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COVID-19: Neurologic complications and management of neurologic conditions

COVID-19: Neurologic complications and management of neurologic conditions
Authors:
Brett L Cucchiara, MD
Igor J Koralnik, MD
Anna S Nordvig, MD
Section Editors:
José Biller, MD, FACP, FAAN, FAHA
Alejandro A Rabinstein, MD
Scott E Kasner, MD
Deputy Editor:
Richard P Goddeau, Jr, DO, FAHA
Literature review current through: Jan 2024.
This topic last updated: Dec 18, 2023.

INTRODUCTION — The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19) [1]. Coronaviruses are important human and animal pathogens in neurological disease [2]. Symptomatic patients with COVID-19 typically present with respiratory symptoms but neurologic complications are common [3,4]. The burden of neurologic symptoms is elevated in hospitalized patients with severe infection and those with baseline neurologic conditions but also occurs in healthy patients and those with milder illness [5,6].

This topic will review the neurologic complications of COVID-19 and the management of patients with neurologic conditions who develop COVID-19. Other aspects of COVID-19 are described separately:

●(See "COVID-19: Epidemiology, virology, and prevention".)

●(See "COVID-19: Clinical features".)

●(See "COVID-19: Diagnosis".)

●(See "COVID-19: Management in hospitalized adults".)

●(See "COVID-19: Management of the intubated adult".)

●(See "COVID-19: Clinical manifestations and diagnosis in children".)

●(See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")".)

NEUROPATHOGENESIS — The underlying mechanisms of neurologic complications in patients with COVID-19 are diverse and, in some cases, multifactorial. Acute neurologic complications frequently arise from systemic response to the infection or immune dysfunction [7,8]. Delayed or chronic neurologic complications may be related to a persistent inflammatory response, immune dysfunction, or genetic susceptibilities. Other mechanisms may also contribute.

Distinct but likely overlapping neuropathologic mechanisms include:

●Neurologic injury due to systemic dysfunction – Patients with severe COVID-19 who are hospitalized for respiratory impairment and/or other organ failure may develop encephalopathy or other neurologic symptoms due to hypoxemia. Severe illness may also lead to acute neurologic injury from associated metabolic derangements or medication effects. In a case series of patients who died from severe COVID-19 infection, acute hypoxic ischemic damage was present in nearly all patients, as well as the presence of hemorrhagic and bland infarcts [8]. Microglial activation with microglial nodules and neuronophagia have been identified at autopsy [8-10]. In other series, neuroimaging findings appeared consistent with a delayed posthypoxic leukoencephalopathy and are similar to those described in patients with acute respiratory distress syndrome (ARDS) unrelated to COVID-19 [11-13].

●Immune dysfunction – A dysregulated immune response to SARS-CoV-2 has been implicated in the genesis of neurologic symptoms [14,15].

•Proinflammatory state – Critically ill patients with COVID-19 can develop signs of severe systemic inflammation consistent with a cytokine release syndrome-like presentation that manifests with persistent fever and laboratory evidence of elevated inflammatory markers (eg, D-dimer, ferritin) and proinflammatory cytokines (eg, peripheral tumor necrosis factor [TNF], TNF-alpha, and interleukin 6 [IL-6]) [16,17]. High levels of circulating proinflammatory cytokines can cause confusion and alteration of consciousness [18,19].

Cytokine release may also lead to brain injury by microglial activation and a systemic inflammatory response. In case series and reports, microglial nodules, neuronophagia, and neuronal expression of elevated cytokines (IL-1 beta and IL-6) were found in brain tissue without evidence of direct viral invasion [8,20,21]. Microglial activation to phagocytose hypoxic neurons has been seen with other viral infections.

A proinflammatory state also may be associated with thrombophilia ("thromboinflammation"), increasing the risk of stroke and other thrombotic events [22]. SARS-CoV-2 utilizes angiotensin converting enzyme 2 (ACE-2), a membrane-bound protein, as its point of entry into cells. By binding to ACE-2, the SARS-CoV-2 virus may damage vascular endothelial cells by inhibiting mitochondrial function and endothelial nitric oxide synthetase activity, resulting in vascular endothelial damage and cardio- and cerebrovascular complications [23]. Complement activation may also lead to thrombotic microvascular injury in patients with severe COVID-19 [24].

A heightened immune system response may also persist after acute infection and contribute to delayed recovery. One study that assessed cerebrospinal fluid (CSF) of participants with persisting cognitive symptoms nine months after COVID-19 infection found patients with persistent cognitive symptoms were likelier to have CSF abnormalities than controls (77 percent [10 of 13] versus none [0 of 4]) [25].

•Autoimmunity – Acute and chronic symptoms have been linked to the presence of autoimmune markers in some studies [26], including autoantibodies against immunomodulatory proteins [27]. COVID-19 has been implicated as a trigger for autoimmune-mediated complications including Guillain-Barré syndrome (GBS), transverse myelitis, and autoimmune encephalitis. The timing of symptoms relative to initial symptoms of COVID-19 infection suggests that Guillain-Barré occurs as a parainfectious rather than a postinfectious complication in most patients. In one case, weakness preceded the onset of fever and respiratory symptoms [28]. Other cases report a longer interval between the onset of viral illness and weakness, consistent with its occurrence as a postinfectious complication. (See 'Guillain-Barré syndrome' below and 'Other acute neurologic manifestations' below.)

The binding of SARS-CoV-2 to the ACE-2 receptor on the endothelial cells may also lead to immune-mediated injury with the generation of antibody complexes [10]. Endothelial damage can contribute to thromboembolic complications including stroke. (See 'Cerebrovascular disease' below.)

●Direct viral invasion of the nervous system – Few reports provide evidence for direct viral invasion of the nervous system [29-31]. In postmortem case series, SARS-CoV-2 was detected in some brain specimens, but these findings were unrelated to the severity of neuropathologic findings and may represent hematogenous contamination during autopsy [8,29,30]. This suggests that neural injury may be due to a systemic inflammatory response triggered by the SARS-CoV-2 virus rather than the infection itself.

It is uncertain if SARS-CoV-2 directly infects the cerebral vessels. Small autopsy studies have reported potential evidence of direct endothelial invasion by the SARS-CoV-2 virus with a possible associated endotheliitis in the lung, heart, kidney, liver, and small intestine [32,33]. However, this remains controversial, as structures on electron microscopy thought to represent viral particles in the endothelium of blood vessels in the kidney may actually be normal structures or artifacts [34,35]. Neuropathologic studies have not confirmed frank cerebral vasculitis with SARS-CoV-2 [8].

●Neurodegeneration – Neuronal changes in limbic and other brain regions have been reported in patients with a prior COVID-19 infection. Among 785 participants of the United Kingdom Biobank study with baseline and follow-up imaging, structural changes were likelier in those following COVID-19 infection [36]. Repeat imaging was performed at a mean of 141 days following COVID-19 infection. Patients with COVID-19 infection were found to have greater reductions in functional connectivity and structural domains (gray matter thickness in the orbitofrontal and parahippocampal cortices and global brain size) compared with controls. In another study, elevated levels of biomarkers associated with neuronal dysfunction were reported in patients with persistent neurologic symptoms following either severe or mild COVID-19 infection [37]. It is unclear whether these structural changes were due to long-term effects from COVID-19 infection or the functional impact of anosmia on the cortex. The persistence of these findings and their functional significance over the long term is also uncertain.

Neurodegenerative markers can be elevated in some patients with COVID-19 infection. In a study of 251 patients hospitalized with COVID-19 (without pre-existing reported dementia or mild cognitive impairment), those with new neurological events during hospitalization were likelier to have elevations in neurodegenerative markers (eg, Tau, neurofilament light chain, ubiquitin) [38]. In another study, elevated levels of biomarkers associated with neuronal dysfunction were reported in patients with persistent neurologic symptoms following either severe or mild COVID-19 infection [37]. However, neurodegenerative markers may also be elevated in other infections, and the long-term effects of these findings in patients with COVID-19 infection remains uncertain. Further study is warranted to assess the role of these findings in patients with post-COVID neurologic symptoms.

ACUTE NEUROLOGIC COMPLICATIONS — Neurologic manifestations can occur in approximately half of hospitalized COVID-19 patients. However, the frequency and severity of neurologic complications of COVID-19 identified at the beginning of the pandemic have decreased due to vaccination, natural immunity, and social distancing strategies, as well as due to the evolving effect of variant forms of SARS-CoV-2 that predominate in the community. Typically, fatigue, myalgias, smell/taste dysfunction, and headache appear to be most common [4].

Smell and taste disorders — Anosmia and dysgeusia have been reported as common early symptoms in patients with COVID-19. In a meta-analysis of 83 studies involving more than 27,000 patients, olfactory dysfunction was reported in 48 percent (95% CI 41.2-54.5) [39]. These symptoms may be an initial manifestation of COVID-19 and can occur in the absence of nasal congestion or discharge; however, these are rarely the only clinical manifestations of COVID-19. (See "COVID-19: Clinical features", section on 'Initial presentation'.)

