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1.
JAMA ; 327(14): 1321-1322, 2022 04 12.
Article in English | MEDLINE | ID: covidwho-1756511
2.
Curr Opin Neurol ; 35(3): 392-398, 2022 06 01.
Article in English | MEDLINE | ID: covidwho-1741071

ABSTRACT

PURPOSE OF REVIEW: As of January 8, 2022, a global pandemic caused by infection with severe acute respiratory syndrome coronavirus (SARS-CoV)-2, a new RNA virus, has resulted in 304,896,785 cases in over 222 countries and regions, with over 5,500,683 deaths (www.worldometers.info/coronavirus/). Reports of neurological and psychiatric symptoms in the context of coronavirus infectious disease 2019 (COVID-19) range from headache, anosmia, and dysgeusia, to depression, fatigue, psychosis, seizures, delirium, suicide, meningitis, encephalitis, inflammatory demyelination, infarction, and acute hemorrhagic necrotizing encephalopathy. Moreover, 30-50% of COVID-19 survivors develop long-lasting neurologic symptoms, including a dysexecutive syndrome, with inattention and disorientation, and/or poor movement coordination. Detection of SARS-CoV-2 RNA within the central nervous system (CNS) of patients is rare, and mechanisms of neurological damage and ongoing neurologic diseases in COVID-19 patients are unknown. However, studies demonstrating viral glycoprotein effects on coagulation and cerebral vasculature, and hypoxia- and cytokine-mediated coagulopathy and CNS immunopathology suggest both virus-specific and neuroimmune responses may be involved. This review explores potential mechanistic insights that could contribute to COVID-19-related neurologic disease. RECENT FINDINGS: While the development of neurologic diseases during acute COVID-19 is rarely associated with evidence of viral neuroinvasion, new evidence suggests SARS-CoV-2 Spike (S) protein exhibits direct inflammatory and pro-coagulation effects. This, in conjunction with immune dysregulation resulting in cytokine release syndrome (CRS) may result in acute cerebrovascular or neuroinflammatory diseases. Additionally, CRS-mediated loss of blood-brain barrier integrity in specific brain regions may contribute to the expression of proinflammatory mediators by neural cells that may impact brain function long after resolution of acute infection. Importantly, host co-morbid diseases that affect vascular, pulmonary, or CNS function may contribute to the type of neurologic disease triggered by SARS-COV-2 infection. SUMMARY: Distinct effects of SARS-CoV-2 S protein and CNS compartment- and region-specific responses to CRS may underlie acute and chronic neuroinflammatory diseases associated with COVID-19.


Subject(s)
Brain Diseases , COVID-19 , Nervous System Diseases , Brain Diseases/virology , COVID-19/complications , Humans , Nervous System Diseases/virology , RNA, Viral , SARS-CoV-2 , Spike Glycoprotein, Coronavirus
3.
J Med Virol ; 93(12): 6818-6821, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1530184

ABSTRACT

Novel coronavirus disease (COVID-19) first described in Wuhan, China in December 2019, has rapidly spread across the world and become a global public health emergency. Literature on the neurological manifestations of COVID-19 is limited. We report a 24-year-old male, who presented with vertigo, dysarthria, and bradyphrenia 3 weeks after being diagnosed with COVID-19 on nasopharyngeal reverse transcription polymerase chain reaction. The patient was diagnosed with acute cerebellitis based on magnetic resonance imaging features and showed improvement posttreatment with intravenous methylprednisone for 5 days. The scope of this article is to highlight the importance of early identification of neurological symptoms and timely management as the outcomes may be catastrophic.


Subject(s)
Brain Diseases/etiology , Brain Diseases/virology , COVID-19/complications , COVID-19/virology , Acute Disease , Adult , Humans , Male , SARS-CoV-2/pathogenicity , Young Adult
5.
Cells ; 10(9)2021 08 31.
Article in English | MEDLINE | ID: covidwho-1390541

ABSTRACT

COVID-19 presents with a wide range of clinical neurological manifestations. It has been recognized that SARS-CoV-2 infection affects both the central and peripheral nervous system, leading to smell and taste disturbances; acute ischemic and hemorrhagic cerebrovascular disease; encephalopathies and seizures; and causes most surviving patients to have long lasting neurological symptoms. Despite this, typical neuropathological features associated with the infection have still not been identified. Studies of post-mortem examinations of the cerebral cortex are obtained with difficulty due to laboratory safety concerns. In addition, they represent cases with different neurological symptoms, age or comorbidities, thus a larger number of brain autoptic data from multiple institutions would be crucial. Histopathological findings described here are aimed to increase the current knowledge on neuropathology of COVID-19 patients. We report post-mortem neuropathological findings of ten COVID-19 patients. A wide range of neuropathological lesions were seen. The cerebral cortex of all patients showed vascular changes, hyperemia of the meninges and perivascular inflammation in the cerebral parenchyma with hypoxic neuronal injury. Perivascular lymphocytic inflammation of predominantly CD8-positive T cells mixed with CD68-positive macrophages, targeting the disrupted vascular wall in the cerebral cortex, cerebellum and pons were seen. Our findings support recent reports highlighting a role of microvascular injury in COVID-19 neurological manifestations.


