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Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 3  |  Page : 560-572

Spectrum of Neurological Manifestations in Covid-19: A Review

Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh, India

Date of Web Publication6-Jul-2020

Correspondence Address:
Dr. Ravindra K Garg
Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh - 226 003
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.289000

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 » Abstract 

COVID-19, in most patients, presents with mild flu-like illness. Elderly patients with comorbidities, like hypertension, diabetes, or lung and cardiac disease, are more likely to have severe disease and deaths. Neurological complications are frequently reported in severely or critically ill patients with comorbidities. In COVID-19, both central and peripheral nervous systems can be affected. The SARS-CoV-2 virus causes the disease COVID-19 and has the potential to invade the brain. The SARS-CoV-2 virus enters the brain either via a hematogenous route or olfactory system. Angiotensin-converting enzyme two receptors, present on endothelial cells of cerebral vessels, are a possible viral entry point. The most severe neurological manifestations, altered sensorium (agitation, delirium, and coma), are because of hypoxic and metabolic abnormalities. Characteristic cytokine storm incites severe metabolic changes and multiple organ failure. Profound coagulopathies may manifest with ischemic or hemorrhagic stroke. Rarely, SARS-CoV-2 virus encephalitis or pictures like acute disseminated encephalomyelitis or acute necrotizing encephalopathy have been reported. Nonspecific headache is a commonly experienced neurological symptom. A new type of headache “personal protection equipment-related headache” has been described. Complete or partial anosmia and ageusia are common peripheral nervous system manifestations. Recently, many cases of Guillain-Barré syndrome in COVID-19 patients have been observed, and a postinfectious immune-mediated inflammatory process was held responsible for this. Guillain-Barré syndrome does respond to intravenous immunoglobulin. Myalgia/fatigue is also common, and elevated creatine kinase levels indicate muscle injury. Most of the reports about neurological complications are currently from China. COVID-19 pandemic is spreading to other parts of the world; the spectrum of neurological complications is likely to widen further.

Keywords: Coronavirus, encephalitis, encephalopathy, Guillain-Barré syndrome, myalgia
Key Messages: COVID-19 is caused by the SARS-COV-2 virus. Several neurological manifestations have been reported. Headache, myalgia, anosmia, and ageusia are common. Cases of encephalitis have been reported but the virus has infrequently been isolated from cerebrospinal fluid. Guillain-Barré syndrome is a postinfectious immune-mediated complication of virus infection.

How to cite this article:
Garg RK. Spectrum of Neurological Manifestations in Covid-19: A Review. Neurol India 2020;68:560-72

How to cite this URL:
Garg RK. Spectrum of Neurological Manifestations in Covid-19: A Review. Neurol India [serial online] 2020 [cited 2023 Sep 23];68:560-72. Available from:

Coronavirus disease 2019 (COVID-19) is a potentially serious condition caused by a novel coronavirus termed as “severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)”. COVID-19 is clinically characterized by respiratory system involvement. COVID-19 disease was first seen in Wuhan, China, in December 2019, when a series of patients presented with pneumonia of unknown etiology. COVID-19 has very rapidly spread worldwide and on March 11, 2020, the World Health Organization officially announced COVID-19 a pandemic.[1]

The majority of patients suffering from COVID-19 have mild to moderate respiratory symptoms. Lungs are the most severely affected organ. Many COVID-19 patients have neurological manifestations as well. Neurological manifestations are common in advanced stages of the disease. In severe COVID-19, systemic disorders like hypoxia, sepsis respiratory and metabolic acidosis, hypercoagulable states, and disseminated intravascular coagulation (DIC) are largely responsible for most of the clinical manifestations, including neurological. Neurological manifestations can also be caused by prolonged stays in the intensive care unit and drug toxicities. The central and peripheral nervous system, both, can be affected in COVID-19. For this article, an extensive literature search was done and all neurological manifestations, seen in COVID-19 patients, were reviewed.

 » Virus Top

The novel coronavirus SARS-CoV-2 was first isolated from the lower respiratory tract, in patients having unexplained pneumonia.[2] Coronaviruses are a group of RNA viruses that dominantly affect the vertebrates. There have been two novel coronavirus outbreaks in the past. In 2002–2003, an outbreak of severe acute respiratory syndrome (SARS) took place that was caused by SARS-CoV. Another outbreak of SARS took place between 2012 that was termed as the Middle East respiratory syndrome (MERS). MERS was caused by MERS-CoV. The current SARS, which is termed as COVID-19, is caused by SARS-CoV-2.[1]


As per the latest World Health Organization report, globally there were 4534731 confirmed COVID-19 cases along with 307537 deaths. COVID-19 has now been reported from 216 countries. India, so far, reported 90727 confirmed cases of COVID-19.[3]

According to the latest meta-analysis (published on April 14, 2020) that analyzed data of 47,344 patients, noted sex ratio (male to a female) of 1.06 and an average age of an affected person was more than 40 years. Diabetes, hypertension, cardiovascular disease, and malignancies were common comorbidities.[4] Another large study, describing data of 5700 hospitalized patients from New York, USA, reported a median age of 63 years (range 1–107 years). There were 40% of females. Common comorbidities were hypertension, obesity, and diabetes. Among patients who were discharged or died (n = 2634), 14% required intensive care management. Approximately, 12% of patients needed mechanical ventilation. In total, 21% of patients had died.[5]


The SARS-CoV-2 virus is a novel coronavirus, consisting of a single-strand positive-sense RNA genome, virus genome lies within a helical nucleocapsid, that is, surrounded by lipid bilayer capsule. SARS-CoV-2 virus entry, into the host cells, is a complex process. After binding to the receptor present on the host cell, the enveloped virus fuses its envelope with the host cell membrane; subsequently, the virus delivers its nucleocapsid into the host cell cytoplasm. In the host cell, viral RNA multiplies and viral proteins are synthesized. Viral proteins reassemble with the viral genome, forming new virus particles. New virus particles are released in new uninfected cells, thus, virus spread takes place.

The SARS-CoV-2 virus utilizes the angiotensin-converting enzyme 2 receptor for entry into the host cell. These receptors are profusely expressed on lung tissues and arterial and venous endothelial cells. Angiotensin-converting enzyme 2 receptors are also expressed in the brain, particularly, in endothelial cells of cerebral capillaries.[6] A unique spike glycoprotein receptor binding domain of SARS-CoV-2 confers affinity of virus for an angiotensin-converting enzyme two receptor.[7] A unique furin-like cleavage site, on the spike protein, plays a crucial role in viral cell entry.[8] Earlier versions of the SARS-CoV virus do not possess a furin-like cleavage site. Transmembrane protease, serine 2 (TMPRSS2) enzyme, is needed to activate the spike protein. A serine protease enzyme inhibitor blocks viral entry into the host cell. This phenomenon can be exploited for developing a treatment of COVID-19, in the future.[6]

Qi and colleagues assessed the expression level of angiotensin-converting enzyme two receptor and TMPRSS2 enzyme in various body organs. Angiotensin-converting enzyme two receptor and TMPRSS2, in the brain, were highly expressed in the oligodendrocyte precursor cells and astrocytes of the substantia nigra and cortex.[9]

