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1.
Neurol Neuroimmunol Neuroinflamm ; 8(5)2021 07.
Article in English | MEDLINE | ID: covidwho-1278138

ABSTRACT

OBJECTIVE: Coronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators. METHODS: In this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2-specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/- sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS). RESULTS: We detected anti-SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10). CONCLUSIONS: Our results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.


Subject(s)
Brain Diseases/etiology , COVID-19/complications , Cytokines/cerebrospinal fluid , Inflammation/etiology , Neurovascular Coupling , SARS-CoV-2/pathogenicity , Adult , Aged , Aged, 80 and over , Antibodies, Viral/cerebrospinal fluid , Brain Diseases/cerebrospinal fluid , Brain Diseases/immunology , Brain Diseases/physiopathology , COVID-19/cerebrospinal fluid , COVID-19/immunology , Critical Care , Cross-Sectional Studies , Cytokines/blood , Electroencephalography , Female , Humans , Immunoglobulin G/cerebrospinal fluid , Inflammation/cerebrospinal fluid , Inflammation/immunology , Interleukin-8/cerebrospinal fluid , Male , Middle Aged , Neurovascular Coupling/immunology , SARS-CoV-2/immunology , Severity of Illness Index , Young Adult
3.
Ann Clin Transl Neurol ; 8(4): 968-979, 2021 04.
Article in English | MEDLINE | ID: covidwho-1155205

ABSTRACT

OBJECTIVE: Many neurological manifestations are associated with COVID-19, including a distinct form of encephalopathy related to cytokine storm, the acute systemic inflammatory syndrome present in a subgroup of COVID-19 patients. Cytokine storm is also associated with immune effector cell-associated neurotoxicity syndrome (ICANS), a complication of chimeric antigen receptor T-cell (CAR-T) therapy, a highly effective treatment for refractory hematological malignancies. We investigated whether COVID-19-related encephalopathy, ICANS, and other encephalopathies associated with cytokine storm, share clinical and investigative findings. METHODS: Narrative literature review. RESULTS: Comparisons between COVID-19-related encephalopathy and ICANS revealed several overlapping features. Clinically, these included dysexecutive syndrome, language disturbances, akinetic mutism and delirium. EEG showed a prevalence of frontal abnormalities. Brain MRI was often unrevealing. CSF elevated cytokine levels have been reported. A direct correlation between cytokine storm intensity and severity of neurological manifestations has been shown for both conditions. Clinical recovery occurred spontaneously or following immunotherapies in most of the patients. Similar clinical and investigative features were also reported in other encephalopathies associated with cytokine storm, such as hemophagocytic lymphohistiocytosis, sepsis, and febrile infection-associated encephalopathies. INTERPRETATION: COVID-19-related encephalopathy and ICANS are characterized by a predominant electro-clinical frontal lobe dysfunction and share several features with other encephalopathies associated with cytokine storm, which may represent the common denominator of a clinical spectrum of neurological disorders. Therefore, we propose a unifying definition of cytokine storm-associated encephalopathy (CySE), and its diagnostic criteria.


Subject(s)
Brain Diseases/physiopathology , Brain/physiopathology , COVID-19/physiopathology , Cytokine Release Syndrome/physiopathology , Immunotherapy, Adoptive/methods , Receptors, Chimeric Antigen , Brain Diseases/epidemiology , Brain Diseases/therapy , COVID-19/epidemiology , COVID-19/therapy , Cytokine Release Syndrome/epidemiology , Cytokine Release Syndrome/therapy , Humans , Immunotherapy, Adoptive/trends
4.
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
5.
IEEE Pulse ; 12(1): 2-6, 2021.
Article in English | MEDLINE | ID: covidwho-1091099

ABSTRACT

In March 2020 -still the early days of the U.K.'s COVID-19 crisis-Rhys Thomas, a neurologist at Newcastle University, got a call at home from a concerned colleague. The colleague's cousin was hospitalized, critically ill with COVID-19, and had developed brainstem encephalitis, a severe inflammatory condition of the brain causing a suite of symptoms, from eye problems to balance problems and drowsiness. He wanted to know if Thomas knew anything about these conditions. At the time, the research coming out of Wuhan, China, only suggested a mild whiff of neurological symptoms-headache, dizziness, and the loss of taste and smell. Clearly the virus could affect the brain in some ways, but it wasn't, Thomas thought then, anything serious. But this report sounded much more concerning. Symptoms like this patient's would mean the virus was accessing more of the nervous system than scientists originally thought.