Subject(s)
COVID-19/pathology , Cerebral Cortex/pathology , Aged , Aged, 80 and over , Autopsy , Brain/pathology , Brain/virology , Brain Diseases/pathology , Brain Diseases/virology , CD8-Positive T-Lymphocytes/pathology , Cerebral Cortex/virology , Female , Humans , Inflammation , Macrophages/pathology , Male , Microvessels/pathology , Microvessels/virology , Middle Aged , Nervous System Diseases/pathology , Nervous System Diseases/virology , SARS-CoV-2/pathogenicity
8.
J Med Virol ; 93(12): 6818-6821, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1326775

ABSTRACT

Novel coronavirus disease (COVID-19) first described in Wuhan, China in December 2019, has rapidly spread across the world and become a global public health emergency. Literature on the neurological manifestations of COVID-19 is limited. We report a 24-year-old male, who presented with vertigo, dysarthria, and bradyphrenia 3 weeks after being diagnosed with COVID-19 on nasopharyngeal reverse transcription polymerase chain reaction. The patient was diagnosed with acute cerebellitis based on magnetic resonance imaging features and showed improvement posttreatment with intravenous methylprednisone for 5 days. The scope of this article is to highlight the importance of early identification of neurological symptoms and timely management as the outcomes may be catastrophic.


Subject(s)
Brain Diseases/etiology , Brain Diseases/virology , COVID-19/complications , COVID-19/virology , Acute Disease , Adult , Humans , Male , SARS-CoV-2/pathogenicity , Young Adult
9.
J Med Case Rep ; 15(1): 220, 2021 Apr 28.
Article in English | MEDLINE | ID: covidwho-1207609

ABSTRACT

BACKGROUND: Current studies show that patients with severe coronavirus disease 2019 (COVID-19) have neurological symptoms manifesting as acute cerebrovascular diseases, impaired consciousness, and skeletal muscle symptoms. Bizarre behavior is an unusual and unique presenting symptom of COVID-19 infection in our patient. CASE PRESENTATION: We report a case of COVID-19 infection in a middle aged Iranian man without underlying disease who presented with bizarre behavior. Results of brain imaging were normal, but COVID-19 pneumonia was detected on chest computed tomography scan. Given the respiratory problem and positive polymerase chain reaction (PCR) test for COVID-19, treatment with hydroxychloroquine was administered, and after 2 days all of the symptoms resolved. CONCLUSIONS: Encephalopathy and encephalitis may be a possible presentation of COVID-19. Clinicians and health care providers should consider the presence of COVID-19 with bizarre behavior during this COVID-19 pandemic.


Subject(s)
Behavioral Symptoms , Brain Diseases , COVID-19 , Behavioral Symptoms/virology , Brain Diseases/virology , COVID-19/complications , COVID-19/diagnosis , COVID-19/epidemiology , Humans , Iran/epidemiology , Male , Middle Aged
10.
J Med Virol ; 93(1): 206-222, 2021 01.
Article in English | MEDLINE | ID: covidwho-1206776

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.


Subject(s)
Brain Diseases/diagnosis , Brain Diseases/virology , COVID-19/complications , Age Factors , Ageusia , Brain Diseases/complications , Critical Care , Critical Illness , Headache , Humans
11.
Signal Transduct Target Ther ; 6(1): 169, 2021 04 24.
Article in English | MEDLINE | ID: covidwho-1199270

ABSTRACT

Neurological manifestations are frequently reported in the COVID-19 patients. Neuromechanism of SARS-CoV-2 remains to be elucidated. In this study, we explored the mechanisms of SARS-CoV-2 neurotropism via our established non-human primate model of COVID-19. In rhesus monkey, SARS-CoV-2 invades the CNS primarily via the olfactory bulb. Thereafter, viruses rapidly spread to functional areas of the central nervous system, such as hippocampus, thalamus, and medulla oblongata. The infection of SARS-CoV-2 induces the inflammation possibly by targeting neurons, microglia, and astrocytes in the CNS. Consistently, SARS-CoV-2 infects neuro-derived SK-N-SH, glial-derived U251, and brain microvascular endothelial cells in vitro. To our knowledge, this is the first experimental evidence of SARS-CoV-2 neuroinvasion in the NHP model, which provides important insights into the CNS-related pathogenesis of SARS-CoV-2.