Central nervous system (CNS) invasion and crossing of the blood–brain barrier

Available pieces of evidence suggest that the SARS-CoV-2 virus can break the blood–brain barrier and enter into the brain. The virus, possibly, travels to the brain by a hematogenous route. The virus can also enter trans-neuronally to the brain via the olfactory system, across the cribriform plate.[10] Angiotensin-converting enzyme 2 receptors that are present on endothelial cells of cerebral vasculature act as cell entry points for virus.[11] Paniz-Mondolfi and co-workers, in an autopsy-based study, demonstrated the presence of the SARS-CoV-2 virus in neural and capillary endothelial cells of the frontal lobe of the brain. The viral particles were specifically present in small vesicles of endothelial cells. Neurons or microglia did not have angiotensin-converting enzyme two receptors.[12] Comorbidities, like diabetes and hypertension, enhance the angiotensin-converting enzyme 2 receptor expression in the brain and neurotropism of the SARS-CoV-2 virus.[13]

In COVID-19, alterations in blood pressure control are another proposed mechanism that has been suggested to explain the increased risk of cerebral vascular complications. Ordinarily, angiotensin-converting enzyme 2 signaling lowers blood pressure.[14] Competitive blockage of angiotensin-converting enzyme 2 by the SARS-CoV-2 virus down-regulates angiotensin-converting enzyme 2 expression leading to uncontrolled blood pressure and the enhanced possibility of cerebrovascular accidents.


Severe COVID-19 is characterized by profound coagulopathy. In the patients of severe COVID-19, coagulopathies are important detrimental factors that are invariably associated with poor outcomes. The hallmark coagulopathy abnormalities in COVID-19 are elevated prothrombin time, raised D-dimer level, and mild thrombocytopenia, but without hypofibrinogenemia. DIC is the severest form of coagulopathy in COVID-19. DIC is characterized by thrombocytopenia, prolonged prothrombin time, and increased D-dimer and markedly elevated D-dimer.[15],[16] Coagulopathies in COVID 19 predispose to stroke and other prothrombotic events.[17],[18],[19]

Cytokine storm

Cytokines are crucial mediators of the inflammation in COVID-19. Severe COVID-19 is characterized by markedly elevated levels of proinflammatory cytokines, lymphopenia, an increased number of neutrophils. This kind of cytokine profile is termed as “cytokine storm.” Interleukin 6 is a key element of the cytokine storm. Other proinflammatory cytokines that are elevated in cytokine storm are interleukin-1β, interleukin-2, interleukin-8, interleukin-17, chemokine ligand 3, granulocyte-colony stimulating factor, granulocyte-macrophage colony-stimulating factor, the human interferon-inducible protein, and tumor necrosis factor-alpha. Cytokine storm is associated with enhanced vascular hyperpermeability, coagulopathies, and multisystem dysfunction.[20] Approximately, 5% of COVID-19 patients develop acute respiratory distress syndrome, septic shock, and/or multiple organ dysfunction. A cytokine storm is held responsible for the pathogenesis of all the complications of severe COVID-19.[21],[22]

The SARS-CoV-2 virus infection can trigger hemophagocytic lymphohistiocytosis. Hemophagocytic lymphohistiocytosis is a rare hyperinflammatory condition that is characterized by a severe hypercytokinaemia with multiorgan failure. The cytokine profiles of severe COVID-19 and hemophagocytic lymphohistiocytosis syndrome are largely similar.[23],[24]


Postinfectious autoimmune reactions can affect neuronal cells. The SARS-CoV-2 virus epitopes bear a structural resemblance to several human proteins. Molecular mimicry between virus epitope and myelin basic protein results in autoimmune postinfectious demyelinating syndromes.[25] Dysregulation of the angiotensin-converting enzyme 2 receptor also contributes to the pathogenesis of experimental autoimmune encephalomyelitis.[26],[27] Spike surface glycoprotein plays a crucial role in immunopathology.

Phases in pathogenesis

The pathogenesis of COVID-19 evolves in three phases. In the early infection phase, the inflammatory response is localized to the mucosa of the upper respiratory tract. During this phase, the patient is infected and transmits the disease to others. In the next pulmonary phase, the virus proliferates and invades the lungs. There are lung damage, hypoxemia, and cardiovascular dysfunction. In the last, inflammatory response phase, there is a cytokine storm. In the last phase, multiple body organs, including the nervous system, are likely to be affected.[28]

Common clinical features

The incubation period for COVID-19 ranges from 4 to 14 days. The average time to hospitalization, after first symptoms, on an average is 7 days. Fever is the most frequent symptom. Fatigue, dry cough, anorexia, myalgia, dyspnea, and expectoration are other common initial symptoms.

According to the severity, Covid-19 is categorized into mild, severe, and critical categories. In mild disease, patients have no pneumonia or mild pneumonia. In severe cases, patients have severe dyspnea (respiratory rate >30/min) and hypoxemia, needing intensive care unit care. At that stage, bilateral pulmonary infiltrates are seen on chest imaging. Critical patients either have respiratory failure requiring mechanical ventilation, septic shock, and/or multiple organ dysfunction.[29],[30] Comorbid conditions, cardiovascular disorders, diabetes mellitus, hypertension, chronic lung disease, systemic malignancies, and chronic renal failure are crucial.


Common laboratory findings include lymphopenia, increased neutrophil count, eosinopenia along with prolonged prothrombin time, raised lactate dehydrogenase, raised alanine aminotransferase, raised aspartate aminotransferase, a high troponin and markedly elevated D-dimer, and C-reactive protein levels. Increased ferritin level is an indicator of the imminent cytokine storm.[31],[32]

Reverse transcription-polymerase chain reaction (RT-PCR) is the gold standard diagnostic procedure for confirming SARS-CoV-2 virus infection. RT-PCR testing is done on nasopharyngeal swabs. RT-PCR test has a specificity that is close to 100%, but the sensitivity is inadequate at 79%. If the results are negative, the RT-PCR test needs to be performed after 3 days.[33],[34]

Recently, IgM and IgG antibody tests to detect antibodies, against SARS-COV-2 infection in human blood, serum/plasma, have been made available. These tests are valuable as they can be used for screening purposes in a large population. However, the World Health Organization has some doubts about the reliability of these tests. IgM and IgG antibody tests need further validation to establish their accuracy.[35]

Neurologic manifestations

In COVID-19, a variety of neurological complications have been reported. Headache, myalgia, and malaise are common initial neurological symptoms. Severe neurological complications are either because of direct viral invasion, immunological reaction, or hypoxic metabolic changes. In COVID-19, both the CNS and peripheral nervous system (PNS) are affected [Table 1] and [Figure 1].[36],[37]
Table 1: Neurological manifestation in COVID-19: review of published original data from two studies, which included patients in large numbers

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Figure 1: Flow diagram depicts common and uncommon central nervous system (CNS) and peripheral nervous system complications on COVID-19