Subject(s)
Brain Diseases/etiology , COVID-19/complications , Pandemics , SARS-CoV-2 , Brain Diseases/physiopathology , Brain Diseases/psychology , COVID-19/drug therapy , COVID-19/physiopathology , COVID-19/psychology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Encephalitis/etiology , Encephalitis/physiopathology , Humans , Nervous System Diseases/etiology , Nervous System Diseases/physiopathology , Nervous System Diseases/psychology , SARS-CoV-2/pathogenicity , Stroke/etiology , Stroke/physiopathology
6.
ACS Chem Neurosci ; 12(4): 573-580, 2021 02 17.
Article in English | MEDLINE | ID: covidwho-1065791

ABSTRACT

Long-COVID is a postviral illness that can affect survivors of COVID-19, regardless of initial disease severity or age. Symptoms of long-COVID include fatigue, dyspnea, gastrointestinal and cardiac problems, cognitive impairments, myalgia, and others. While the possible causes of long-COVID include long-term tissue damage, viral persistence, and chronic inflammation, the review proposes, perhaps for the first time, that persistent brainstem dysfunction may also be involved. This hypothesis can be split into two parts. The first is the brainstem tropism and damage in COVID-19. As the brainstem has a relatively high expression of ACE2 receptor compared with other brain regions, SARS-CoV-2 may exhibit tropism therein. Evidence also exists that neuropilin-1, a co-receptor of SARS-CoV-2, may be expressed in the brainstem. Indeed, autopsy studies have found SARS-CoV-2 RNA and proteins in the brainstem. The brainstem is also highly prone to damage from pathological immune or vascular activation, which has also been observed in autopsy of COVID-19 cases. The second part concerns functions of the brainstem that overlap with symptoms of long-COVID. The brainstem contains numerous distinct nuclei and subparts that regulate the respiratory, cardiovascular, gastrointestinal, and neurological processes, which can be linked to long-COVID. As neurons do not readily regenerate, brainstem dysfunction may be long-lasting and, thus, is long-COVID. Indeed, brainstem dysfunction has been implicated in other similar disorders, such as chronic pain and migraine and myalgic encephalomyelitis or chronic fatigue syndrome.


Subject(s)
Brain Diseases/physiopathology , Brain Stem/physiopathology , COVID-19/complications , Inflammation/physiopathology , Thrombosis/physiopathology , Angiotensin-Converting Enzyme 2/metabolism , Brain Diseases/metabolism , Brain Diseases/virology , Brain Stem/blood supply , Brain Stem/metabolism , Brain Stem/virology , COVID-19/metabolism , COVID-19/physiopathology , Humans , Inflammation/metabolism , Inflammation/virology , Neuropilin-1/metabolism , RNA, Viral/isolation & purification , RNA, Viral/metabolism , Receptors, Coronavirus/metabolism , SARS-CoV-2/genetics , SARS-CoV-2/pathogenicity , Thrombosis/metabolism , Thrombosis/virology , Viral Tropism
7.
Seizure ; 84: 66-68, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-1065590

ABSTRACT

Symptoms of COVID-19, as reported during the SARS-CoV-2 pandemic in 2019-2020, are primarily respiratory and gastrointestinal, with sparse reports on neurological manifestations. We describe the case of a 17-year old female with Cornelia de Lange syndrome and well controlled epilepsy, who sustained significant cortical injury during a COVID-19 associated multi-inflammatory syndrome.