Subject(s)
Brain Diseases/metabolism , Brain/metabolism , COVID-19/metabolism , Olfactory Bulb/metabolism , SARS-CoV-2/metabolism , Animals , Astrocytes/metabolism , Astrocytes/pathology , Astrocytes/virology , Brain/pathology , Brain/virology , Brain Diseases/pathology , Brain Diseases/virology , COVID-19/pathology , Disease Models, Animal , Humans , Macaca mulatta , Microglia/metabolism , Microglia/pathology , Microglia/virology , Neurons/metabolism , Neurons/pathology , Neurons/virology , Olfactory Bulb/pathology , Olfactory Bulb/virology
12.
Can Assoc Radiol J ; 73(1): 179-186, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1197333

ABSTRACT

PURPOSE: Coronavirus disease (COVID-19) has been associated with neurologic sequelae and neuroimaging abnormalities in several case series previously. In this study, the neuroimaging findings and clinical course of adult patients admitted with COVID-19 to a tertiary care hospital network in Canada were characterized. METHODS: This is a retrospective observational study conducted at a tertiary hospital network in Ontario, Canada. All adult patients with PCR-confirmed COVID-19 admitted from February 1, 2020 to July 22, 2020 who received neuroimaging related to their COVID-19 admission were included. CT and MR images were reviewed and categorized by fellowship-trained neuroradiologists. Demographic and clinical data were collected and correlated with imaging findings. RESULTS: We identified 422 patients admitted with COVID-19 during the study period. 103 (24.4%) met the inclusion criteria and were included: 30 ICU patients (29.1%) and 73 non-ICU patients (70.9%). A total of 198 neuroimaging studies were performed: 177 CTs and 21 MRIs. 17 out of 103 imaged patients (16.8%) had acute abnormalities on neuroimaging: 10 had macrohemorrhages (58.8%), 9 had acute ischemia (52.9%), 4 had SWI abnormalities (23.5%), and 1 had asymmetric sulcal effacement suggesting possible focal encephalitis (5.8%). ICU patients were more likely to have positive neuroimaging findings, more specifically acute ischemia and macrohemorrhages (P < 0.05). Macrohemorrhages were associated with increased mortality (P < 0.05). CONCLUSION: Macrohemorrhages, acute ischemia and SWI abnormalities were the main neuroimaging abnormalities in our cohort of hospitalized COVID-19 patients. Acute ischemia and hemorrhage were associated with worse clinical status.


Subject(s)
Brain Diseases/diagnostic imaging , Brain Diseases/virology , COVID-19/complications , Neuroimaging/methods , Adult , Canada , Humans , Magnetic Resonance Imaging , Male , Pandemics , Retrospective Studies , SARS-CoV-2 , Tomography, X-Ray Computed
13.
J Neurovirol ; 27(3): 507-509, 2021 06.
Article in English | MEDLINE | ID: covidwho-1193170

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represents respiratory symptoms as the most common clinical manifestations. Similar to some other viral infections, it can cause severe neurological damages. Here, we describe a 40-year-old man case who initially was admitted to a major hospital with presenting 7 days with weak flu-like symptoms (cough) and fever then presented neurology signs for 3 days. Physical examination and brain magnetic resonance imaging (MRI) showed cerebral vasculopathy. Molecular testing was performed on nasopharyngeal swab by real-time reverse transcription polymerase chain reaction (RT-PCR) which was positive for SARS-CoV-2. The patient received supportive cares and was treated with routine antiplatelet therapy. He was improved and discharged 10 days after admission with no symptoms. Our findings report a 40-year-old man with flu-like symptoms that indicate cerebral vasculopathy that was discharged with no symptoms. Therefore, physicians should be monitor patients with worsening or progressive central nervous system results. The pathobiology of this virus is still incompletely known; therefore, extensive studies are needed to reveal the effect of COVID-19 on the nervous system.


Subject(s)
Arteritis/virology , Brain Diseases/virology , COVID-19/complications , Adult , Humans , Iran , Male , SARS-CoV-2
14.
Pan Afr Med J ; 38: 139, 2021.
Article in English | MEDLINE | ID: covidwho-1175753

ABSTRACT

Case numbers reported in literature with neurological manifestations potentially linked to COVID-19 is constantly increasing. Most often it is sudden anosmia, headache, encephalopathy or stroke. Pathophysiology of this neurological involvement is still poorly understood. While viral genome is very rarely detected in cerebrospinal fluid, inflammatory involvement is often very significant. We report a case of SARS-CoV-2 encephalopathy without respiratory distress or cytokine storm.