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Helms and co-workers recorded neurological manifestations in 58 severely ill patients. The median age of these patients was 63 years. Agitation was the most frequent neurological complication (69%; 40/58). On examination, diffuse pyramidal signs were recorded in 39 (67%) patients. A dysexecutive syndrome, consisting of inattention, disorientation, or poorly organized movements, was common sequelae among one-third of the survivors.[36]

In another retrospective study, Mao and co-workers from China noted that among 214 severely affected patients, 78 (36.4%) had neurological complications. CNS involvement was noted in 53 (24.8%) patients. In total, 19 (8.9%) patients had peripheral nervous system involvement. Rest, 23 (10.7%) had skeletal muscle injury. The commonest CNS manifestations were dizziness and headache. More serious CNS manifestations included acute cerebrovascular disease 6 (5 ischemic stroke and 1 hemorrhage). Impaired consciousness was recorded in 16 patients. The majority of serious patients had multiple organ dysfunction. The commonest peripheral manifestations were anosmia and ageusia. Three patients had vision impairment, and five patients had neuralgic pain. Muscle injuries were associated with elevated creatine kinase levels.[37]

 » Central Nervous System Top


Altered sensorium, in severe COVID-19, ranges from confusion, delirium, stupor to coma. Delirium is often associated with systemic inflammation and prolonged hypoxia. Middle-aged and older adults with severe disease are more likely to be affected.[37] Metabolic alterations in an isolated case manifested with posterior reversible encephalopathy syndrome. Kaya and colleagues reported a 38 man, who presented with cortical blindness and MRI hyperintensities in the visual cortex. Both blindness and imaging abnormalities resolved soon after stopping chloroquine and starting corticosteroids.[38] Altered sensorium, in COVID-19, is associated with an increased risk of death.[39]


The SARS-CoV-2 virus has the potential to enter the brain. Xiang and co-workers, in Beijing, China, claimed to isolate the first SARS-CoV-2 virus in cerebrospinal fluid (CSF).[40] So far seven additional cases of SARS-CoV-2 associated encephalitis, encephalopathy, or meningitis have been reported. Four cases presented with features were consistent with encephalitis. Only in two patients, the SARS-CoV-2 virus in CSF was isolated; in one such case, the SARS-CoV-2 virus was not identified in a throat swab. Neuroimaging, usually, in patients with SARS-CoV-2 encephalitis is normal. In a case of COVID-19-associated encephalitis, MRI revealed the involvement of the limbic system. It was likely that the SARS-CoV-2 virus travelled down from nasal mucosa to olfactory bulb then spreading to the piriform cortex. In the majority of patients with encephalitis, computed tomography (CT) thorax demonstrated the ground-glass appearance of the lungs. The majority of the patients had recovered completely.[41],[42],[43],[44],[45],[46],[47],[48],[49] Patients also presented with corticosteroid-responsive encephalopathy, acute disseminated encephalomyelitis, and immune-mediated acute hemorrhagic necrotizing encephalopathy.[50],[51],[52],[53] In the case with hemorrhagic necrotizing encephalopathy, hemorrhagic lesions in thalamus were noted [Table 2].[50]
Table 2: Encephalitis/meningitis in COVID-19: review of all published isolated cases

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SARS-CoV-2 virus-associated medullary respiratory center dysfunction is now held responsible for respiratory distress. Many experts noted that patients of COVID-19 lacked dyspnea; instead, these patients had marked tachypnoea and tachycardia.[54] Li and colleagues argue that the SARS-CoV-2 virus spreads to the medulla oblongata and contributes to the pathogenesis of acute respiratory failure.[55]

In an interesting isolated case, SARS-CoV-2 virus-associated brainstem encephalitis has been described. MRI showed hyperintense signal changes in the brainstem and the upper cervical cord. Clinical manifestations indicated dysfunction of the medulla, pons as well as the midbrain. The patient had marked hepatic insufficiency. Virus possibly travelled from olfactory mucosa to brainstem.[56]


Spinal cord involvement is uncommon. Zhao and co-workers described acute myelitis in a 66-year-old patient. The patient developed acute flaccid paraplegia with spinal sensory level at T10 and urinary incontinence. The patient was treated with intravenous immunoglobulin and corticosteroids, and he responded well to the treatment. The cytokine storm and exaggerated inflammatory changes resulted in acute transverse myelitis.[57]


In COVID-19, coagulopathies enhance the risk of cerebral arterial and venous thrombosis. Li and co-workers, in a retrospective study, noted that out of 221, 11 patients had an acute ischemic stroke. One patient each had cerebral venous thrombosis and cerebral hemorrhage. Majority stroke patients were elderly and were suffering from severe COVID-19. Comorbidities were common.[58] Beyrouti and co-workers, in a report of six severely affected patients with large cerebral infarcts, noted elevated D-dimer levels (≥1000 μg/L), indicating a coagulopathy.[59]

COVID-19-related strokes happen in young patients as well. Oxley and colleagues, from New York, USA, described five cases of large-vessel infarct in young (>50; 33–49 years). Three patients had prior risk factors (diabetes and hypertension). National Institutes of Health Stroke Scale scores, on hospitalization, ranged from 13 to 19. On follow up, all five patients deteriorated. In four patients, either the endovascular intervention or thrombolysis was done. Covid-19-associated coagulopathy and vascular endothelial dysfunction were plausible mechanisms.[60] In patients of stroke, the SARS-CoV-2 virus could not be demonstrated in CSF.[61]

Administration of exogenous soluble angiotensin-converting enzyme 2 receptors (human recombinant soluble angiotensin-converting enzyme 2 receptors), in experimental conditions, found to prevent SARS-CoV-2 virus infection of engineered human blood vessels. Soluble angiotensin-converting enzyme 2 acts as a virus trap. This treatment has the potential to prevent multiorgan failure and stroke.[19],[62]


Seizures are not common manifestation in COVID-19. Mao and co-workers noted that among 214 patients admitted in intensive care units, the seizure was recorded only in one patient.[37] A multicentric Chinese retrospective study noted that among 304 COVID-19 patients (108 with severe disease) in none of the patients acute symptomatic seizures or status epilepticus were observed despite the presence of severe metabolic alterations.[63] In many case reports, authors had described new-onset seizures that were triggered by the SARS-CoV-2 virus infection. Even convulsive and nonconvulsive status epilepticus triggered by SARS-CoV-2 virus infection has also been described. Status epilepticus patients had responded well to parenteral levetiracetam.[64],[65]

Vollono and colleagues published a report of nonconvulsive status epilepticus triggered by Covid-19, in an elderly patient. Electroencephalography showed intermittent epileptiform discharges over the left temporal area. MRI brain revealed extensive gliosis and atrophy of left temporo-parietal lobe. After the resolution of fever, the patient had improved.[66] Dugue and co-workers, from the USA, described a six-week-old child, who presented with an acute episode of seizure. His CSF examination and neuroimaging were normal. The child initially had a fever; authors considered this episode as a manifestation of febrile seizures.[67]