Subject(s)
Brain Diseases/physiopathology , COVID-19/physiopathology , De Lange Syndrome/complications , Epilepsy/physiopathology , Seizures/physiopathology , Systemic Inflammatory Response Syndrome/physiopathology , Acute Kidney Injury/etiology , Adolescent , Airway Extubation , Anticonvulsants/therapeutic use , Blood Coagulation Disorders/etiology , Bone Marrow Failure Disorders , Brain Diseases/diagnostic imaging , Brain Diseases/etiology , Brain Diseases/pathology , Brain Edema/diagnostic imaging , Brain Edema/etiology , C-Reactive Protein/immunology , COVID-19/complications , COVID-19/immunology , COVID-19/therapy , Disease Progression , Electroencephalography , Epilepsy/complications , Epilepsy/drug therapy , Female , Ferritins/metabolism , Humans , Influenza B virus , Influenza, Human/complications , Levetiracetam/therapeutic use , Magnetic Resonance Imaging , Midazolam/therapeutic use , Necrosis , Phenobarbital/therapeutic use , Pseudomonas Infections/complications , Respiration, Artificial , Rhabdomyolysis/complications , Rhabdomyolysis/etiology , SARS-CoV-2 , Seizures/drug therapy , Seizures/etiology , Sepsis/etiology , Sepsis/physiopathology , Sepsis/therapy , Systemic Inflammatory Response Syndrome/complications , Systemic Inflammatory Response Syndrome/immunology , Systemic Inflammatory Response Syndrome/therapy , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/physiopathology , Tachycardia, Ventricular/therapy
9.
Lancet Child Adolesc Health ; 5(3): 167-177, 2021 03.
Article in English | MEDLINE | ID: covidwho-978470

ABSTRACT

BACKGROUND: The CNS manifestations of COVID-19 in children have primarily been described in case reports, which limit the ability to appreciate the full spectrum of the disease in paediatric patients. We aimed to identify enough cases that could be evaluated in aggregate to better understand the neuroimaging manifestations of COVID-19 in the paediatric population. METHODS: An international call for cases of children with encephalopathy related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and abnormal neuroimaging findings was made. Clinical history and associated plasma and cerebrospinal fluid data were requested. These data were reviewed by a central neuroradiology panel, a child neurologist, and a paediatric infectious diseases expert. The children were categorised on the basis of their time of probable exposure to SARS-CoV-2. In addition, cases were excluded when a direct link to SARS-CoV-2 infection could not be established or an established alternate diagnostic cause could be hypothesised. The accepted referral centre imaging data, from ten countries, were remotely reviewed by a central panel of five paediatric neuroradiologists and a consensus opinion obtained on the imaging findings. FINDINGS: 38 children with neurological disease related to SARS-CoV-2 infection were identified from France (n=13), the UK (n=8), the USA (n=5), Brazil (n=4), Argentina (n=4), India (n=2), Peru (n=1), and Saudi Arabia (n=1). Recurring patterns of disease were identified, with neuroimaging abnormalities ranging from mild to severe. The most common imaging patterns were postinfectious immune-mediated acute disseminated encephalomyelitis-like changes of the brain (16 patients), myelitis (eight patients), and neural enhancement (13 patients). Cranial nerve enhancement could occur in the absence of corresponding neurological symptoms. Splenial lesions (seven patients) and myositis (four patients) were predominantly observed in children with multisystem inflammatory syndrome. Cerebrovascular complications in children were less common than in adults. Significant pre-existing conditions were absent and most children had favourable outcomes. However, fatal atypical CNS co-infections developed in four previously healthy children infected with SARS-CoV-2. INTERPRETATION: Acute-phase and delayed-phase SARS-CoV-2-related CNS abnormalities are seen in children. Recurring patterns of disease and atypical neuroimaging manifestations can be found and should be recognised being as potentially due to SARS-CoV-2 infection as an underlying aetiological factor. Studies of paediatric specific cohorts are needed to better understand the effects of SARS-CoV-2 infection on the CNS at presentation and on long-term follow-up in children. FUNDING: American Society of Pediatric Neuroradiology, University of Manchester (Manchester, UK). VIDEO ABSTRACT.


Subject(s)
COVID-19/complications , Central Nervous System Diseases/diagnostic imaging , Central Nervous System Diseases/etiology , Neuroimaging , Adolescent , Argentina/epidemiology , Brain Diseases/diagnostic imaging , Brain Diseases/physiopathology , Brazil/epidemiology , COVID-19/physiopathology , Child , Child, Preschool , Coinfection/mortality , Encephalomyelitis, Acute Disseminated/diagnostic imaging , Encephalomyelitis, Acute Disseminated/physiopathology , Female , France/epidemiology , Humans , India/epidemiology , Infant , Male , Peru/epidemiology , SARS-CoV-2/pathogenicity , Saudi Arabia/epidemiology , Systemic Inflammatory Response Syndrome/physiopathology , United Kingdom/epidemiology , United States/epidemiology
12.
Ann Clin Transl Neurol ; 8(1): 300-301, 2021 01.
Article in English | MEDLINE | ID: covidwho-925534

ABSTRACT

A 69-year-old man with uncontrolled type 2 diabetes presented to an outside hospital with altered mental status. He progressed from being argumentative to encephalopathic and agitated by the evening with urinary frequency, urinary urgency, nausea, and vomiting. His vital signs were normal, and he had no focal neurological deficits on presentation. He was generally encephalopathic, only groaning with no ability to follow commands. He was found to have diabetic ketoacidosis on initial labs. A left parietal hypodensity on CT Head was found, and he was positive for Sars-COV-2.


