the evaluation and management of COVID-19 patients who present with associated neurological problems.


Subject(s)
COVID-19 , Diabetic Ketoacidosis , Encephalitis , Aged , Disease Progression , Encephalitis/complications , Female , Humans , SARS-CoV-2
2.
BMC Neurol ; 21(1): 414, 2021 Oct 27.
Article in English | MEDLINE | ID: covidwho-1486559

ABSTRACT

BACKGROUND: While Covid-19 predominantly affects the respiratory system, neurological manifestations including encephalitis occur in some patients, possibly affecting the course and outcome of the disease. Here, we describe a unique case of a young man with Covid-19 and transient MOG-positive encephalitis, with a benign course. CASE PRESENTATION: A 22-year-old male, with PCR confirmed Covid-19 infection was admitted because of persistent headache. The clinical examination was normal. Neuropsychological testing revealed distinct executive deficits. Brain MRI and cerebrospinal fluid (CSF) analysis were suggestive for encephalitis. Further laboratory examination revealed a serum MOG antibody titre. The headache improved with analgetic treatment and i.v. methylprednisolone. Consequently, the MOG antibody titer decreased and MRI lesions were resolving. The patient made a full recovery, with no signs of deterioration over the following months. CONCLUSIONS: Covid-19 manifestations in the CNS include encephalitis with variable course and prognosis. This case highlights a possible association between inflammation due to COVID-19 and transient secondary autoimmunity with transient MOG antibodies and atypical clinical presentation.


Subject(s)
COVID-19 , Encephalitis , Adult , Antibodies , Encephalitis/complications , Humans , Male , Myelin-Oligodendrocyte Glycoprotein , SARS-CoV-2 , Young Adult
4.
Neurol Sci ; 42(9): 3527-3530, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1274855

ABSTRACT

Neurological manifestations of SARS-CoV-2 are increasingly being recognised and can arise as a result of direct viral invasion, para-infectious or postinfectious immune mechanisms. We report a delayed presentation of COVID-19 postinfectious immune-mediated encephalitis and status epilepticus occurring in a 47-year-old woman 4 weeks after SARS-CoV-2 pulmonary disease. SARS-CoV-2-specific IgG and IgM antibodies were detected in her cerebrospinal fluid with features of encephalitis evident in both magnetic resonance imaging of the brain and electroencephalogram. She made a complete recovery following treatment with high-dose intravenous corticosteroids and intravenous immunoglobulins. Diagnosis of COVID-19 postinfectious encephalitis may prove challenging in patients presenting many weeks following the initial infection. A high index of clinical suspicion and testing intrathecal SARS-CoV-2-specific antibodies are key to its diagnosis. Early immunotherapy is likely to result in a good outcome.


Subject(s)
COVID-19 , Encephalitis , Electroencephalography , Encephalitis/complications , Female , Humans , Magnetic Resonance Imaging , Middle Aged , SARS-CoV-2
5.
J Nucl Med ; 61(12): 1726-1729, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-993173

ABSTRACT

We report the case of a 72-y-old man with concomitant autoimmune encephalitis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The patient presented with subacute cerebellar syndrome and myoclonus several days after general infectious symptoms began. Methods: Clinical examination, CT, PET, MRI, and autoantibody testing were performed. Results: The oropharyngeal swab test was positive for SARS-CoV-2. The brain MRI results were normal. Cerebrospinal fluid testing showed normal cell counts, a negative result on reverse-transcription polymerase chain reaction testing, and no oligoclonal banding. Brain 18F-FDG PET showed diffuse cortical hypometabolism associated with putaminal and cerebellum hypermetabolism, compatible with encephalitis and especially cerebellitis. The immunologic study revealed high titers of IgG autoantibodies in serum and cerebrospinal fluid directed against the nuclei of Purkinje cells, striatal neurons, and hippocampal neurons. Whole-body 18F-FDG PET and CT scans did not show neoplasia. Treatment with steroids allowed a rapid improvement in symptoms. Conclusion: This clinical case argues for a possible relationship between SARS-CoV-2 infection and autoimmune encephalitis and for the use of 18F-FDG PET in such a context.