Sporadic electroencephalographic epileptiform discharges, in acutely ill patients of COVID-19, have been described. Epileptiform discharges were dominantly localized to frontal lobes. These patients never had a definite seizure episode. Electroencephalography was done either because the patient had encephalopathy or had some seizure-like event.[68]


In many meta-analyses, headache has now been recognized as one of the common initial symptom of COVID-19. In these meta-analyses and systematic reviews, the incidence of headache ranged from 10% to 15% [Table 3].[69],[70],[71],[72] A recent European study noted a different clinical profile of younger (median 37 years) COVID-19 patients. In 1,420 mild-to-moderate Covid-19 patients, headache (70%) was the most prevalent symptom. Other common neurological symptoms were loss of smell (70%), asthenia (63%), myalgia (63%), and loss of taste (54%). A fewer number of patients reported a reduction in visual acuity (n = 6), vertigo (n = 6), and tinnitus (n = 5). Fever was not a common symptom and was reported only by 45% of patients.[73] Exact reasons for headache remained unexplained. Increased mental stress, excessive anxiety, and changes in lifestyle are possible reasons for early headaches. Pre-existing migraine may get worse because of COVID-19-related stress.[74] Belvis in a recent communication opined that COVID-19-associated acute headaches can be because of systemic viral infection, primary cough headache, and tension-type headache. Early headaches respond well to acetaminophen. Headaches appearing between the 7th and the 10th days of illness can be related to cytokine storm.[75]
Table 3: The most common presenting symptoms of COVID-19: review of three meta-analysis analyzing large number of patients

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Personal protection equipment (PPE) can because of new-onset headaches. Ong and co-workers, among hospital staff performing Covid-19 related duties, described a new kind of PPE-associated headache. In a cross-sectional study, the authors noted that most healthcare workers had either PPE-associated headache or there was the aggravation of their pre-existing headaches. In a questionnaire-based study, 81% (128/158) respondents experienced de novo PPE-associated headaches. The majority (42/46) of participants with pre-existing headaches experienced that prolonged PPE usage triggered the disabling headache.[76]

Subjective neurological symptoms

Frequently, the neurological symptoms that patients complain are subjective. Liguori and colleagues assessed 103 patients with SARS-CoV2 virus infection and noted that 91.3% of participants had one or more subjective neurological complaints. Sleep disturbances were the most common complaint. Other complaints were dysgeusia, headache, hyposmia, depression, dizziness, numbness/paraesthesia, daytime sleepiness, and muscle ache. These subjective neurological complaints were more common in females.[77]

Neuroimaging brain

In critically ill patients of Covid-19, a variety of neuroimaging abnormalities of the brain has been described. Kandemirli and co-workers demonstrated nonspecific T2/FLAIR cortical, subcortical, and deep white-matter signal abnormalities in 37% (10/27) critically ill patients. One patient each had transverse sinus thrombosis and right middle cerebral artery infarct. In patients with neuroimaging abnormalities, CSF protein levels (range 59.9 – 109.7 mg/dL) were elevated. The SARS-CoV-2 virus in CSF was not demonstrated.[78]

Coleen and co-workers performed MRI in 19 deceased patients of severe COVID-19, within 24 h after death. White-matter cortical abnormalities were noted in four deceased patients. These changes were intracranial vasculopathy, subcortical micro- and macrobleeds, and changes similar to posterior reversible encephalopathy syndrome.[79]

 » Peripheral Nervous System Top

Loss of smell and taste

A complete or partial loss of smell sensation (anosmia) and taste sensation (ageusia) is the most frequent neurological manifestation of COVID-19. Anosmia and ageusia are common even in mild to moderate cases.[80] Smell sensation is more severely affected than a taste sensation. In a French study, Lechien and co-workers reported that out of 417 mild-to-moderate COVID-19 patients, 86% and 88% of patients, respectively, reported anosmia and ageusia. Anosmia in many patients was the first manifestation of Covid-19.[81] Beltrán-Corbellini and co-workers noted that anosmia and ageusia were more frequent in Covid-19 than in influenza. The SARS-CoV-2 virus utilizes angiotensin-converting enzyme 2 receptors, presents in the olfactory epithelium, to enter into the neuronal cells, and then via the olfactory nerve, it spreads to the olfactory bulb.[82]

Other cranial nerves

Isolated cranial neuropathies are rare in COVID-19. Wei and co-workers described a case of acute unilateral isolated oculomotor nerve palsy in a severely ill patient. CT chest demonstrated multiple ground-glass opacities of the lungs. The inflammatory reaction against the SARS-CoV-2 virus and inflammation of vessels supplying to nerve trunk was a possible reason for cranial nerve damage.[83]

Guillain-Barré syndrome

Guillain-Barré syndrome is a frequently encountered neurological complication of COVID-19. Zhao and co-workers described the first patient of Guillain-Barré syndrome in a patient with COVID-19.[84] After this, 18 more patients, of Guillain-Barré syndrome in COVID-19, have been described. All patients presented with classical clinical manifestations – acute symmetric flaccid, areflexic quadriparesis. CSF examination, in the majority, revealed albumin-cytologic dissociation. Treatment with intravenous immunoglobulins led to complete or partial recovery, in the majority. Few patients needed ventilatory support.[85],[86],[87],[88],[89],[90],[91],[92],[93],[94],[95],[96],[97],[98]

Miller Fisher syndrome is a variant of Guillain-Barré syndrome and is characterized by ophthalmoplegia, ataxia, and areflexia. Miller Fisher syndrome has also been described in patients with Covid-19. An albumin-cytologic dissociation in CSF and positive GD1b-IgG antibodies indicated an inflammatory pathology.[99],[100] A postinfectious immune-mediated mechanism was the putative mechanism proposed for the pathogenesis of COVID-19 associated Guillain-Barré syndrome and Miller Fisher syndrome [Table 4].
Table 4: Guillain-Barré syndrome in COVID-19: review of all published isolated cases

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General muscle pain or myalgia and fatigue are common initial symptoms of COVID-19. Several meta-analyses noted that myalgia, muscle soreness, and fatigue occurred in up to 35% of patients [Table 3].

Mao and co-workers noted muscle injury in 10% (23/214) of COVID-19 patients. Muscle involvement was much more common in severe cases. Creatine kinase levels were elevated in all patients with muscle disease. Rhabdomyolysis, a life-threatening disorder, has been described in Covid-19. Rhabdomyolysis is clinically characterized by myalgia, fatigue, and haemoglobinuria. If not recognized and treated promptly, acute renal failure may set in.[37],[101] Rhabdomyolysis can be a heralding manifestation of COVID-19. A COVID-19 patient, presenting with localized muscle pain or generalized weakness, a high index of suspicion for rhabdomyolysis should be kept.[102],[103] It has been hypothesized that via angiotensin-converting enzyme 2 receptor, virus enter in the muscles and can cause muscle injury.[104]

Beydon and co-workers recently described myositis in a critically ill patient of COVID-19. The patient presented with acute myalgias, difficulty in waking, and proximal weakness. Creatine kinase level (25384 IU/L) was markedly elevated. Four days later, the patient became febrile and tested positive for the SARS-CO-V-2 virus. A thoracic CT scan revealed ground-glass opacities of lungs. Limb MRI revealed external obturator muscle and quadricipital edema, suggesting myositis.[105]


Drugs that have been repurposed for use in COVID-19 have the potential to cause neurological toxicities.[106] Hydroxychloroquine-associated retinal toxicity is well recognized and can occur in up to 7.5% of patients.[107] Hydroxychloroquine myopathy/myositis is another rarely encountered neurological condition. Hydroxychloroquine induced myositis is clinically characterized by proximal muscle weakness and normal creatinine kinase levels. Electron microscopy of biopsied muscle tissue demonstrates vacuolar changes and curvilinear bodies.[108],[109],[110] Hydroxychloroquine myopathy should be clinically and pathologically considered in the differential diagnosis of Pompe disease and other limb-girdle muscle disorders.[111] In isolated instances, hydroxychloroquine has also been implicated as a trigger for seizure.[112],[113]


Currently, no drug has proven efficacy in the treatment of COVID-19.