Subject(s)
Brain Diseases/physiopathology , COVID-19/physiopathology , Cerebral Veins , Diabetic Ketoacidosis/physiopathology , Sinus Thrombosis, Intracranial/physiopathology , Aged , Brain Diseases/etiology , COVID-19/complications , COVID-19/diagnostic imaging , Diabetes Mellitus, Type 2/complications , Diabetic Ketoacidosis/etiology , Humans , Magnetic Resonance Imaging , Male , SARS-CoV-2 , Sinus Thrombosis, Intracranial/diagnostic imaging , Sinus Thrombosis, Intracranial/etiology , Thrombosis/diagnostic imaging , Thrombosis/etiology , Thrombosis/physiopathology , Tomography, X-Ray Computed
13.
Brain Dev ; 43(2): 230-233, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-856505

ABSTRACT

BACKGROUND: Reversible splenial lesion syndrome (RESLES) is characterized by a temporary lesion in the splenium of the corpus callosum, emerging related to encephalitis, seizures, antiepileptic drug withdrawal, or metabolic disturbances. Among RESLES, mild encephalitis/encephalopathy with reversible splenial lesion (MERS) has been defined as a distinct clinicoradiologic syndrome associated with viral infections. CASE PRESENTATION: We report two children with multisystem inflammatory syndrome-children related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) who developed RESLES during the disease course. Encephalopathy was the main central nervous system symptom. Both of the children showed a rapid recovery, and brain magnetic resonance imaging revealed complete resolution of the splenial lesion within 1 week. CONCLUSION: The complete resolution of the splenial lesion and rapid recovery from encephalopathy in RESLES associated with SARS CoV-2 were similar to observed in MERS.


Subject(s)
Brain Diseases/diagnostic imaging , COVID-19/diagnosis , Corpus Callosum/diagnostic imaging , Systemic Inflammatory Response Syndrome/diagnostic imaging , Brain Diseases/drug therapy , Brain Diseases/physiopathology , COVID-19/diagnostic imaging , COVID-19/drug therapy , COVID-19/physiopathology , Child , Dyspnea/physiopathology , Electroencephalography , Exanthema/physiopathology , Female , Fever/physiopathology , Glucocorticoids/therapeutic use , Hallucinations/physiopathology , Humans , Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Magnetic Resonance Imaging , Male , Methylprednisolone/therapeutic use , Neurocognitive Disorders/diagnostic imaging , Neurocognitive Disorders/physiopathology , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/physiopathology , Tachypnea/physiopathology
14.
Ann Clin Transl Neurol ; 7(11): 2221-2230, 2020 11.
Article in English | MEDLINE | ID: covidwho-813302

ABSTRACT

OBJECTIVE: Covid-19 can involve multiple organs including the nervous system. We sought to characterize the neurologic manifestations, their risk factors, and associated outcomes in hospitalized patients with Covid-19. METHODS: We examined neurologic manifestations in 509 consecutive patients admitted with confirmed Covid-19 within a hospital network in Chicago, Illinois. We compared the severity of Covid-19 and outcomes in patients with and without neurologic manifestations. We also identified independent predictors of any neurologic manifestations, encephalopathy, and functional outcome using binary logistic regression. RESULTS: Neurologic manifestations were present at Covid-19 onset in 215 (42.2%), at hospitalization in 319 (62.7%), and at any time during the disease course in 419 patients (82.3%). The most frequent neurologic manifestations were myalgias (44.8%), headaches (37.7%), encephalopathy (31.8%), dizziness (29.7%), dysgeusia (15.9%), and anosmia (11.4%). Strokes, movement disorders, motor and sensory deficits, ataxia, and seizures were uncommon (0.2 to 1.4% of patients each). Severe respiratory disease requiring mechanical ventilation occurred in 134 patients (26.3%). Independent risk factors for developing any neurologic manifestation were severe Covid-19 (OR 4.02; 95% CI 2.04-8.89; P < 0.001) and younger age (OR 0.982; 95% CI 0.968-0.996; P = 0.014). Of all patients, 362 (71.1%) had a favorable functional outcome at discharge (modified Rankin Scale 0-2). However, encephalopathy was independently associated with worse functional outcome (OR 0.22; 95% CI 0.11-0.42; P < 0.001) and higher mortality within 30 days of hospitalization (35 [21.7%] vs. 11 [3.2%] patients; P < 0.001). INTERPRETATION: Neurologic manifestations occur in most hospitalized Covid-19 patients. Encephalopathy was associated with increased morbidity and mortality, independent of respiratory disease severity.