Transient anosmia may be related to inflammatory changes in the sustentacular cells within the nasal epithelium rather than direct injury to the olfactory neurons [40]. Magnetic resonance imaging (MRI) signal abnormalities in one or both olfactory bulbs have been described in patients with COVID-19, which can resolve on follow-up imaging [41-45]. In one MRI-based study of 20 patients with anosmia, edematous obstruction was identified in the olfactory cleft of the nasal cavities [46]. At one-month follow-up, olfactory function correlated with improvement of obstruction.

Robust data on long-term prognosis are lacking [47]. In one series, among the 33 percent of affected patients who had recovered olfactory function, the mean symptom duration was eight days [48]. In a survey of nonhospitalized patients with olfactory dysfunction from Italy, 83 percent reported complete recovery at a mean of 37 days after symptom onset [49]. Among 51 patients with anosmia who underwent objective olfactory testing, full recovery at four and eight months was reported in 84 and 96 percent, respectively [50]. In some patients, anosmia and dysgeusia may persist for several months, along with other neurologic or systemic symptoms after acute COVID-19 infection [51]. (See 'Persistent neurologic symptoms after SARS-CoV-2 infection' below.)

Taste and olfactory dysfunction can occur with other viral infections and other causes; an approach to evaluation is discussed separately. (See "Taste and olfactory disorders in adults: Evaluation and management".)

Encephalopathy — Encephalopathy is common in critically ill patients with COVID-19. Encephalopathy may be more common in COVID-19 than in other severe respiratory illnesses [52]. In a cohort study of 2088 patients with COVID-19 admitted to an intensive care unit, delirium was common, occurring in 55 percent [53].

Underlying causes and risk factors — Critically ill patients, including those with COVID-19, are subject to at least the same causes of encephalopathy as are other critically ill patients. Common causes of agitated or hypoactive delirium are varied and include toxic metabolic encephalopathy, medication effects, cerebrovascular disease, nonconvulsive seizures, and others as outlined in more detail in the table (table 1). The underlying causes of delirium are discussed in detail separately. (See "Diagnosis of delirium and confusional states".)

Encephalopathy may be a presenting feature and/or a clinical component of other overlapping neurologic conditions. Other neurologic complications of COVID-19 that may also produce encephalopathy include:

●Ischemic or hemorrhagic stroke.

●Encephalitis.

●Reversible posterior leukoencephalopathy syndrome (RPLS).

●Multisystem inflammatory syndrome.

●Postinfectious demyelinating disease.

The clinical features of these other neurologic complications are discussed separately. (See 'Cerebrovascular disease' below and 'Other acute neurologic manifestations' below.)

Severe COVID-19 infection and medical comorbidities are common risk factors for encephalopathy. In a study of 509 hospitalized COVID-19 patients, 32 percent had encephalopathy, and those patients were older than those without encephalopathy (66 versus 55 years), had a shorter time from symptom onset to hospitalization (six versus seven days), were more likely to be male, and were more likely to have medical comorbidities (including a history of any neurologic disorder, cancer, cerebrovascular disease, chronic kidney disease, diabetes, dyslipidemia, heart failure, hypertension, or smoking) [3]. Factors associated with a higher risk of delirium among patients with COVID-19 admitted to an intensive care unit included mechanical ventilation, vasopressor use, use of restraints, benzodiazepine or continuous opioid infusions, and lack of family visitation [53].

Clinical features — Patients with COVID-19 may develop prominent delirium and agitation requiring sedation; others manifest encephalopathy with somnolence and a decreased level of consciousness [54,55]. Corticospinal tract signs (eg, hyperreflexia, extensor plantar responses) are common; seizures are described along with encephalopathy in patients with COVID-19, just as they can occur in toxic-metabolic encephalopathy in other settings [56,57]. These signs and symptoms are described separately. (See "Diagnosis of delirium and confusional states", section on 'Clinical presentation'.)

In most cases, encephalopathy develops in patients who become critically ill. In exceptional cases, delirium may be an early, and even a presenting, feature [58,59], especially in older adult patients [60,61]. Cases of transient global amnesia have also been reported [62,63].

Diagnostic test findings — Patients with acute encephalopathy typically have no evidence of brain inflammation on clinical neuroimaging studies or on cerebrospinal fluid (CSF) analysis, although there are exceptions.

●MRI findings – A spectrum of neuroimaging abnormalities have been described in patients with COVID-19-related encephalopathy; some but not all of these findings indicate a specific, alternative (and/or additional) diagnosis for the patient's mental state, such as stroke, encephalitis, RPLS, and others [11,45,55,64-66]. (See 'Other acute neurologic manifestations' below.)

Approximately half of neuroimaging studies in patients with COVID-19-related encephalopathy demonstrate an acute abnormality, the most common of which are cortical fluid-attenuated inversion recovery (FLAIR) signal abnormality, acute ischemic stroke, leptomeningeal enhancement (often subtle), and other manifestations of encephalitis [11,13,45,55,64,66,67]. Impaired perfusion may be found in hospitalized patients using arterial spin labeling MRI sequences [68]. One series reported results of MRI studies in 190 patients with severe COVID-19, most of whom had symptoms consistent with encephalopathy [64]. After excluding patients with ischemic stroke or chronic unrelated lesions, abnormalities were reported in 37 patients. Patterns of MRI abnormality included multifocal hyperintense lesions on T2-weighted and diffusion-weighted sequences in the white matter or medial temporal lobe, often with associated microhemorrhages.

Hyperintense lesions on MRI have been reported in the splenium of the corpus callosum in adult patients with COVID-19-related encephalopathy [64,66,69,70] as well as in a few children with multisystem inflammatory syndrome in COVID-19 [65]. (See "COVID-19: Multisystem inflammatory syndrome in children (MIS-C) clinical features, evaluation, and diagnosis".)

●Cerebrospinal fluid – Abnormal findings in the CSF are nonspecific and appear in a minority of cases, including patients presenting with acute neurologic symptoms [71]. A 2021 systemic review of individual reports and case series involving 430 patients identified SARS-CoV-2 in the CSF of only 17 patients (6 percent) [71]. Oligoclonal bands were found in three patients among the 132 patients tested.

Evaluation and management — Patients with COVID-19 infection who develop encephalopathy should be evaluated for underlying causes that may occur in patients with other systemic illnesses (table 1). Specific testing depends on the clinical scenario and may include MRI with and without gadolinium, electroencephalography (EEG) to exclude subclinical seizures, and cerebrospinal fluid evaluation to rule out central nervous system infection. The evaluation of patients with encephalopathy is described in detail separately. (See "Diagnosis of delirium and confusional states", section on 'Evaluation'.)

The general management of patients with COVID-19 and encephalopathy is directed toward the underlying cause and is the same as the management of other patients with delirium. (See "Delirium and acute confusional states: Prevention, treatment, and prognosis", section on 'Management' and "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

Additional factors for patients with COVID-19 infection and encephalopathy include:

●Initial supportive care – As with other critically ill patients, improvement in neurologic dysfunction may be delayed beyond the period when symptoms of the acute illness have resolved. Clinicians should exercise caution about withdrawal of life support measures in patients with encephalopathy in the absence of structural brain injury on neuroimaging or other evidence of futility.

Our clinical experience, as well as some published reports, suggest that some patients with a prolonged disorder of consciousness in the setting of severe COVID-19 may awaken up to several days to weeks following cessation of sedating medications and later recover [3,72-74]. In one series of 795 hospitalized patients with severe COVID-19 infection who were intubated for at least seven days, among the nearly 72 percent who eventually recovered consciousness, the median time to recovery of command following was 30 days [75]. Variables associated with prolonged recovery included hypoxemia, duration of exposure to paralytic or sedative medications, age, and male sex. Approximately one-third of patients with encephalopathy and COVID-19 infection who subsequently recover remained subjectively cognitively impaired at the time of hospital discharge [3,55,76].

●The role of immunomodulatory therapies – The role of glucocorticoids or other immunomodulatory therapies in the management of patients with COVID-19 and encephalopathy is uncertain. Case series have identified a small number of patients with severe encephalopathy who have improved neurologically after receiving glucocorticoids with or without plasma exchange [77,78]. However, glucocorticoids or other immunomodulatory therapies should not be considered routine therapeutic options for patients with COVID-19-related encephalopathy unless additional data emerge to help identify immunotherapy-responsive cases.

The role of glucocorticoids in the general management of severely ill patients with COVID-19 is discussed in further detail separately. (See "COVID-19: Management in hospitalized adults", section on 'Dexamethasone and other glucocorticoids'.)