Subject(s)
Autoantibodies/metabolism , COVID-19/complications , COVID-19/diagnostic imaging , Encephalitis/complications , Fluorodeoxyglucose F18 , Hashimoto Disease/complications , Neurons/immunology , Positron-Emission Tomography , Aged , COVID-19/immunology , COVID-19/therapy , Humans , Male
6.
BMJ Case Rep ; 13(9)2020 Sep 18.
Article in English | MEDLINE | ID: covidwho-823795

ABSTRACT

Bickerstaff's brainstem encephalitis (BBE) is a Guillain-Barré syndrome (GBS) spectrum disorder associated with predominantly central nervous system predilection. Patients exhibit a variable constellation of depressed consciousness, bilateral external ophthalmoplegia, ataxia and long tract signs. Although the pathophysiology is not fully understood, it has been associated with anti-GQ1b antibodies in two-thirds of patients. We present a patient with clinical features consistent with BBE and positive anti-GM1 and anti-GD1a antibodies. A diagnostic approach to the acutely unwell patient with brainstem encephalitis is explored in this clinical context with a literature review of the aforementioned ganglioside antibody significance. Intravenous immunoglobulin therapy is highlighted in BBE using up-to-date evidence-based extrapolation from GBS.


Subject(s)
Ataxia/immunology , Autoantibodies/blood , Brain Stem/immunology , Encephalitis/diagnosis , Ophthalmoplegia/immunology , Adult , Ataxia/blood , Autoantibodies/immunology , Diagnosis, Differential , Electroencephalography , Encephalitis/blood , Encephalitis/complications , Encephalitis/immunology , G(M1) Ganglioside/immunology , Gangliosides/immunology , Glasgow Coma Scale , Humans , Male , Ophthalmoplegia/blood
8.
J Neurovirol ; 26(5): 619-630, 2020 10.
Article in English | MEDLINE | ID: covidwho-728290

ABSTRACT

The recent pandemic outbreak of coronavirus is pathogenic and a highly transmittable viral infection caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2). In this time of ongoing pandemic, many emerging reports suggested that the SARS-CoV-2 has inimical effects on neurological functions, and even causes serious neurological damage. The neurological symptoms associated with COVID-19 include headache, dizziness, depression, anosmia, encephalitis, stroke, epileptic seizures, and Guillain-Barre syndrome along with many others. The involvement of the CNS may be related with poor prognosis and disease worsening. Here, we review the evidence of nervous system involvement and currently known neurological manifestations in COVID-19 infections caused by SARS-CoV-2. We prioritize the 332 human targets of SARS-CoV-2 according to their association with brain-related disease and identified 73 candidate genes. We prioritize these 73 genes according to their spatio-temporal expression in the different regions of brain and also through evolutionary intolerance analysis. The prioritized genes could be considered potential indicators of COVID-19-associated neurological symptoms and thus act as a possible therapeutic target for the prevention and treatment of CNS manifestations associated with COVID-19 patients.


Subject(s)
Betacoronavirus/pathogenicity , Brain/metabolism , Coronavirus Infections/genetics , Host-Pathogen Interactions/genetics , Nerve Tissue Proteins/genetics , Pneumonia, Viral/genetics , Viral Proteins/genetics , Brain/pathology , Brain/virology , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/pathology , Coronavirus Infections/virology , Depression , Dizziness/complications , Dizziness/genetics , Dizziness/pathology , Dizziness/virology , Encephalitis/complications , Encephalitis/genetics , Encephalitis/pathology , Encephalitis/virology , Guillain-Barre Syndrome/complications , Guillain-Barre Syndrome/genetics , Guillain-Barre Syndrome/pathology , Guillain-Barre Syndrome/virology , Headache/complications , Headache/genetics , Headache/pathology , Headache/virology , Humans , Nerve Tissue Proteins/classification , Nerve Tissue Proteins/metabolism , Olfaction Disorders/complications , Olfaction Disorders/genetics , Olfaction Disorders/pathology , Olfaction Disorders/virology , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , Protein Interaction Mapping , SARS-CoV-2 , Seizures/complications , Seizures/genetics , Seizures/pathology , Seizures/virology , Severity of Illness Index , Stroke/complications , Stroke/genetics , Stroke/pathology , Stroke/virology , Viral Proteins/metabolism
9.
J Psychiatr Res ; 130: 215-217, 2020 11.
Article in English | MEDLINE | ID: covidwho-713999