Subject(s)
Brain Diseases/physiopathology , Coronavirus Infections/physiopathology , Dizziness/physiopathology , Dysgeusia/physiopathology , Headache/physiopathology , Myalgia/physiopathology , Olfaction Disorders/physiopathology , Pneumonia, Viral/physiopathology , Adult , Aged , Aged, 80 and over , Ataxia/physiopathology , Betacoronavirus , COVID-19 , Chicago , Coronavirus Infections/mortality , Coronavirus Infections/therapy , Female , Humans , Male , Middle Aged , Mortality , Movement Disorders/physiopathology , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/therapy , Prognosis , Respiration, Artificial , Retrospective Studies , Risk Factors , SARS-CoV-2 , Seizures/physiopathology , Severity of Illness Index , Stroke/physiopathology
15.
Clin Neurophysiol ; 132(1): 218-225, 2021 01.
Article in English | MEDLINE | ID: covidwho-807009

ABSTRACT

OBJECTIVE: Encephalopathy is a major neurological complication of severe Coronavirus Disease 2019 (COVID-19), but has not been fully defined yet. Further, it remains unclear whether neurological manifestations are primarily due to neurotropism of the virus, or indirect effects, like cerebral hypoxia. METHODS: We analysed the electroencephalograms (EEGs) of 19 consecutive patients with laboratory-confirmed COVID-19, performed at peak disease severity as part of their clinical management. Disease severity, respiratory failure, immune and metabolic dysfunction, sedation status, and neurological examination on the day of the EEG were noted. RESULTS: Severe encephalopathy was confirmed in 13 patients, all with severe COVID-19; 10 remained comatose off sedation, and five of them had alpha coma (AC). Disease severity, sedation, immune and metabolic dysfunction were not different between those with AC and those without. CONCLUSIONS: Severe COVID-19 encephalopathy is a principal cause of persisting coma after sedation withdrawal. The relatively high incidence of the rare AC pattern may reflect direct SARS-CoV-2 neurotropism with a predilection for the brainstem ascending reticular system. SIGNIFICANCE: Systematic early EEG detection of encephalopathy related to severe COVID-19 is important for the acute care and the management of long-term neurological and cognitive sequelae, and may help our better understanding of its pathophysiology.


Subject(s)
Brain Diseases/physiopathology , Brain/physiopathology , COVID-19/physiopathology , Coma/physiopathology , Adult , Aged , Aged, 80 and over , Brain Diseases/etiology , COVID-19/complications , Coma/etiology , Electroencephalography , Female , Humans , Male , Middle Aged , Retrospective Studies
16.
Ann Neurol ; 88(3): 626-630, 2020 09.
Article in English | MEDLINE | ID: covidwho-763027

ABSTRACT

In March 2020, we treated a cohort of 26 critically ill hospitalized SARS-CoV-2-infected patients who underwent electroencephalography to assess unexplained altered mental status, loss of consciousness, or poor arousal and responsiveness. Of the 26 patients studied, 5 patients had electroencephalograms that showed periodic discharges consisting of high-amplitude frontal monomorphic delta waves with absence of epileptic activity. These findings may suggest central nervous system injury potentially related to COVID-19 in these patients. ANN NEUROL 2020;88:626-630.