Cerebrovascular disease

Epidemiology — Cerebrovascular events appear to be relatively infrequent in the setting of acute COVID-19 infection. Incidence rates according to stroke subtype have been assessed in multiple retrospective series:

●Ischemic stroke – 0.4 to 2.4 percent [79-84]

●Intracranial hemorrhage – 0.2 to 0.9 percent [82,83]

●Cerebral venous thrombosis (CVT) – 0.08 percent [85,86]

The risk of stroke varies according to the severity of COVID-19. Early case series suggest that for patients with mild illness, the risk is <1 percent, while for patients in intensive care, the risk may be as high as 6 percent [54].

Most often, stroke occurs one to three weeks after onset of COVID-19 symptoms, although stroke has been the initial symptom leading to hospitalization in a minority of reported patients [80,81,87-89].

The mean age of patients with COVID-19 and stroke appears similar to that of those without COVID-19. In a systematic analysis of 10 studies including 160 COVID-19 patients with ischemic stroke, the median age was 65 years [90]. In a United States national stroke registry that included 1143 patients with COVID-19 and acute stroke, the median age at presentation was 68 years compared with 71 years for patients without COVID-19 during the same period [91].

The incidence of stroke may be elevated beyond the acute period of COVID-19 infection. In a study of approximately 5.8 million United States veterans, the incidence of stroke at one year was higher in patients with prior COVID-19 infection than controls (hazard ratio 1.52, 95% CI 1.4-1.6) [92]. Cerebrovascular risk was higher for patients hospitalized with COVID-19 than for patients with less severe symptoms. The etiology of this finding is uncertain and may include a proinflammatory state or endothelial dysfunction following infection or suboptimal follow-up and management of vascular risk factors during the pandemic. (See 'Risk factors and mechanisms' below.)

Risk factors and mechanisms

●Traditional stroke risk factors – Most patients with ischemic stroke associated with COVID-19 are older patients with vascular risk factors [80,82,83,93]. Traditional stroke risk factors such as hypertension, hyperlipidemia, atrial fibrillation, and/or diabetes mellitus have been identified in these patients.

●Hypercoagulability and proinflammatory state associated with infection – Thrombophilia associated with SARS-CoV-2 or the host immune response appears to be an important mechanism of ischemic stroke in some patients with COVID-19 infection, as suggested by elevated markers of hypercoagulability and inflammation [22]. Markedly elevated D-dimer levels commonly found in patients with severe COVID-19 infection also appear to be present specifically in some patients with ischemic stroke [94-96]. D-dimer levels >10,000 ng/mL have been proposed to identify patients with cryptogenic stroke potentially attributable to COVID-19 hypercoagulability [97]. (See "COVID-19: Hypercoagulability".)

Evidence suggests that serious infections can trigger acute stroke, potentially due to increased inflammation and consequent thrombosis [98-100]. Influenza, sepsis, and minor respiratory and urinary tract infections were associated with increased stroke risk in analyses of administrative datasets [101-103]. COVID-19 appears to be associated with a higher risk of ischemic stroke compared with influenza. In a retrospective cohort study comparing patients with emergency department visits or hospitalizations for COVID-19 (n = 1916) or influenza (n = 1486), the incidence of ischemic stroke was higher among patients with COVID-19 (1.6 percent, versus 0.2 percent with influenza; adjusted odds ratio 7.6, 95% CI 2.3-25.2) [81].

Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare prothrombotic condition that may cause CVT; VITT is associated with adenovirus vector-based COVID-19 vaccines and is discussed in greater detail separately. (See "COVID-19: Vaccine-induced immune thrombotic thrombocytopenia (VITT)".)

●Cardioembolism – Cardiac dysfunction associated with COVID-19 infection may also serve as a potential embolic stroke mechanism, either directly due to SARS-CoV-2 myocarditis or indirectly due to cardiac injury or dysfunction related to general critical illness. COVID-19 has been associated with several cardiac manifestations, including arrhythmia, heart failure, and myocardial infarction, many of which may predispose to cardioembolic stroke. (See "COVID-19: Evaluation and management of cardiac disease in adults" and "COVID-19: Myocardial infarction and other coronary artery disease issues".)

●Coagulopathy and anticoagulation – Cases of spontaneous intraparenchymal and cortical subarachnoid hemorrhage have been reported with coagulopathy or anticoagulation [45]. One report of 278 hospitalized patients with COVID-19 and available neuroimaging identified intracerebral hemorrhage in 10 patients. Most of the patients had been treated with full-dose anticoagulation.

Some hemorrhages may represent unrecognized ischemic events with subsequent hemorrhagic conversion. In one report of 3824 hospitalized patients with COVID-19, intracerebral hemorrhage was reported in 33 (0.9 percent) [104]. Based upon the radiologic appearance, the investigators inferred that approximately three-quarters of these may have resulted from hemorrhagic transformation of ischemic stroke.

Intracranial hemorrhage with COVID-19 has also been associated with use of extracorporeal membrane oxygenation (ECMO) [105-107]. In an international registry, 145 of 2346 (6 percent) patients on ECMO with COVID-19 had an intracranial hemorrhage [106]. Patients on ECMO are also at increased risk of brain ischemia, including due to air embolism. (See "COVID-19: Extracorporeal membrane oxygenation (ECMO)", section on 'Complications'.)

Management — The initial diagnostic approach should be similar to the approach generally used for all patients with suspected stroke aside from necessary precautions related to infection control [108-110]. (See "Initial assessment and management of acute stroke" and "Approach to reperfusion therapy for acute ischemic stroke".)

●Thrombolytic and reperfusion therapies – Evaluation for intravenous thrombolytic therapy and mechanical thrombectomy should be undertaken for patients with acute stroke, with or without COVID-19. Some observational data suggest there may be an elevated risk of hemorrhage with thrombolysis and thrombectomy among patients with acute COVID-19 infection [111]. However, there may be an increased risk of reocclusion after initial recanalization in patients with COVID-19, potentially related to hypercoagulability associated with the infection. (See "Mechanical thrombectomy for acute ischemic stroke" and 'Risk factors and mechanisms' above.)

●Acute antithrombotic therapy – For patients with ischemic stroke and an unambiguous indication for full-dose anticoagulation (eg, atrial fibrillation, severe heart failure), early initiation is reasonable given the high thrombotic risk seen in patients with COVID-19, provided the bleeding risk is tolerable. For other patients with ischemic stroke, early use of aspirin is generally indicated regardless of COVID-19 infection status.

For patients without a defined mechanism for ischemic stroke associated with COVID-19, our approach to testing for a hypercoagulable state is otherwise similar to the approach used for patients without COVID-19. (See "COVID-19: Hypercoagulability", section on 'Routine testing' and "Overview of the evaluation of stroke", section on 'Hypercoagulable studies'.)

●Management for patients with VITT – For patients who develop cerebral venous thrombosis due to VITT after COVID-19 vaccination, anticoagulation with a nonheparin agent (eg, a direct oral anticoagulant) and intravenous immune globulin treatment have been suggested [112]. This is discussed in greater detail separately. (See "COVID-19: Vaccine-induced immune thrombotic thrombocytopenia (VITT)", section on 'Management'.)

Other aspects of the evaluation and management of adults hospitalized with COVID-19 are discussed in detail elsewhere. (See "COVID-19: Management in hospitalized adults".)

Neuromuscular conditions

Guillain-Barré syndrome — Cases of Guillain-Barré syndrome (GBS) have been reported after COVID-19 infection [113-116]. However, a potential causal association of COVID-19 with the risk of GBS remains uncertain. A cohort study from the United Kingdom failed to show a specific association between GBS and COVID-19 infection [117]. The role of COVID-19 infection as a trigger for GBS is discussed in greater detail separately. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis", section on 'Infection'.)

Most patients with GBS and COVID-19 presented with progressive, ascending limb weakness evolving over one to four days [118]. The interval between the onset of viral illness and the development of muscle weakness is 5 to 16 days, similar to that observed for other viral infections associated with GBS [119]. In a report of 11 patients in the International GBS Outcome Study (IGOS) who developed GBS after COVID-19 infection, sensorimotor features were found in 73 percent including facial palsy in 64 percent [114]. In other series, the Miller Fisher syndrome [45,120] and other variant forms of GBS [121] have also been described in patients with COVID-19. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis".)

The possible risk of GBS after vaccination against COVID-19 is discussed in greater detail separately. (See "COVID-19: Vaccines", section on 'Guillain-Barré syndrome'.)

Other acute neuromuscular syndromes

●Myositis – Myalgia and fatigue are common symptoms in COVID-19, however, myositis appears to be uncommon. Three case reports have described rhabdomyolysis with CK >12,000 units/L [122-124]. In one case, muscle biopsy in one patient with COVID-19 and myopathy showed perivascular inflammation and deposition of myxovirus resistance protein A, a type I interferon-inducible protein [124].