Patients with mild disease are usually treated at home. The clinical condition of the patient should be keenly monitored. Severe and critically ill patients require intensive care treatment and mechanical ventilation. The focus is on prevention of transmission of the virus to the others.

 » Conclusions Top

Information regarding SARS-CoV-2-related neurological manifestations is available in the form of a few large studies and case series, but bulk information is available only in the form of case reports. Neurological manifestations of the SARS-CoV-2 are seen in severe cases of Covid-19. Reports on SARS-CoV-2 encephalitis are in the form of isolated reports, and virus in CSF is not readily demonstrated. Guillain-Barré syndrome is another common complication of COVID-19. Several newly developed vaccines are currently in various phases of clinical trial. Vaccines are always at risk of inciting neurological complications. Even newer drugs, that are being tried, can have neurological complications.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

World Health Organization. Rolling updates on coronavirus disease (COVID-19). Updated 24 April 2020. Available from: [Last assessed on 2020 Apr 29].  Back to cited text no. 1
Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med 2020;382:727-33.  Back to cited text no. 2
World Health Organization. Coronavirus disease (COVID-19) outbreak situation. Available from: [Last assessed on 2020 May 19].  Back to cited text no. 3
Hu Y, Sun J, Dai Z, Deng H, Li X, Huang Q, et al. Prevalence and severity of coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis. J Clin Virol 2020;127:104371.  Back to cited text no. 4
Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, et al. Presenting characteristics, comorbidities, and outcomes among 5700 patients hospitalized with COVID-19 in the New York City area. JAMA 2020;323:2052-9.  Back to cited text no. 5
Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 2020;181:271-80.e8.  Back to cited text no. 6
Wrapp D, Wang N, Corbett KS, Goldsmith JA, Hsieh CL, Abiona O, et al. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Science 2020;367:1260-3.  Back to cited text no. 7
Coutard B, Valle C, de Lamballerie X, Canard B, Seidah NG, Decroly E. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. Antiviral Res 2020;176:104742.  Back to cited text no. 8
Qi J, Zhou Y, Hua J, Zhang L, Bian J, Liu B, et al. The scRNA-seq expression profiling of the receptor ACE2 and the cellular protease TMPRSS2 reveals human organs susceptible to COVID-19 infection. bioRxiv 2020. doi: 10.1101/2020.04.16.045690.  Back to cited text no. 9
Natoli S, Oliveira V, Calabresi P, Maia LF, Pisani A. Does SARS-Cov-2 invade the brain? Translational lessons from animal models. Eur J Neurol 2020. doi: 10.1111/ene. 14277.  Back to cited text no. 10
Li MY, Li L, Zhang Y, Wang XS. Expression of the SARS-CoV-2 cell receptor gene ACE2 in a wide variety of human tissues. Infect Dis Poverty 2020;9:45.  Back to cited text no. 11
Paniz-Mondolfi A, Bryce C, Grimes Z, Gordon RE, Reidy J, Lednicky J, et al. Central nervous system involvement by severe acute respiratory syndrome coronavirus -2 (SARS-CoV-2). J Med Virol 2020. doi: 10.1002/jmv. 25915.  Back to cited text no. 12
Puelles VG, Lütgehetmann M, Lindenmeyer MT, Sperhake JP, Wong MN, Allweiss L, et al. Multiorgan and renal tropism of SARS-CoV-2. N Engl J Med 2020. doi: 10.1056/NEJMc2011400.  Back to cited text no. 13
Zhu H, Rhee JW, Cheng P, Waliany S, Chang A, Witteles RM, et al. Cardiovascular complications in patients with COVID-19: Consequences of viral toxicities and host immune response. Curr Cardiol Rep 2020;22:32.  Back to cited text no. 14
Mucha SR, Dugar S, McCrae K, Joseph DE, Bartholomew J, Sacha G, et al. Coagulopathy in COVID-19. Cleve Clin J Med 2020. doi: 10.3949/ccjm. 87a.ccc024.  Back to cited text no. 15
Lillicrap D. Disseminated intravascular coagulation in patients with 2019-nCoV pneumonia. J Thromb Haemost 2020;18:786-7.  Back to cited text no. 16
Kollias A, Kyriakoulis KG, Dimakakos E, Poulakou G, Stergiou GS, Syrigos K. Thromboembolic risk and anticoagulant therapy in COVID-19 patients: Emerging evidence and call for action. Br J Haematol 2020;189:846-7.  Back to cited text no. 17
Bikdeli B, Madhavan MV, Jimenez D, Chuich T, Dreyfus I, Driggin E, et al. COVID-19 and thrombotic or thromboembolic disease: Implications for prevention, antithrombotic therapy, and follow-up. J Am Coll Cardiol 2020:S0735-1097 (20) 35008-7. doi: 10.1016/j.jacc. 2020.04.031.  Back to cited text no. 18
Hess DC, Eldahshan W, Rutkowski E. COVID-19-related stroke. Transl Stroke Res 2020;11:322-5.  Back to cited text no. 19
Jose RJ, Manuel A. COVID-19 cytokine storm: The interplay between inflammation and coagulation. Lancet Respir Med 2020:S2213-2600(20)30216-2. doi: 10.1016/S2213-2600(20)30216-2.  Back to cited text no. 20
Feng Y, Ling Y, Bai T, Xie Y, Huang J, Li J, Xiong W, et al. COVID-19 with Different severity: A multi-center study of clinical features. Am J Respir Crit Care Med 2020;201:1380-8.  Back to cited text no. 21
Yang F, Shi S, Zhu J, Shi J, Dai K, Chen X. Analysis of 92 deceased patients with COVID-19. J Med Virol 2020. doi: 10.1002/jmv. 25891.  Back to cited text no. 22
McGonagle D, Sharif K, O'Regan A, Bridgewood C. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease. Autoimmun Rev 2020;19:102537.  Back to cited text no. 23
Radmanesh F, Rodriguez-Pla A, Pincus MD, Burns JD. Severe cerebral involvement in adult-onset hemophagocytic lymphohistiocytosis. J Clin Neurosci 2020;76:236-7.  Back to cited text no. 24