Subject(s)
Brain Diseases/virology , COVID-19/complications , SARS-CoV-2/isolation & purification , Aged , Brain Diseases/diagnosis , COVID-19/diagnosis , Humans , Male
15.
J Med Virol ; 93(7): 4374-4381, 2021 07.
Article in English | MEDLINE | ID: covidwho-1156881

ABSTRACT

Severe acute respiratory coronavirus 2 (SARS-CoV-2) has been associated with neurological complications, including acute encephalopathy. To better understand the neuropathogenesis of this acute encephalopathy, we describe a series of patients with coronavirus disease 2019 (COVID-19) encephalopathy, highlighting its phenomenology and its neurobiological features. On May 10, 2020, 707 patients infected by SARS-CoV-2 were hospitalized at the Geneva University Hospitals; 31 (4.4%) consecutive patients with an acute encephalopathy (64.6 ± 12.1 years; 6.5% female) were included in this series, after exclusion of comorbid neurological conditions, such as stroke or meningitis. The severity of the COVID-19 encephalopathy was divided into severe and mild based on the Richmond Agitation Sedation Scale (RASS): severe cases (n = 14, 45.2%) were defined on a RASS < -3 at worst presentation. The severe form of this so-called COVID-19 encephalopathy presented more often a headache. The severity of the pneumonia was not associated with the severity of the COVID-19 encephalopathy: 28 of 31 (90%) patients did develop an acute respiratory distress syndrome, without any difference between groups (p = .665). Magnetic resonance imaging abnormalities were found in 92.0% (23 of 25 patients) with an intracranial vessel gadolinium enhancement in 85.0% (17 of 20 patients), while an increased cerebrospinal fluid/serum quotient of albumin suggestive of blood-brain barrier disruption was reported in 85.7% (6 of 7 patients). Reverse transcription-polymerase chain reaction for SARS-CoV-2 was negative for all patients in the cerebrospinal fluid. Although different pathophysiological mechanisms may contribute to this acute encephalopathy, our findings suggest the hypothesis of disturbed brain homeostasis and vascular dysfunction consistent with a SARS-CoV-2-induced endotheliitis.


Subject(s)
Brain Diseases/pathology , Brain Diseases/virology , Brain/pathology , COVID-19/pathology , Aged , Albumins/cerebrospinal fluid , Electroencephalography , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , SARS-CoV-2 , Severity of Illness Index , Switzerland
17.
J Clin Neurophysiol ; 38(2): e5-e10, 2021 Mar 01.
Article in English | MEDLINE | ID: covidwho-1150060

ABSTRACT

SUMMARY: Neurological manifestations of coronavirus disease 2019 most commonly present in severe cases and range from mild complications, such as headache and dizziness, to severe complications, such as encephalopathy and acute cerebrovascular disease. Seizures, however, are an underreported neurological manifestation of this disease. We present three critically ill coronavirus disease 2019 patients with EEG monitoring who developed new-onset seizures and encephalopathy up to three-and-a-half weeks after symptom onset. There are several speculated etiologies for the development of new-onset seizures; however, the pathogenic mechanism remains unknown. Testing of coronavirus disease 2019 in the cerebrospinal fluid in addition to extensive research on neurological manifestations is warranted.


Subject(s)
Brain Diseases/virology , COVID-19/complications , Dizziness/virology , Headache/virology , Seizures/virology , Adult , Aged , Female , Humans , Male , Middle Aged , SARS-CoV-2
18.
Am J Case Rep ; 22: e930135, 2021 Mar 24.
Article in English | MEDLINE | ID: covidwho-1148367

ABSTRACT

BACKGROUND During the coronavirus disease 2019 (COVID-19) pandemic of 2020, varied presentations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been reported. The present report is of a case of hyponatremia and encephalopathy due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) as the main presentation of SARS-CoV-2 infection in a 55-year-old woman. CASE REPORT A 55-year-old woman with type II diabetes mellitus presented with confusion and slurring of speech, with a temperature of 38.5°C, heart rate of 120 bpm, blood pressure of 159/81 mmHg, and oxygen saturation of 98% on room air. She did not have edema on examination. Laboratory testing showed a low sodium level of 116 mEq/L (reference range, 135-145 mEq/L) with urine osmolarity of 364 mOsm/kg, urinary sodium of 69 mEq/L, urinary potassium of 15.6 mEq/L, and serum osmolarity of 251 mOsm/kg. The patient had normal serum thyroid-stimulating hormone and cortisol levels. A chest X-ray should no pulmonary infiltrates nor did a lumbar puncture reveal signs of infection. A real-time SARS-CoV-2 polymerase chain reaction assay was positive for COVID-19. Brain imaging with computed tomography was negative for acute infarct, intracranial hemorrhage, and mass effect. Based on findings from laboratory testing and physical examination, a diagnosis of SIADH was made. The patient was treated with 3% hypertonic saline, followed by salt tablets and fluid restriction, with improvement in her clinical symptoms and serum sodium level. CONCLUSIONS The present report is of a rare but previously reported association with SARS-CoV-2 infection. Encephalopathy and hyponatremia associated with SIADH without pneumonia or other symptoms of infection should be an indication for testing for SARS-CoV-2 infection.