●Focal and multifocal neuropathies – Several peripheral nerve and plexus syndromes have been reported in patients with COVID-19. These include:

•Facial nerve palsy [115,125]

•Ocular motor neuropathies [45,126]

•Lower cranial neuropathies (eg, vagus, spinal accessory, hypoglossal, Tapia syndrome) [127,128]

•Multiple cranial neuropathies [120,126]

•Neuralgic amyotrophy [129,130]

•Autonomic neuropathy or dysautonomia [131,132]

●Critical illness neuropathy and myopathy – This complication occurs in patients hospitalized with severe illness, typically those who are mechanically ventilated for several days. Clinical features include flaccid muscle weakness often with failure to wean from ventilatory support. Critical illness neuropathy and myopathy tends to develop late in the course of COVID-19 infection [133,134]. (See "Neuromuscular weakness related to critical illness".)

●Peripheral nerve injuries after prone positioning – Patients placed in prone positioning for COVID-19-related acute respiratory distress syndrome may develop peripheral nerve, typically brachial plexus, injuries [135-137]. In one study of 83 patients admitted to a rehabilitation facility after severe COVID-19 infection, 12 (15 percent) were diagnosed with a peripheral nerve injury, 11 of whom had been placed in prone positioning [136]. Nerve injuries were most frequently axonal and in the upper limb. (See "Prone ventilation for adult patients with acute respiratory distress syndrome", section on 'Complications'.)

Other acute neurologic manifestations — Isolated case series and reports have described several other neurologic syndromes in patients with COVID-19:

●Seizures and status epilepticus – New seizures and status epilepticus can occur in patients with severe COVID-19 infection [138,139]. A meta-analysis of studies that reported seizures among more than 250,000 patients with COVID-19 infection reported a prevalence rate of 1 percent [140]. In one series of 32 patients with COVID-19 who presented to the hospital with seizures, 40 percent had no history of epilepsy or other central nervous system diagnoses [141]. In rare instances, seizures have been the presenting symptom for patients without signs of infection who have tested positive for COVID-19 [141,142]. A systematic review of case series and reports identified 47 patients with COVID-19 who developed status epilepticus [143]. Most patients had preceding respiratory symptoms and no history of prior seizures. Neuroimaging was abnormal in approximately half of patients and four patients had a positive SARS-CoV-2 in the CSF. (See "Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis".)

●Meningoencephalitis – Viral meningoencephalitis has been reported in patients presenting with encephalopathy or seizures and COVID-19. CSF analysis has identified SARS-CoV-2 in some [144,145], but not all [135,146-148], cases. Other cases of brainstem encephalitis or isolated cerebellitis have been reported in adults and children with COVID-19 infection [149-153]. A parainfectious inflammatory cause has been suggested. Some patients with fulminant disease and brainstem compression received external ventricular drainage for hydrocephalus [151].

An autoimmune mechanism has been postulated for some cases. Some patients have clinical syndromes and MRI findings that appear similar to autoimmune encephalitis [154]. One patient was found to have anti-N-methyl-d-aspartate (anti-NMDA) receptor antibodies [148]. Many of these patients appeared to respond to immunomodulatory treatment with glucocorticoids [135,147], plasma exchange [155], and/or intravenous immunoglobulin [148]. (See "Autoimmune (including paraneoplastic) encephalitis: Clinical features and diagnosis".)

●Acute disseminated encephalomyelitis (ADEM) and acute hemorrhagic necrotizing encephalopathy – A few case reports have described patients with clinical and neuroimaging findings consistent with ADEM [18,135,156-158]. Some patients have had myelitis with or without brain involvement [135]. Other patients present with hemorrhagic findings consistent with the hemorrhagic leukoencephalitis variant form of ADEM [135,159,160]. (See "Acute disseminated encephalomyelitis (ADEM) in adults".)

●Acute transverse myelitis – Paraparesis or quadriparesis due to acute transverse myelitis is an uncommon complication, typically occurring in symptomatic adults or children days to weeks after onset of COVID-19 infection [161-163]. Some patients also have clinical features and diagnostic evidence of coexisting ADEM or acute motor neuropathies. (See "Transverse myelitis: Etiology, clinical features, and diagnosis".)

●Multisystem inflammatory syndrome in children – Some children with COVID-19 develop a multisystem inflammatory syndrome (MIS-C), similar to incomplete Kawasaki disease, which can include neurocognitive symptoms (eg, headache, lethargy, confusion). The clinical features of MIS-C are discussed separately. (See "COVID-19: Multisystem inflammatory syndrome in children (MIS-C) clinical features, evaluation, and diagnosis".)

●Generalized myoclonus – Generalized myoclonus may occur as an apparent postinfectious, rare complication of COVID-19. In one report, generalized myoclonus developed in symptomatic patients who were not severely ill at the time [164]. The myoclonus could not be explained by hypoxia, metabolic cause, or drug effect. Patients were treated symptomatically with levetiracetam, valproate, clonazepam, and/or propofol sedation and appeared to recover gradually with immunotherapy such as methylprednisolone and/or plasma exchange. (See "Symptomatic (secondary) myoclonus".)

●Reversible posterior leukoencephalopathy syndrome (RPLS) – RPLS has been reported in patients with COVID-19 and may be due to hypertension and renal failure in some [43,45,83,84,165-169]. In one neuroimaging case series early in the pandemic, findings consistent with RPLS were seen in more than 1 percent of hospitalized patients [45]. (See "Reversible posterior leukoencephalopathy syndrome".)

●Reversible cerebral vasoconstriction syndrome (RCVS) – RCVS has been reported in adults and children with COVID-19 infection [170-172]. Corresponding features on brain imaging of patients with a severe syndrome included subarachnoid hemorrhagic, intracerebral hemorrhage, and ischemic stroke. (See "Reversible cerebral vasoconstriction syndrome".)

PERSISTENT NEUROLOGIC SYMPTOMS AFTER SARS-COV-2 INFECTION — Patients recovering from a severe illness or after hospitalization may report prolonged neurologic symptoms. Likewise, some patients who were hospitalized with COVID-19 report symptoms that persist for weeks to years after the acute infection [173,174].

In addition, patients with milder acute COVID-19 symptoms who never required hospitalization for pneumonia or hypoxemia may also report prolonged neurologic and systemic symptoms [175-177]. Common neurologic symptoms that may interfere with activities of daily life include cognitive impairment, paresthesia, headache, dysgeusia, anosmia, myalgia, dizziness, blurred vision, and tinnitus. Persistent neurologic symptoms lasting >4 weeks after the initial infection may be part of the "long COVID" syndrome [178], also called "postacute sequelae of SARS-CoV-2 infection (PASC)" [179]. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")", section on 'Persistent symptoms'.)

Prior COVID-19 infection has also been reported to unmask symptoms of neurodegenerative disease in presymptomatic individuals [180,181]. One nationwide study in Sweden reported that dementia has been underdiagnosed and undertreated in the pandemic [182].

Neuroimaging with brain MRI is typically normal in patients with persisting neurologic symptoms after COVID-19 infection. However, small studies using functional neuroimaging with fluorodeoxyglucose-positron emission tomography (FDG-PET) have identified multiple areas of glucose hypometabolism in some patients with persisting symptoms, including the orbitofrontal gyrus, hippocampus, amygdala, thalamus, and insular cortex [183-186].

MANAGEMENT OF PATIENTS WITH NEUROLOGIC CONDITIONS — Strategies to optimize both prevention and treatment of COVID-19 are important for patients with baseline disabling neurologic conditions due to the associated elevated risk of poor prognosis with COVID-19 infection. Neurologic conditions associated with an elevated risk of complications with COVID-19 infection in cohort studies include:

●Cerebrovascular disease [187,188]

●Epilepsy [189]

●Amyotrophic lateral sclerosis [190]

●Myasthenia gravis [191]

●Multiple sclerosis (MS) [192,193]

●Dementia [194]

Several conditions have also been identified by the United States Centers for Disease Control and Prevention (CDC) as risk factors for severe infection with SARS-CoV-2 (table 2). These conditions are discussed in greater detail separately. (See "COVID-19: Clinical features", section on 'Risk factors for severe illness'.)

Prevention — Several preventive strategies may be used to help reduce the transmission and burden of COVID-19, including for patients with neurologic conditions. These include vaccination, infection control measures, and screening with viral testing. General preventive strategies for all patients are discussed in detail separately. (See "COVID-19: Epidemiology, virology, and prevention", section on 'Prevention'.)