Lyons-Weiler J. Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity. J Transl Autoimmun 2020;3:100051.  Back to cited text no. 25
Pérez CA. Looking ahead: The risk of neurologic complications due to COVID-19. Neurol Clin Pract 2020. doi: 10.1212/CPJ.0000000000000836.  Back to cited text no. 26
Guidon AC, Amato AA. COVID-19 and neuromuscular disorders. Neurology 2020;94:959-69.  Back to cited text no. 27
Shi Y, Wang Y, Shao C, Huang J, Gan J, Huang X, et al. COVID-19 infection: The perspectives on immune responses. Cell Death Differ 2020;27:1451-4.  Back to cited text no. 28
Gandhi RT, Lynch JB, Del Rio C. Mild or moderate Covid-19. N Engl J Med 2020. doi: 10.1056/NEJMcp2009249.  Back to cited text no. 29
Berlin DA, Gulick RM, Martinez FJ. Severe Covid-19. N Engl J Med 2020. doi: 10.1056/NEJMcp2009575.  Back to cited text no. 30
Babiker A, Myers CW, Hill CE, Guarner J. SARS-CoV-2 testing. Am J Clin Pathol 2020;153:706-8.  Back to cited text no. 31
Lippi G, Plebani M. Laboratory abnormalities in patients with COVID-2019 infection. Clin Chem Lab Med 2020. doi: 10.1515/cclm-2020-0198.  Back to cited text no. 32
World Health Organization. Laboratory testing for coronavirus disease (COVID-19) in suspected human cases. Interim guidance. Available from: cases-20200117. [Last accessed on 2020 May 15].  Back to cited text no. 33
He JL, Luo L, Luo ZD, Lyu JX, Ng MY, Shen XP, et al. Diagnostic performance between CT and initial real-time RT-PCR for clinically suspected 2019 coronavirus disease (COVID-19) patients outside Wuhan, China. Respir Med 2020;168:105980.  Back to cited text no. 34
World Health Organization. “Immunity passports” in the context of COVID-19 scientific brief. April 24, 2020. Available from:  Back to cited text no. 35
Helms J, Kremer S, Merdji H, Clere-Jehl R, Schenck M, Kummerlen C, et al. Neurologic features in severe SARS-CoV-2 infection. N Engl J Med 2020;382:2268-70.  Back to cited text no. 36
Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, et al. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol 2020;e201127. doi: 10.1001/jamaneurol. 2020.1127.  Back to cited text no. 37
Kaya Y, Kara S, Akinci C, Kocaman AS. Transient cortical blindness in covid-19 pneumonia; a PRES-like syndrome: A case report. J Neurol Sci 2020;413:116858.  Back to cited text no. 38
Chen T, Wu D, Chen H, Yan W, Yang D, Chen G, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: Retrospective study. BMJ 2020;368:m1091. Erratum in: BMJ 2020;368:m1295.  Back to cited text no. 39
Xiang P, Xu XM, Gao LL, Wang HZ, Xiong HF, Li RH. First case of 2019 novel coronavirus disease with Encephalitis. ChinaXiv T. 2020;202003:00015.  Back to cited text no. 40
Moriguchi T, Harii N, Goto J, Harada D, Sugawara H, Takamino J, et al. A first case of meningitis/encephalitis associated with SARS-Coronavirus-2. Int J Infect Dis 2020;94:55-8.  Back to cited text no. 41
Ye M, Ren Y, Lv T. Encephalitis as a clinical manifestation of COVID-19. Brain Behav Immun 2020:S0889-1591(20)30465-7. doi: 10.1016/j.bbi. 2020.04.017.  Back to cited text no. 42
Duong L, Xu P, Liu A. Meningoencephalitis without respiratory failure in a young female patient with COVID-19 infection in Downtown Los Angeles, early April 2020. Brain Behav Immun 2020:S0889-1591 (20) 30509-2. doi: 10.1016/j.bbi. 2020.04.024.  Back to cited text no. 43
Yin R, Feng W, Wang T, Chen G, Wu T, Chen D, et al. Concomitant neurological symptoms observed in a patient diagnosed with coronavirus disease 2019. J Med Virol 2020. doi: 10.1002/jmv. 25888.  Back to cited text no. 44
Filatov A, Sharma P, Hindi F, Espinosa PS. Neurological complications of coronavirus disease (COVID-19): Encephalopathy. Cureus 2020;12:e7352.  Back to cited text no. 45
McAbee GN, Brosgol Y, Pavlakis S, Agha R, Gaffoor M. Encephalitis associated with COVID-19 infection in an 11-year-old child. Pediatr Neurol 2020. doi: 10.1016/j.pediatrneurol. 2020.04.013.  Back to cited text no. 46
Bernard-Valnet R, Pizzarotti B, Anichini A, Demars Y, Russo E, Schmidhauser M, et al. Two patients with acute meningo-encephalitis concomitant to SARS-CoV-2 infection. Eur J Neurol 2020. doi: 10.1111/ene. 14298.  Back to cited text no. 47
Packwood R, Galletta G, Tennyson J. An unusual case report of covid-19 presenting with meningitis symptoms and shingles. Clin Pract Cases Emerg Med 2020. doi: 10.5811/cpcem. 2020.4.47557.  Back to cited text no. 48
Hanna Huang Y, Jiang D, Huang JT. SARS-CoV-2 detected in cerebrospinal fluid by PCR in a case of COVID-19 encephalitis. Brain Behav Immun 2020:S0889-1591 (20) 30770-4. doi: 10.1016/j.bbi. 2020.05.012.  Back to cited text no. 49
Poyiadji N, Shahin G, Noujaim D, Stone M, Patel S, Griffith B. COVID-19-associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI features. Radiology 2020:201187. doi: 10.1148/radiol. 2020201187.  Back to cited text no. 50
Sachs JR, Gibbs KW, Swor DE, Sweeney AP, Williams DW, Burdette JH, et al. COVID-19-associated leukoencephalopathy. Radiology 2020:201753. doi: 10.1148/radiol. 2020201753.  Back to cited text no. 51
Zhang T, Rodricks MB, Hirsh E. COVID-19-associated acute disseminated encephalomyelitis – A case report. medRxiv 2020. doi: 10.1101/2020.04.16.20068148.  Back to cited text no. 52
Pilotto A, Odolini S, Masciocchi S, Comelli A, Volongh I, Gazzina S, et al. Steroid-responsive severe encephalopathy in SARS-CoV-2 infection. Ann Neurol 2020. doi: 10.1002/ana. 25783.  Back to cited text no. 53
Bertran Recasens B, Martinez-Llorens JM, Rodriguez-Sevilla JJ, Rubio MA. Lack of dyspnea in Covid-19 patients; another neurological conundrum? Eur J Neurol 2020. doi: 10.1111/ene. 14265.  Back to cited text no. 54