Subject(s)
Brain Diseases/physiopathology , Brain Diseases/virology , COVID-19/complications , COVID-19/physiopathology , Aged , Brain/physiopathology , Critical Illness , Electroencephalography , Humans , Male , Middle Aged
17.
Epilepsia ; 61(10): 2097-2105, 2020 10.
Article in English | MEDLINE | ID: covidwho-740235

ABSTRACT

OBJECTIVE: There is evidence for central nervous system complications of coronavirus disease 2019 (COVID-19) infection, including encephalopathy. Encephalopathy caused by or arising from seizures, especially nonconvulsive seizures (NCS), often requires electroencephalography (EEG) monitoring for diagnosis. The prevalence of seizures and other EEG abnormalities among COVID-19-infected patients is unknown. METHODS: Medical records and EEG studies of patients hospitalized with confirmed COVID-19 infections over a 2-month period at a single US academic health system (four hospitals) were reviewed to describe the distribution of EEG findings including epileptiform abnormalities (seizures, periodic discharges, or nonperiodic epileptiform discharges). Factors including demographics, remote and acute brain injury, prior history of epilepsy, preceding seizures, critical illness severity scores, and interleukin 6 (IL-6) levels were compared to EEG findings to identify predictors of epileptiform EEG abnormalities. RESULTS: Of 111 patients monitored, most were male (71%), middle-aged or older (median age 64 years), admitted to an intensive care unit (ICU; 77%), and comatose (70%). Excluding 11 patients monitored after cardiac arrest, the most frequent EEG finding was moderate generalized slowing (57%), but epileptiform findings were observed in 30% and seizures in 7% (4% with NCS). Three patients with EEG seizures did not have epilepsy or evidence of acute or remote brain injury, although all had clinical seizures prior to EEG. Only having epilepsy (odds ratio [OR] 5.4, 95% confidence interval [CI] 1.4-21) or seizure(s) prior to EEG (OR 4.8, 95% CI 1.7-13) was independently associated with epileptiform EEG findings. SIGNIFICANCE: Our study supports growing evidence that COVID-19 can affect the central nervous system, although seizures are unlikely a common cause of encephalopathy. Seizures and epileptiform activity on EEG occurred infrequently, and having a history of epilepsy or seizure(s) prior to EEG testing was predictive of epileptiform findings. This has important implications for triaging EEG testing in this population.


Subject(s)
Brain Diseases/physiopathology , Brain Diseases/virology , COVID-19/complications , Aged , COVID-19/physiopathology , Electroencephalography , Humans , Male , Middle Aged , Neurophysiological Monitoring , New York , SARS-CoV-2
20.
Seizure ; 81: 198-200, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-733627

ABSTRACT

PURPOSE: Neurological manifestations of COVID-19 infection include impaired consciousness, strokes, and seizures. Limited reports describing EEG abnormalities in patients with COVID-19 have been published. These articles reported nonspecific encephalopathic patterns, epileptiform discharges, and rarely seizures. Our primary aim was to assess EEG abnormalities in patients with COVID-19 and evaluate for epileptiform activity or seizures. METHODS: We identified five critically ill adult patients with COVID-19 who underwent EEG monitoring. All patients had Ceribell™ rapid response EEG initially and two continued with conventional long-term video EEG. RESULTS: All 5 patients had encephalopathy and 3 also had seizure-like movements, thus prompting EEG monitoring. EEGs all showed nonspecific markers of encephalopathy including diffuse slowing and generalized rhythmic delta activity. Two also had epileptiform discharges reaching 2-3 Hz at times, with one patient in nonconvulsive status epilepticus and the other developing clinical status epilepticus with myoclonic movements. EEG and clinical symptoms improved with anti-seizure medications. CONCLUSION: Status epilepticus was present in 2 out of our cohort of 5 critically ill patients who underwent EEG monitoring. These findings highlight the importance of EEG monitoring in high-risk patients with COVID-19 and encephalopathy. EEG recordings in such patients can identify pathological patterns that will benefit from treatment with anti-seizure medications.


Subject(s)
Brain Diseases/physiopathology , Coronavirus Infections/physiopathology , Pneumonia, Viral/physiopathology , Seizures/physiopathology , Status Epilepticus/physiopathology , Adult , Betacoronavirus , Brain Diseases/diagnosis , COVID-19 , Electroencephalography , Female , Humans , Male , Middle Aged , Pandemics , Retrospective Studies , SARS-CoV-2 , Seizures/diagnosis , Status Epilepticus/diagnosis
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