Vaccination against COVID-19 — Based on available data from the general population, we recommend vaccination against COVID-19, in agreement with observational data and guidelines from the American Association of Neuromuscular and Electrodiagnostic Medicine and the National Multiple Sclerosis Society [195-197]. COVID-19 vaccination has been associated with a reduced risk of neurologic complications of COVID-19 infection, including stroke [198]. Vaccination has also been associated with improved symptoms in some patients with postacute persistent COVID-19 symptoms. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")", section on 'Persistent symptoms' and "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")".)

Immunosuppressive medications may reduce the immunogenicity and effectiveness of vaccination against COVID-19. Patients with neurologic conditions who are receiving immunosuppressive therapy may warrant additional vaccine doses following the primary series. Strategies to optimize effectiveness of vaccination against COVID-19 infection in patients taking immunosuppressive therapy are discussed separately. (See "COVID-19: Vaccines", section on 'Immunocompromised individuals'.)

Adverse neurologic effects from vaccination against COVID-19 are rare. Vaccine-related neurologic conditions include:

●Vaccine-associated immune thrombotic thrombocytopenia (VITT) – Rare cases of thrombotic events with thrombocytopenia, including cerebral venous thrombosis (CVT) with and without hemorrhage, have been reported in patients immunized with the adenovirus-vector AstraZeneca (ChAdOx1 nCoV-19/AZD122) COVID-19 and Janssen/Johnson & Johnson (Ad26.COV2.S) COVID-19 vaccines [199-203]. DNA from adenovirus vectors binds to platelet factor 4 to trigger the production of autoantibodies and subsequent thrombosis. Patients present with thrombocytopenia and symptoms related to thrombosis. This syndrome occurs between 5 and 30 days postvaccination. The epidemiology, clinical features, and management of vaccine-associated thrombotic thrombocytopenia are discussed in greater detail separately. (See "COVID-19: Vaccine-induced immune thrombotic thrombocytopenia (VITT)".)

●Guillain-Barré syndrome – Cases of Guillain-Barré syndrome (GBS) have been observed with the adenovirus vector Janssen/Johnson & Johnson (Ad26.COV2.S) and AstraZeneca (ChAdOx1 nCoV-19/AZD1222) COVID-19 vaccines in the United States and Europe [204-207], although a causal link has not been established. Adenovirus vector vaccines are no longer available in the United States. This finding has not been reported with other COVID-19 vaccines [208]. This possible risk is discussed in greater detail separately. (See "COVID-19: Vaccines", section on 'Guillain-Barré syndrome'.)

●Other neurologic syndromes – Very rare cases of other neurologic symptoms following COVID-19 vaccination have been reported. These include cognitive impairment, facial palsy, transverse myelitis, and seizures [209-212]. A causal role has not been established.

Clinicians and patients are encouraged to report adverse events to the Vaccine Adverse Event Reporting System.

The benefits of vaccination to prevent the morbidity and mortality associated with COVID-19 infection greatly outweigh the risks, including the risks of VITT and GBS [213-215]. The risk of thromboembolism from COVID-19 infection appears higher than the risk of VITT [86,216]. Similarly, the risk of GBS appears higher in the setting of COVID-19 infection than after vaccination [115,217]. (See "COVID-19: Vaccines", section on 'Rare but serious associated events'.)

Among patients with a history of GBS or chronic immune neuropathies, the overall risk of recurrence following COVID-19 vaccination appears low to negligible [218]. Because of the possible increased risk of GBS associated with the adenovirus vector Janssen/Johnson & Johnson (Ad26.COV2.S) and AstraZeneca (ChAdOx1 nCoV-19/AZD1222) COVID-19 vaccines, for patients with a history of GBS, we suggest other available COVID-19 vaccines. (See "Guillain-Barré syndrome in adults: Treatment and prognosis", section on 'Subsequent immunizations'.)

Health care utilization — Telemedicine is being increasingly used during the pandemic to manage outpatients with chronic neurologic disease. Routine outpatient cerebrovascular visits can often be conducted safely and effectively using telehealth [219,220]. Building on developments in the use of rapid outpatient evaluation for transient ischemic attack (TIA) patients, telehealth follow-up of patients with TIA may be safe and effective [221]. In a survey of 143 patients with epilepsy, reduced availability of ambulatory care occurred in approximately one-third of patients and was associated with exacerbation of seizures [222]. (See "COVID-19: Issues related to wound care and telehealth management", section on 'Telehealth'.)

Patients with neurologic diseases should develop rescue treatment plans that can be administered at home, if appropriate [223]. This may include patients with conditions such as migraine or epilepsy who may need acute or rescue therapies for established patients with exacerbations that may not require evaluation and management in a hospital setting, where exposure to infection may be elevated.

Managing immunosuppressive therapy — For most patients with neurologic conditions, chronic immunosuppressive therapy should be continued; generally, immunosuppressive therapy should be discontinued only if severe COVID-19 infection develops [224-228]. The role of switching agents or amending treatment protocols may be appropriate for some patients and is determined by assessing individual risks. Patients with neurologic disease who are treated with immunosuppressive therapy do not appear to be at increased risk of COVID-19 infection.

●Multiple sclerosis – Patients with MS treated with B cell-depleting anti-CD20 or sphingosine-1-phosphate receptor disease-modifying therapies (DMTs) may have a lower antibody response to SARS-CoV-2 infection than those treated with other DMTs. Patients with MS should be given vaccination prior to starting an anti-CD20 DMT, if possible. For patients already on an anti-CD20 DMT, timing the infusion in selected stable patients to occur several weeks after vaccination may be used to improve humoral response and possibly vaccine effectiveness. Decisions should be individualized based on disease severity and activity. The selection and administration of DMTs for MS are discussed in greater detail separately. (See "Overview of disease-modifying therapies for multiple sclerosis", section on 'COVID-19 and DMTs'.)

For patients with MS who develop COVID-19, the decision to continue or stop DMT until recovery should be individualized according to the risks associated with specific DMT, MS disease activity level, and other comorbid conditions that may impact the severity of the acute illness. These issues are discussed in greater detail separately. (See "Overview of disease-modifying therapies for multiple sclerosis", section on 'COVID-19 and DMTs'.)

●Myasthenia gravis – Immunosuppressive medications for patients with myasthenia gravis are typically continued to minimize the risk of neuromuscular deterioration. Alternative treatments may also be considered for some patients who develop COVID-19 while taking immunosuppressive therapy. As examples, immunoglobulin therapy, complement inhibitor therapy, and plasma exchange are not expected to increase the risk of COVID-19; however, such treatments are not appropriate in all patients and indiscriminate switching to these treatments is not advised [227].

Additional advice specific to the management of patients with myasthenia gravis is presented separately. (See "Overview of the treatment of myasthenia gravis", section on 'Guidance during COVID-19 pandemic'.)

Other acute treatment issues — Some patients with neurologic conditions who develop a COVID-19 infection are at risk for severe illness, such as those with dementia or neuroinflammatory disorders treated with immunosuppressive medications (table 2). The indications for and approach to COVID-19-specific therapy in symptomatic patients vary by clinical setting and risk profile for severe illness. In addition, COVID-19-specific treatments may help reduce the incidence of neurologic complications in patients with severe symptoms [229]. The approach to COVID-19-specific therapy is discussed separately. (See "COVID-19: Management in hospitalized adults", section on 'COVID-19-specific therapy' and "COVID-19: Management of adults with acute illness in the outpatient setting", section on 'Treatment with COVID-19-specific therapies'.)

Patients presenting with new, acute neurologic symptoms such as stroke, seizure, or encephalopathy should be tested for COVID-19 infection, even in the absence respiratory symptoms. Neurologic symptoms may be the presenting feature of COVID-19 for some patients with pre-existing neurologic conditions, risk factors for neurologic conditions, and others.

Other aspects of the evaluation and management of adults hospitalized with COVID-19 include infection control, the prevention of venous thromboembolism, and the management of baseline medications. These issues are discussed in detail elsewhere. (See "COVID-19: Management in hospitalized adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: COVID-19 overview (The Basics)" and "Patient education: COVID-19 and pregnancy (The Basics)" and "Patient education: COVID-19 and children (The Basics)" and "Patient education: COVID-19 vaccines (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Acute neurologic complications of COVID-19 infection – Neurologic manifestations occur in approximately half of hospitalized COVID-19 patients. Fatigue, myalgias, smell/taste dysfunction, and headache appear to be most common. (See 'Acute neurologic complications' above.)

•Smell and taste disorders – Anosmia and dysgeusia have been reported as common early symptoms in patients with COVID-19. (See 'Smell and taste disorders' above.)

•Encephalopathy – Encephalopathy is common in critically ill patients with COVID-19, occurring in up to 55 percent. Encephalopathy may be a presenting feature and/or a clinical component of other overlapping neurologic conditions such as ischemic or hemorrhagic stroke, encephalitis, reversible posterior leukoencephalopathy syndrome (RPLS), multisystem inflammatory syndrome, or demyelinating diseases. (See 'Encephalopathy' above.)