Li YC, Bai WZ, Hashikawa T. The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients. J Med Virol 2020. doi: 10.1002/jmv. 25728.  Back to cited text no. 55
Wong PF, Craik S, Newman P, Makan A, Srinivasan K, Crawford E, et al. Lessons of the month 1: A case of rhombencephalitis as a rare complication of acute COVID-19 infection. Clin Med (Lond) 2020:clinmed. 2020-0182. doi: 10.7861/clinmed. 2020-0182.  Back to cited text no. 56
Zhao K, Huang J, Dai D, Feng Y, Liu L, Nie S. Acute myelitis after SARS-CoV-2 infection: A case report. medRxiv 2020. doi: 10.1101/2020.03.16.20035105.  Back to cited text no. 57
Li Y, Wang M, Zhou Y, Chang J, Xian Y, Mao L, et al. Acute cerebrovascular disease following COVID-19: A single center, retrospective, observational study. SSRN Electron J 2020. doi: 10.2139/ssrn. 3550025.  Back to cited text no. 58
Beyrouti R, Adams ME, Benjamin L, Cohen H, Farmer SF, Goh YY, et al. Characteristics of ischaemic stroke associated with COVID-19. J Neurol Neurosurg Psychiatry 2020:jnnp-2020-323586. doi: 10.1136/jnnp-2020-323586.  Back to cited text no. 59
Oxley TJ, Mocco J, Majidi S, Kellner CP, Shoirah H, Singh IP, et al. Large-vessel stroke as a presenting feature of Covid-19 in the young. N Engl J Med 2020;382:e60. doi: 10.1056/NEJMc2009787.  Back to cited text no. 60
Al Saiegh F, Ghosh R, Leibold A, Avery MB, Schmidt RF, Theofanis T, et al. Status of SARS-CoV-2 in cerebrospinal fluid of patients with COVID-19 and stroke. J Neurol Neurosurg Psychiatry 2020:jnnp-2020-323522. doi: 10.1136/jnnp-2020-323522.  Back to cited text no. 61
Monteil V, Kwon H, Prado P, Hagelkrüys A, Wimmer RA, Stahl M, et al. Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2. Cell 2020;181:905-13.e7.  Back to cited text no. 62
Lu L, Xiong W, Liu D, Liu J, Yang D, Li N, et al. New-onset acute symptomatic seizure and risk factors in Corona Virus Disease 2019: A retrospective multicenter study. Epilepsia 2020. doi: 10.1111/epi. 16524.  Back to cited text no. 63
Somani S, Pati S, Gaston T, Chitlangia A, Agnihotri S. De novo status epilepticus in patients with COVID-19. Ann Clin Transl Neurol 2020. doi: 10.1002/acn3.51071.  Back to cited text no. 64
Balloy G, Mahé PJ, Leclair-Visonneau L, Péréon Y, Derkinderen P, Magot A, et al. Non-lesional status epilepticus in a patient with coronavirus disease 2019. Clin Neurophysiol 2020. doi: 10.1016/j.clinph. 2020.05.005.  Back to cited text no. 65
Vollono C, Rollo E, Romozzi M, Frisullo G, Servidei S, Borghetti A, et al. Focal status epilepticus as unique clinical feature of COVID-19: A case report. Seizure 2020;78:109-12.  Back to cited text no. 66
Dugue R, Cay-Martínez KC, Thakur K, Garcia JA, Chauhan LV, Williams SH, et al. Neurologic manifestations in an infant with COVID-19. Neurology 2020. doi: 10.1212/WNL.0000000000009653.  Back to cited text no. 67
Galanopoulou AS, Ferastraoaru V, Correa DJ, Cherian K, Duberstein S, Gursky J, et al. EG findings in acutely ill patients investigated for SARS-CoV2/COVID-19: A small case series preliminary report. Epilepsia Open 2020. doi: 10.1002/epi4.12399.  Back to cited text no. 68
Zhu J, Ji P, Pang J, Zhong Z, Li H, He C, et al. Clinical characteristics of 3,062 COVID-19 patients: A meta-analysis. J Med Virol 2020. doi: 10.1002/jmv. 25884.  Back to cited text no. 69
Fu L, Wang B, Yuan T, Chen X, Ao Y, Fitzpatrick T, et al. Clinical characteristics of coronavirus disease 2019 (COVID-19) in China: A systematic review and meta-analysis. J Infect 2020;80:656-65.  Back to cited text no. 70
Cao Y, Liu X, Xiong L, Cai K. Imaging and clinical features of patients with 2019 novel coronavirus SARS-CoV-2: A systematic review and meta-analysis. J Med Virol 2020. doi: 10.1002/jmv. 25822.  Back to cited text no. 71
Rodriguez-Morales AJ, Cardona-Ospina JA, Gutiérrez-Ocampo E, Villamizar-Peña R, Holguin-Rivera Y, et al. Clinical, laboratory and imaging features of COVID-19: A systematic review and meta-analysis. Travel Med Infect Dis 2020:101623. doi: 10.1016/j.tmaid. 2020.101623.  Back to cited text no. 72
Lechien JR, Chiesa-Estomba CM, Place S, Van Laethem Y, Cabaraux P, Mat Q, Huet K, et al. Clinical and epidemiological characteristics of 1,420 European patients with mild-to-moderate coronavirus disease 2019. J Intern Med 2020. doi: 10.1111/joim. 13089.  Back to cited text no. 73
Silvestro M, Tessitore A, Tedeschi G, Russo A. Migraine in the time of COVID-19. Headache 2020;60:988-9.  Back to cited text no. 74
Belvis R. Headaches during COVID-19: My clinical case and review of the literature. Headache 2020. doi: 10.1111/head. 13841.  Back to cited text no. 75
Ong JJY, Bharatendu C, Goh Y, Tang JZY, Sooi KWX, Tan YL, et al. Headaches associated with personal protective equipment-A cross-sectional study among frontline healthcare workers during COVID-19. Headache 2020;60:864-77.  Back to cited text no. 76
Liguori C, Pierantozzi M, Spanetta M, Sarmati L, Cesta N, Iannetta M, et al. Subjective neurological symptoms frequently occur in patients with SARS-CoV2 infection. Brain Behav Immun 2020:S0889-1591(20)30876-X. doi: 10.1016/j.bbi. 2020.05.037.  Back to cited text no. 77
Kandemirli SG, Dogan L, Sarikaya ZT, Kara S, Akinci C, Kaya D, et al. Brain MRI findings in patients in the intensive care unit with COVID-19 infection. Radiology 2020:201697. doi: 10.1148/radiol. 2020201697.  Back to cited text no. 78
Coolen T, Lolli V, Sadeghi N, Rovai A, Trotta N, Fabio S, et al. Early postmortem brain MRI findings in COVID-19 non-survivors. medRxiv 2020. doi: 10.1101/2020.05.04.20090316.  Back to cited text no. 79
Moein ST, Hashemian SMR, Mansourafshar B, Khorram-Tousi A, Tabarsi P, Doty RL. Smell dysfunction: A biomarker for COVID-19. Int Forum Allergy Rhinol 2020. doi: 10.1002/alr. 22587.  Back to cited text no. 80