Subject(s)
Brain Diseases/virology , COVID-19/complications , Hyponatremia/virology , Inappropriate ADH Syndrome/virology , COVID-19/diagnosis , Diabetes Mellitus, Type 2/complications , Female , Humans , Middle Aged , Saline Solution, Hypertonic/therapeutic use , Sodium/blood , Sodium Chloride/therapeutic use
19.
Mol Neurobiol ; 58(7): 3347-3361, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1120777

ABSTRACT

The severity of COVID-19 infection is surging day by day. With the cases increasing daily, it is becoming more and more essential to understand the pathogenic mechanisms underlying the severity of the disease. It is now well known that the infection manifests itself primarily as respiratory, but the involvement of the other organ systems has now been documented in many studies. SARS-CoV-2 can invade the nervous system by a multitude of proposed mechanisms that have been discussed in this review. NF-κB and Nrf2 are transcription factors that regulate genes responsible for inflammatory and anti-oxidant response respectively. Specific focus in this review has been given to NF-κB and Nrf2 pathways that are involved in the cytokine storm and oxidative stress that are the hallmarks of COVID-19. As the immune injury is an important mechanism of neuro-invasion and neuroinflammation, there is the possible involvement of these two pathways in the neurological complications. The crosstalk mechanisms of these signaling pathways have also been discussed. Immuno-modulators both synthetic and natural are promising candidates in catering to the pathologies targeted in the aforementioned pathways.


Subject(s)
Brain Diseases/virology , Brain/metabolism , COVID-19/complications , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism , Oxidative Stress/physiology , Brain Diseases/metabolism , COVID-19/metabolism , Humans , Signal Transduction/physiology
20.
BMJ Case Rep ; 14(3)2021 Mar 02.
Article in English | MEDLINE | ID: covidwho-1115107

ABSTRACT

The COVID-19 pandemic has dealt a devastating blow to healthcare systems globally. Approximately 3.2% of patients infected with COVID-19 require invasive ventilation during the course of the illness. Within this population, 25% of patients are affected with neurological manifestations. Among those who are affected by severe neurological manifestations, some may have acute cerebrovascular complications (5%), impaired consciousness (15%) or exhibit skeletal muscle hypokinesis (20%). The cause of the severe cognitive impairment and hypokinesis is unknown at this time. Potential causes include COVID-19 viral encephalopathy, toxic metabolic encephalopathy, post-intensive care unit syndrome and cerebrovascular pathology. We present a case of a 60 year old patient who sustained a prolonged hospitalization with COVID-19, had a cerebrovascular event and developed a persistent unexplained encephalopathy along with a hypokinetic state. He was treated successfully with modafinil and carbidopa/levodopa showing clinical improvement within 3-7 days and ultimately was able to successfully discharge home.


Subject(s)
Brain Diseases , COVID-19 , Carbidopa/administration & dosage , Hypokinesia , Ischemic Stroke , Levodopa/administration & dosage , Modafinil/administration & dosage , Rehabilitation/methods , SARS-CoV-2/isolation & purification , Blood Coagulation , Brain Diseases/physiopathology , Brain Diseases/virology , COVID-19/blood , COVID-19/complications , COVID-19/physiopathology , COVID-19/therapy , Central Nervous System Stimulants/administration & dosage , Cognitive Dysfunction/diagnosis , Cognitive Dysfunction/etiology , Critical Care/methods , Drug Combinations , Humans , Hypokinesia/diagnosis , Hypokinesia/etiology , Hypokinesia/therapy , Ischemic Stroke/diagnostic imaging , Ischemic Stroke/etiology , Ischemic Stroke/physiopathology , Ischemic Stroke/therapy , Magnetic Resonance Imaging/methods , Male , Middle Aged , Respiration, Artificial/methods , Severity of Illness Index , Treatment Outcome , Ventilator Weaning/methods
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