The evaluation and management of patients with COVID-19 and encephalopathy is directed toward the underlying cause and is the same as with other patients with delirium. Clinicians should exercise caution about withdrawal of life support measures in patients with encephalopathy in the absence of structural brain injury on neuroimaging or other evidence of futility.

•Cerebrovascular disease – Cerebrovascular events appear to be relatively infrequent in the setting of acute COVID-19 infection, occurring in up to 2.4 percent of patients. The risk of stroke is <1 percent for patients with mild illness, while for patients in intensive care, the risk may be as high as 6 percent. (See 'Cerebrovascular disease' above.)

Most often, stroke occurs one to three weeks after onset of COVID-19 symptoms, although stroke has been the initial symptom leading to hospitalization in a minority of reported patients.

Evaluation for intravenous thrombolytic therapy and mechanical thrombectomy should be undertaken for patients with acute stroke, with or without COVID-19. For patients with ischemic stroke and an unambiguous indication for full-dose anticoagulation (eg, atrial fibrillation, severe heart failure), early initiation is reasonable given the high thrombotic risk seen in patients with COVID-19.

•Neuromuscular disorders – Rare cases of Guillain-Barré syndrome (GBS) have been reported after COVID-19 infection; however, a potential causal association of COVID-19 with the risk of GBS remains uncertain. Other acute neuromuscular disorders occurring in patients with COVID-19 infection include myositis, focal and multifocal neuropathies, and critical illness neuropathy and myopathy. (See 'Neuromuscular conditions' above.)

•Other acute neurologic manifestations – Isolated case series and reports have described several other neurologic syndromes in patients with COVID-19, including seizures and status epilepticus, encephalitis, acute disseminated encephalomyelitis (ADEM), acute transverse myelitis, multisystem inflammatory syndrome in children (MIS-C), myoclonus, reversible posterior leukoencephalopathy syndrome (RPLS), and reversible cerebral vasoconstriction syndrome (RCVS). (See 'Other acute neurologic manifestations' above.)

●Persistent neurologic symptoms after COVID-19 infection – Some patients who were hospitalized with COVID-19 report symptoms that persist for weeks to years after the acute infection. In addition, patients with milder acute COVID-19 symptoms who never required hospitalization for pneumonia or hypoxemia may also report prolonged neurologic and systemic symptoms. Cognitive impairment, paresthesias, headache, dysgeusia, anosmia, and myalgia are common. (See 'Persistent neurologic symptoms after SARS-CoV-2 infection' above.)

●Management of patients with neurologic conditions – Strategies to optimize both prevention and treatment of COVID-19 are important for patients with baseline disabling neurologic conditions due to the associated elevated risk of poor prognosis with COVID-19 infection. (See 'Management of patients with neurologic conditions' above.)

•Vaccination – Patients with neurologic conditions should receive vaccination against COVID-19. COVID-19 vaccination has been associated with a reduced risk of neurologic complications of COVID-19 infection. Patients with neurologic conditions who are receiving immunosuppressive therapy may warrant additional vaccine doses following the primary series. (See 'Vaccination against COVID-19' above and "COVID-19: Vaccines".)

•Chronic immunosuppressive therapy – For most patients with neurologic conditions, chronic immunosuppressive therapy should be continued. For patients who develop COVID-19 infection, the decision to continue or discontinue immunosuppressive therapy depends on many variables including the specific medication and the severity of the condition for which it is prescribed. (See 'Managing immunosuppressive therapy' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Mitchell SV Elkind, MD, MS, FAAN, MD, who contributed to earlier versions of this topic review.

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  229. Grundmann A, Wu CH, Hardwick M, et al. Fewer COVID-19 Neurological Complications with Dexamethasone and Remdesivir. Ann Neurol 2023; 93:88.
Topic 128153 Version 35.0

References

1 : World Health Organization. Director-General's remarks at the media briefing on 2019-nCoV on 11 February 2020. Available at: http://www.who.int/dg/speeches/detail/who-director-general-s-remarks-at-the-media-briefing-on-2019-ncov-on-11-february-2020 (Accessed on February 12, 2020).

2 : Potential Neurologic Manifestations of COVID-19.

3 : Frequent neurologic manifestations and encephalopathy-associated morbidity in Covid-19 patients.

4 : Frequency of Neurologic Manifestations in COVID-19: A Systematic Review and Meta-analysis.

5 : Neurologic manifestations in hospitalized patients with COVID-19: The ALBACOVID registry.

6 : New onset neurologic events in people with COVID-19 in 3 regions in China.

7 : Lifting the mask on neurological manifestations of COVID-19.

8 : COVID-19 neuropathology at Columbia University Irving Medical Center/New York Presbyterian Hospital.

9 : Neuropathological Features of Covid-19.

10 : Neurovascular injury with complement activation and inflammation in COVID-19.

11 : Brain MRI Findings in Patients in the Intensive Care Unit with COVID-19 Infection.

12 : COVID-19-associated Diffuse Leukoencephalopathy and Microhemorrhages.

13 : Cerebral Microbleeds and Leukoencephalopathy in Critically Ill Patients With COVID-19.

14 : Reply to the Letter "COVID-19-Associated Encephalopathy and Cytokine-Mediated Neuroinflammation".

15 : COVID-19-Associated Encephalopathy and Cytokine-Mediated Neuroinflammation.

16 : Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.

17 : An interferon-gamma-related cytokine storm in SARS patients.

18 : COVID-19: A Global Threat to the Nervous System.

19 : Neurobiology of COVID-19.

20 : Neuronophagia and microglial nodules in a SARS-CoV-2 patient with cerebellar hemorrhage.

21 : COVID-19 induces CNS cytokine expression and loss of hippocampal neurogenesis.

22 : Thromboinflammation and the hypercoagulability of COVID-19.

23 : SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2.

24 : Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases.

25 : Risk factors and abnormal cerebrospinal fluid associate with cognitive symptoms after mild COVID-19.

26 : Clinical and Autoimmune Characteristics of Severe and Critical Cases of COVID-19.

27 : Diverse functional autoantibodies in patients with COVID-19.

28 : Guillain-Barrésyndrome associated with SARS-CoV-2 infection: causality or coincidence?

29 : Neuropathology of patients with COVID-19 in Germany: a post-mortem case series.

30 : Olfactory transmucosal SARS-CoV-2 invasion as a port of central nervous system entry in individuals with COVID-19.

31 : Neuroinvasion of SARS-CoV-2 in human and mouse brain.

32 : Endothelial cell infection and endotheliitis in COVID-19.

33 : Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19.

34 : Electron microscopy of SARS-CoV-2: a challenging task.

35 : Electron microscopy of SARS-CoV-2: a challenging task - Authors' reply.

36 : SARS-CoV-2 is associated with changes in brain structure in UK Biobank.

37 : Plasma Biomarkers of Neuropathogenesis in Hospitalized Patients With COVID-19 and Those With Postacute Sequelae of SARS-CoV-2 Infection.

38 : Comparison of serum neurodegenerative biomarkers among hospitalized COVID-19 patients versus non-COVID subjects with normal cognition, mild cognitive impairment, or Alzheimer's dementia.

39 : Prevalence of Olfactory Dysfunction in Coronavirus Disease 2019 (COVID-19): A Meta-analysis of 27,492 Patients.

40 : Expression of the SARS-CoV-2 Entry Proteins, ACE2 and TMPRSS2, in Cells of the Olfactory Epithelium: Identification of Cell Types and Trends with Age.

41 : Anosmia in COVID-19 Associated with Injury to the Olfactory Bulbs Evident on MRI.

42 : Anosmia and olfactory tract neuropathy in a case of COVID-19.

43 : Early postmortem brain MRI findings in COVID-19 non-survivors.

44 : Bilateral transient olfactory bulb edema during COVID-19-related anosmia.

45 : Brain Imaging of Patients with COVID-19: Findings at an Academic Institution during the Height of the Outbreak in New York City.

46 : Loss of smell in patients with COVID-19: MRI data reveal a transient edema of the olfactory clefts.

47 : COVID-19 and anosmia: A review based on up-to-date knowledge.

48 : Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): a multicenter European study.

49 : Olfactory and Gustatory Outcomes in COVID-19: A Prospective Evaluation in Nonhospitalized Subjects.

50 : Clinical Outcomes for Patients With Anosmia 1 Year After COVID-19 Diagnosis.

51 : Post-COVID syndrome in non-hospitalised patients with COVID-19: a longitudinal prospective cohort study.

52 : Acquired agitation in acute respiratory distress syndrome with COVID-19 compared to influenza patients: a propensity score matching observational study.

53 : Prevalence and risk factors for delirium in critically ill patients with COVID-19 (COVID-D): a multicentre cohort study.

54 : Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China.

55 : Neurologic Features in Severe SARS-CoV-2 Infection.