ABSTRACT

Coronavirus Disease 2019 (COVID-19), caused by SARS-CoV-2, is a disaster due to not only its psychosocial impact but it also to its direct effects on the brain. The latest evidence suggests it has neuroinvasive mechanisms, in addition to neurological manifestations, and as seen in past pandemics, long-term sequelae are expected. Specific and well-structured interventions are necessary, and that's why it's important to ensure a continuity between primary care, emergency medicine, and psychiatry. Evidence shows that 2003 SARS (Severe Acute Respiratory Syndrome) survivors developed persistent psychiatric comorbidities after the infection, in addition to Chronic Fatigue Syndrome. A proper stratification of patients according not only to psychosocial factors but also an inflammatory panel and SARS-Cov-2's direct effects on the central nervous system (CNS) and the immune system, may improve outcomes. The complexity of COVID-19's pathology and the impact on the brain requires appropriate screening that has to go beyond the psychosocial impact, taking into account how stress and neuroinflammation affects the brain. This is a call for a clinical multidisciplinary approach to treat and prevent Sars-Cov-2 mental health sequelae.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Coronavirus Infections/psychology , Mental Disorders/complications , Mental Disorders/psychology , Neurosciences/methods , Pneumonia, Viral/complications , Pneumonia, Viral/psychology , COVID-19 , Encephalitis/complications , Encephalitis/prevention & control , Encephalitis/psychology , Humans , Mental Disorders/prevention & control , Pandemics , SARS-CoV-2 , Stress, Physiological
10.
Int J Mol Sci ; 21(15)2020 Jul 31.
Article in English | MEDLINE | ID: covidwho-693402

ABSTRACT

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called "cytokine storm"), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.


Subject(s)
Betacoronavirus/physiology , Central Nervous System/virology , Coronavirus Infections/pathology , Pneumonia, Viral/pathology , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/isolation & purification , Blood-Brain Barrier/metabolism , Blood-Brain Barrier/virology , Brain Diseases/complications , Brain Diseases/pathology , COVID-19 , Central Nervous System/metabolism , Coronavirus Infections/virology , Encephalitis/complications , Encephalitis/pathology , Humans , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/virology , SARS-CoV-2
11.
Ann Neurol ; 88(2): 423-427, 2020 08.
Article in English | MEDLINE | ID: covidwho-600958

ABSTRACT

Coronavirus disease 2019 (COVID-19) infection has the potential for targeting the central nervous system, and several neurological symptoms have been described in patients with severe respiratory distress. Here, we described the case of a 60-year-old patient with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection but only mild respiratory abnormalities who developed an akinetic mutism attributable to encephalitis. Magnetic resonance imaging was negative, whereas electroencephalography showed generalized theta slowing. Cerebrospinal fluid analyses during the acute stage were negative for SARS-CoV-2, positive for pleocytosis and hyperproteinorrachia, and showed increased interleukin-8 and tumor necrosis factor-α concentrations. Other infectious or autoimmune disorders were excluded. A progressive clinical improvement along with a reduction of cerebrospinal fluid parameters was observed after high-dose steroid treatment, thus arguing for an inflammatory-mediated brain involvement related to COVID-19. ANN NEUROL 2020;88:423-427.


Subject(s)
Akinetic Mutism/physiopathology , Antiviral Agents/therapeutic use , Coronavirus Infections/drug therapy , Encephalitis/drug therapy , Glucocorticoids/therapeutic use , Methylprednisolone/therapeutic use , Pneumonia, Viral/drug therapy , Betacoronavirus , COVID-19 , Coronavirus Infections/cerebrospinal fluid , Coronavirus Infections/complications , Coronavirus Infections/physiopathology , Drug Combinations , Electroencephalography , Encephalitis/cerebrospinal fluid , Encephalitis/complications , Encephalitis/physiopathology , Humans , Hydroxychloroquine/therapeutic use , Interleukin-6/cerebrospinal fluid , Interleukin-8/cerebrospinal fluid , Lopinavir/therapeutic use , Magnetic Resonance Imaging , Male , Middle Aged , Pandemics , Pneumonia, Viral/cerebrospinal fluid , Pneumonia, Viral/complications , Pneumonia, Viral/physiopathology , Ritonavir/therapeutic use , SARS-CoV-2 , Treatment Outcome , Tumor Necrosis Factor-alpha/cerebrospinal fluid , beta 2-Microglobulin/cerebrospinal fluid
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