56 : De Novo Status Epilepticus in patients with COVID-19.

57 : Seizure with CSF lymphocytosis as a presenting feature of COVID-19 in an otherwise healthy young man.

58 : Delirium in COVID-19: A case series and exploration of potential mechanisms for central nervous system involvement.

59 : A Unique Presentation of Delirium in a Patient with Otherwise Asymptomatic COVID-19.

60 : Delirium in Older Patients With COVID-19 Presenting to the Emergency Department.

61 : The Importance of Delirium and Delirium Prevention in Older Adults During Lockdowns.

62 : Transient global amnesia with bilateral hippocampal lesions during the COVID-19 global outbreak.

63 : Transient Global Amnesia as a Possible First Manifestation of COVID-19.

64 : Brain MRI Findings in Severe COVID-19: A Retrospective Observational Study.

65 : Neurologic and Radiographic Findings Associated With COVID-19 Infection in Children.

66 : Neurologic and neuroimaging findings in patients with COVID-19: A retrospective multicenter study.

67 : More on Neurologic Features in Severe SARS-CoV-2 Infection.

68 : Cerebral perfusion using ASL in patients with COVID-19 and neurological manifestations: A retrospective multicenter observational study.

69 : Nervous System Involvement in Coronavirus Disease 2019: Results from a Retrospective Consecutive Neuroimaging Cohort.

70 : Retrospective Observational Study of Brain MRI Findings in Patients with Acute SARS-CoV-2 Infection and Neurologic Manifestations.

71 : Cerebrospinal fluid in COVID-19: A systematic review of the literature.

72 : Intact Brain Network Function in an Unresponsive Patient with COVID-19.

73 : Prolonged Unconsciousness Following Severe COVID-19.

74 : Disorders of Consciousness Associated With COVID-19: A Prospective Multimodal Study of Recovery and Brain Connectivity.

75 : Prolonged Unconsciousness is Common in COVID-19 and Associated with Hypoxemia.

76 : Psychiatric and neuropsychiatric presentations associated with severe coronavirus infections: a systematic review and meta-analysis with comparison to the COVID-19 pandemic.

77 : COVID-19-related encephalopathy responsive to high-dose glucocorticoids.

78 : Severe COVID-19-related encephalitis can respond to immunotherapy.

79 : Acute Ischemic Stroke and COVID-19: An Analysis of 27 676 Patients.

80 : SARS-CoV-2 and Stroke in a New York Healthcare System.

81 : Risk of Ischemic Stroke in Patients With Coronavirus Disease 2019 (COVID-19) vs Patients With Influenza.

82 : Acute Cerebrovascular Events in Hospitalized COVID-19 Patients.

83 : COVID-19 and Stroke: Incidence and Etiological Description in a High-Volume Center.

84 : Cerebrovascular disease in patients with COVID-19: neuroimaging, histological and clinical description.

85 : Cerebral Venous Thrombosis in COVID-19: A New York Metropolitan Cohort Study.

86 : Cerebral venous thrombosis and severe acute respiratory syndrome coronavirus-2 infection: A systematic review and meta-analysis.

87 : Health Disparities and the Coronavirus Disease 2019 (COVID-19) Pandemic in the USA.

88 : Cerebrovascular Complications of COVID-19.

89 : Risk of acute myocardial infarction and ischaemic stroke following COVID-19 in Sweden: a self-controlled case series and matched cohort study.

90 : Stroke risk, phenotypes, and death in COVID-19: Systematic review and newly reported cases.

91 : Acute Ischemic Stroke in Patients With COVID-19: An Analysis From Get With The Guidelines-Stroke.

92 : Long-term cardiovascular outcomes of COVID-19.

93 : Characteristics and Outcomes Among US Patients Hospitalized for Ischemic Stroke Before vs During the COVID-19 Pandemic.

94 : Characteristics of ischaemic stroke associated with COVID-19.

95 : Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study.

96 : Characteristics and outcomes of COVID-19 associated stroke: a UK multicentre case-control study.

97 : Biomarkers of Coagulation and Inflammation in COVID-19-Associated Ischemic Stroke.

98 : Why now? Moving from stroke risk factors to stroke triggers.

99 : Hospitalization for infection and risk of acute ischemic stroke: the Cardiovascular Health Study.

100 : Hospitalized Infection as a Trigger for Acute Ischemic Stroke: The Atherosclerosis Risk in Communities Study.

101 : Influenza-like illness as a trigger for ischemic stroke.

102 : Risk of Acute Stroke After Hospitalization for Sepsis: A Case-Crossover Study.

103 : Risk of myocardial infarction and stroke after acute infection or vaccination.

104 : Hemorrhagic stroke and anticoagulation in COVID-19.

105 : Hemorrhagic stroke in setting of severe COVID-19 infection requiring Extracorporeal Membrane Oxygenation (ECMO).

106 : Hemorrhagic stroke in setting of severe COVID-19 infection requiring Extracorporeal Membrane Oxygenation (ECMO).

107 : A Case Series of Devastating Intracranial Hemorrhage During Venovenous Extracorporeal Membrane Oxygenation for COVID-19.

108 : Acute Stroke Care in the Coronavirus Disease 2019 Pandemic.

109 : Preserving stroke care during the COVID-19 pandemic: Potential issues and solutions.

110 : Pandemic Guidance for Stroke Centers Aiding COVID-19 Treatment Teams.

111 : Safety and Outcome of Revascularization Treatment in Patients With Acute Ischemic Stroke and COVID-19: The Global COVID-19 Stroke Registry.

112 : Diagnosis and Management of Cerebral Venous Sinus Thrombosis With Vaccine-Induced Immune Thrombotic Thrombocytopenia.

113 : Incidence, clinical, risk factors and outcomes of Guillain-Barréin Covid-19.

114 : Guillain-Barrésyndrome after SARS-CoV-2 infection in an international prospective cohort study.

115 : Association between covid-19 vaccination, SARS-CoV-2 infection, and risk of immune mediated neurological events: population based cohort and self-controlled case series analysis.

116 : Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review.

117 : Epidemiological and cohort study finds no association between COVID-19 and Guillain-Barrésyndrome.

118 : Guillain-BarréSyndrome Associated with SARS-CoV-2.

119 : SARS-CoV-2-associated Guillain-Barrésyndrome is a para-infectious disease.

120 : Miller Fisher syndrome and polyneuritis cranialis in COVID-19.

121 : Facial diplegia, a possible atypical variant of Guillain-BarréSyndrome as a rare neurological complication of SARS-CoV-2.

122 : Rhabdomyolysis as a Presentation of 2019 Novel Coronavirus Disease.

123 : Rhabdomyolysis as Potential Late Complication Associated with COVID-19.

124 : Covid-19-Associated Myopathy Caused by Type I Interferonopathy.

125 : Pearls&Oy-sters: Facial nerve palsy in COVID-19 infection.

126 : COVID-19 presenting with ophthalmoparesis from cranial nerve palsy.

127 : Tapia syndrome at the time of the COVID-19 pandemic: Lower cranial neuropathy following prolonged intubation.

128 : Isolated bulbar palsy after SARS-CoV-2 infection.

129 : Pure sensory neuralgic amyotrophy in COVID-19 infection.

130 : Neuralgic amyotrophy following infection with SARS-CoV-2.

131 : Assessment of Autonomic Nervous System Dysfunction in the Early Phase of Infection With SARS-CoV-2 Virus.

132 : Autonomic Dysfunction during Acute SARS-CoV-2 Infection: A Systematic Review.

133 : COVID-19 and neuromuscular disorders.

134 : Critical illness polyneuropathy, myopathy and neuronal biomarkers in COVID-19 patients: A prospective study.

135 : The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings.

136 : Injury-prone: peripheral nerve injuries associated with prone positioning for COVID-19-related acute respiratory distress syndrome.

137 : Imaging Review of Peripheral Nerve Injuries in Patients with COVID-19.

138 : Outcomes of seizures, status epilepticus, and EEG findings in critically ill patient with COVID-19.

139 : Seizure in patients with COVID-19.

140 : Prevalence and risk factors for seizures in adult COVID-19 patients: A meta-analysis

141 : A follow-up study of patients with COVID-19 presenting with seizures.

142 : Seizure as the presenting symptom of COVID-19: A retrospective case series.

143 : Status epilepticus and COVID-19: A systematic review.

144 : A first case of meningitis/encephalitis associated with SARS-Coronavirus-2.

145 : SARS-CoV-2 Detected in Cerebrospinal Fluid by PCR in a Case of COVID-19 Encephalitis.

146 : Two patients with acute meningoencephalitis concomitant with SARS-CoV-2 infection.

147 : Steroid-Responsive Encephalitis in Coronavirus Disease 2019.

148 : Anti-NMDA receptor encephalitis in a psychiatric Covid-19 patient: A case report.

149 : A First Case of Acute Cerebellitis Associated with Coronavirus Disease (COVID-19): a Case Report and Literature Review.

150 : Acute Cerebellar Ataxia in COVID-19 Infection: A Case Report.

151 : Acute Fulminant Cerebellitis in Children with COVID-19 Infection: A Rare But Treatable Complication.

152 : SARS-CoV-2 Encephalitis Presenting as a Clinical Cerebellar Syndrome: A Case Report.

153 : Expanding the Spectrum of Acute Cerebellitis due to SARS-Cov-2.

154 : AI-CoV Study: Autoimmune Encephalitis Associated With COVID-19 and Its Vaccines-A Systematic Review.

155 : Plasmapheresis treatment in COVID-19-related autoimmune meningoencephalitis: Case series.

156 : SARS-CoV-2 can induce brain and spine demyelinating lesions.

157 : Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology.

158 : COVID-19-associated acute necrotising encephalopathy successfully treated with steroids and polyvalent immunoglobulin with unusual IgG targeting the cerebral fibre network.

159 : Hemorrhagic encephalopathy associated with COVID-19.

160 : COVID-19-associated Acute Hemorrhagic Necrotizing Encephalopathy: Imaging Features.

161 : Acute Transverse Myelitis (ATM):Clinical Review of 43 Patients With COVID-19-Associated ATM and 3 Post-Vaccination ATM Serious Adverse Events With the ChAdOx1 nCoV-19 Vaccine (AZD1222).

162 : Acute transverse myelitis in COVID-19 infection.

163 : COVID-19-Associated Acute Transverse Myelitis: A Case Series of a Rare Neurologic Condition.

164 : Generalized myoclonus in COVID-19.

165 : Hemorrhagic Posterior Reversible Encephalopathy Syndrome as a Manifestation of COVID-19 Infection.

166 : Transient cortical blindness in COVID-19 pneumonia; a PRES-like syndrome: Case report.

167 : Posterior reversible encephalopathy syndrome (PRES) as a neurological association in severe Covid-19.

168 : Reversible Encephalopathy Syndrome (PRES) in a COVID-19 patient.

169 : Posterior reversible encephalopathy syndrome in patients with COVID-19.

170 : Reversible Cerebral Vasoconstriction Syndrome and Multisystem Inflammatory Syndrome in Children With COVID-19.

171 : Fulminant Reversible Cerebral Vasoconstriction Syndrome in Breakthrough COVID 19 Infection.

172 : Reversible Cerebral Vasoconstriction Syndrome in Patients with Coronavirus Disease: A Multicenter Case Series.

173 : Persistent symptoms 3 months after a SARS-CoV-2 infection: the post-COVID-19 syndrome?

174 : Fatigue and cognitive impairment in Post-COVID-19 Syndrome: A systematic review and meta-analysis.

175 : Persistent neurologic symptoms and cognitive dysfunction in non-hospitalized Covid-19 "long haulers".

176 : Post-acute COVID-19 syndrome in patients after 12 months from COVID-19 infection in Korea.

177 : Evolution of neurologic symptoms in non-hospitalized COVID-19 "long haulers".

178 : Evolution of neurologic symptoms in non-hospitalized COVID-19 "long haulers".

179 : Evolution of neurologic symptoms in non-hospitalized COVID-19 "long haulers".

180 : One-Year Trajectory of Cognitive Changes in Older Survivors of COVID-19 in Wuhan, China: A Longitudinal Cohort Study.

181 : New-Onset Dementia Among Survivors of Pneumonia Associated With Severe Acute Respiratory Syndrome Coronavirus 2 Infection.

182 : Changes in dementia diagnoses in Sweden during the COVID-19 pandemic.

183 : Long COVID: cognitive complaints (brain fog) and dysfunction of the cingulate cortex.

184 : 18F-FDG brain PET hypometabolism in patients with long COVID.

185 : Long COVID hallmarks on [18F]FDG-PET/CT: a case-control study.

186 : Correction to: The cerebral network of COVID-19-related encephalopathy: a longitudinal voxel-based 18F-FDG-PET study.

187 : Clinical Characteristics and Outcomes of COVID-19 Patients With a History of Stroke in Wuhan, China.

188 : History of Stroke Is Independently Associated With In-Hospital Death in Patients With COVID-19.

189 : Epilepsy and the risk of severe coronavirus disease 2019 outcomes: A systematic review, meta-analysis, and meta-regression.

190 : Clinical characteristics and outcomes of inpatients with neurologic disease and COVID-19 in Brescia, Lombardy, Italy.

191 : Impact of Coronavirus Disease 2019 in a French Cohort of Myasthenia Gravis.

192 : Clinical Characteristics and Outcomes in Patients With Coronavirus Disease 2019 and Multiple Sclerosis.

193 : Associations of Disease-Modifying Therapies With COVID-19 Severity in Multiple Sclerosis.

194 : Correlations between COVID-19 and burden of dementia: An ecological study and review of literature.

195 : Doctor-Should I get the COVID-19 vaccine? Infection and immunization in individuals with neuromuscular disorders.

196 : Doctor-Should I get the COVID-19 vaccine? Infection and immunization in individuals with neuromuscular disorders.

197 : Safety and immunogenicity of mRNA COVID-19 vaccine in inpatients with muscular dystrophy.

198 : Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection.

199 : Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection.

200 : Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection.

201 : US Case Reports of Cerebral Venous Sinus Thrombosis With Thrombocytopenia After Ad26.COV2.S Vaccination, March 2 to April 21, 2021.

202 : Clinical Features of Vaccine-Induced Immune Thrombocytopenia and Thrombosis.

203 : Characteristics and Outcomes of Patients With Cerebral Venous Sinus Thrombosis in SARS-CoV-2 Vaccine-Induced Immune Thrombotic Thrombocytopenia.

204 : Characteristics and Outcomes of Patients With Cerebral Venous Sinus Thrombosis in SARS-CoV-2 Vaccine-Induced Immune Thrombotic Thrombocytopenia.

205 : Guillain-BarréSyndrome Variant Occurring after SARS-CoV-2 Vaccination.

206 : Guillain-BarréSyndrome following ChAdOx1-S/nCoV-19 Vaccine.

207 : Association of Receipt of the Ad26.COV2.S COVID-19 Vaccine With Presumptive Guillain-BarréSyndrome, February-July 2021.

208 : Incidence of Guillain-BarréSyndrome After COVID-19 Vaccination in the Vaccine Safety Datalink.

209 : Development of facial palsy following COVID-19 vaccination: A systematic review.

210 : Rare Heterogeneous Adverse Events Associated with mRNA-Based COVID-19 Vaccines: A Systematic Review.

211 : Spectrum of neurological complications following COVID-19 vaccination.

212 : COVID-19 vaccination-related exacerbation of seizures in persons with epilepsy.

213 : AstraZeneca vaccine: Blood clots are "extremely rare" and benefits outweigh risks, regulators conclude.

214 : No, it's not 1976 all over again.

215 : Age- and Sex-Specific Incidence of Cerebral Venous Sinus Thrombosis Associated With Ad26.COV2.S COVID-19 Vaccination.

216 : Age- and Sex-Specific Incidence of Cerebral Venous Sinus Thrombosis Associated With Ad26.COV2.S COVID-19 Vaccination.

217 : Neurological complications after first dose of COVID-19 vaccines and SARS-CoV-2 infection.

218 : SARS-CoV-2 Vaccination Safety in Guillain-BarréSyndrome, Chronic Inflammatory Demyelinating Polyneuropathy, and Multifocal Motor Neuropathy.

219 : Teleneurology during the COVID-19 pandemic: A step forward in modernizing medical care.

220 : Temporary Emergency Guidance to US Stroke Centers During the Coronavirus Disease 2019 (COVID-19) Pandemic: On Behalf of the American Heart Association/American Stroke Association Stroke Council Leadership.

221 : Safety and Feasibility of a Rapid Outpatient Management Strategy for Transient Ischemic Attack and Minor Stroke: The Rapid Access Vascular Evaluation-Neurology (RAVEN) Approach.

222 : Recalling the COVID-19 lockdown: Insights from patients with epilepsy.

223 : Keeping people with epilepsy safe during the COVID-19 pandemic.

224 : Neurological Implications of COVID-19 Infections.

225 : Treating multiple sclerosis and neuromyelitis optica spectrum disorder during the COVID-19 pandemic.

226 : An Italian programme for COVID-19 infection in multiple sclerosis.

227 : Guidance for the management of myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome (LEMS) during the COVID-19 pandemic.

228 : Guidance for the care of neuromuscular patients during the COVID-19 pandemic outbreak from the French Rare Health Care for Neuromuscular Diseases Network.

229 : Fewer COVID-19 Neurological Complications with Dexamethasone and Remdesivir.

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