Lechien JR, Chiesa-Estomba CM, De Siati DR, Horoi M, Le Bon SD, Rodriguez A, et al. Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): A multicenter European study. Eur Arch Otorhinolaryngol 2020:1-11. doi: 10.1007/s00405-020-05965-1.  Back to cited text no. 81
Beltrán-Corbellini Á, Chico-García JL, Martínez-Poles J, Rodríguez-Jorge F, Natera-Villalba E, Gómez-Corral J, et al. Acute-onset smell and taste disorders in the context ofCovid-19: A pilot multicenter PCR-based case-control study. Eur J Neurol 2020. doi: 10.1111/ene. 14273.  Back to cited text no. 82
Wei H, Yin H, Huang M, Guo Z. The 2019 novel cornoavirus pneumonia with onset of oculomotor nerve palsy: A case study. J Neurol 2020;267:1550-3.  Back to cited text no. 83
Zhao H, Shen D, Zhou H, Liu J, Chen S. Guillain-Barré syndrome associated with SARS-CoV-2 infection: Causality or coincidence? Lancet Neurol 2020;19:383-4.  Back to cited text no. 84
Camdessanche JP, Morel J, Pozzetto B, Paul S, Tholance Y, Botelho-Nevers E. COVID-19 may induce Guillain-Barré syndrome. Rev Neurol (Paris) 2020;176:516-8.  Back to cited text no. 85
Padroni M, Mastrangelo V, Asioli GM, Pavolucci L, Abu-Rumeileh S, Piscaglia MG, et al. Guillain-Barré syndrome following COVID-19: New infection, old complication? J Neurol 2020:1-3. doi: 10.1007/s00415-020-09849-6.  Back to cited text no. 86
Virani A, Rabold E, Hanson T, Haag A, Elrufay R, Cheema T, et al. Guillain-Barré syndrome associated with SARS-CoV-2 infection. IDCases 2020:e00771. doi: 10.1016/j.idcr. 2020.e00771.  Back to cited text no. 87
Sedaghat Z, Karimi N. Guillain Barre syndrome associated with COVID-1 infection: A case report. J Clin Neurosci 2020;76:233-5.  Back to cited text no. 88
Toscano G, Palmerini F, Ravaglia S, Ruiz L, Invernizzi P, Cuzzoni MG, et al. Guillain-Barré syndrome associated with SARS-CoV-2. N Engl J Med 2020. doi: 10.1056/NEJMc2009191.  Back to cited text no. 89
Alberti P, Beretta S, Piatti M, Karantzoulis A, Piatti ML, Santoro P, et al. Guillain-Barré syndrome related to COVID-19 infection. Neurol Neuroimmunol Neuroinflamm 2020;7:e741.  Back to cited text no. 90
Otmani HE, Moutawakil BE, Rafai MA, Benna NE, Kettani CE, Soussi M, et al. Covid-19 and Guillain-Barré syndrome: More than a coincidence! Rev Neurol (Paris) 2020;176:518-9.  Back to cited text no. 91
Coen M, Jeanson G, Alejandro Culebras Almeida L, Hübers A, Stierlin F, Najjar I, et al. Guillain-Barré syndrome as a complication of SARS-CoV-2 infection. Brain Behav Immun 2020:S0889-1591(20)30698-X. doi: 10.1016/j.bbi. 2020.04.074.  Back to cited text no. 92
Galán AV, Saucedo PDS, Postigo FP, Paniagua EB. Guillain-Barré syndrome associated with SARS-CoV-2 infection. Neurologia 2020:S0213-4853(20)30072-4. doi: 10.1016/j.nrl. 2020.04.007.  Back to cited text no. 93
Marta-Enguita J, Rubio-Baines I, Gastón-Zubimendi I. Fatal Guillain-Barre syndrome after infection with SARS-CoV-2. Neurologia 2020:S0213-4853(20)30069-4. doi: 10.1016/j.nrleng. 2020.04.004.  Back to cited text no. 94
Scheidl E, Canseco DD, Hadji-Naumov A, Bereznai B. Guillain-Barre syndrome during SARS-CoV-2 pandemic: A case report and review of recent literature. J Peripher Nerv Syst 2020. doi: 10.1111/jns. 12382.  Back to cited text no. 95
Arnaud S, Budowski C, Ng Wing Tin S, Bertrand Degos B. Post SARS-CoV-2 Guillain-Barré syndrome. Clin Neurophysiol 2020;131:1652-4.  Back to cited text no. 96
Ottaviani D, Boso F, Tranquillini E, Gapeni I, Pedrotti G, Cozzio S, et al. Early Guillain-Barré syndrome in coronavirus disease 2019 (COVID-19): A case report from an Italian COVID-hospital. Neurol Sci 2020:1-4. doi: 10.1007/s10072-020-04449-8.  Back to cited text no. 97
Caamaño DSJ, Beato RA. Facial diplegia, a possible atypical variant of Guillain-Barré Syndrome as a rare neurological complication of SARS-CoV-2. J Clin Neurosci 2020. doi: 10.1016/j.jocn. 2020.05.016.  Back to cited text no. 98
Dinkin M, Gao V, Kahan J, Bobker S, Simonetto M, Wechsler P, et al. COVID-19 presenting with ophthalmoparesis from cranial nerve palsy. Neurology 2020. doi: 10.1212/WNL.0000000000009700.  Back to cited text no. 99
Gutiérrez-Ortiz C, Méndez A, Rodrigo-Rey S, San Pedro-Murillo E, Bermejo-Guerrero L, Gordo-Mañas R, et al. Miller Fisher syndrome and polyneuritis cranialis in COVID-19. Neurology 2020. doi: 10.1212/WNL.0000000000009619.  Back to cited text no. 100
Jin M, Tong Q. Rhabdomyolysis as potential late complication associated with COVID-19. Emerg Infect Dis 2020:26. doi: 10.3201/eid2607.200445.  Back to cited text no. 101
Suwanwongse K, Shabarek N. Rhabdomyolysis as a presentation of 2019 novel coronavirus disease. Cureus 2020;12:e7561.  Back to cited text no. 102
Chan KH, Farouji I, Abu Hanoud A, Slim J. Weakness and elevated creatinine kinase as the initial presentation of coronavirus disease 2019 (COVID-19). Am J Emerg Med 2020:S0735-6757(20)30353-3. doi: 10.1016/j.ajem. 2020.05.015.  Back to cited text no. 103
Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 2004;203:631-7.  Back to cited text no. 104
Beydon M, Chevalier K, Al Tabaa O, Hamroun S, Delettre AS, Thomas M, et al. Myositis as a manifestation of SARS-CoV-2. Ann Rheum Dis 2020. doi: 10.1136/annrheumdis-2020-217573.  Back to cited text no. 105
Ruamviboonsuk P, Lai TYY, Chang A, Lai CC, Mieler WF, Lam DSC, et al. Chloroquine and hydroxychloroquine retinal toxicity consideration in the treatment of COVID-19. Asia Pac J Ophthalmol (Phila) 2020;9:85-7.  Back to cited text no. 106
Mack HG, Kowalski T, Lucattini A, Symons RA, Wicks I, Hall AJ. Genetic susceptibility to hydroxychloroquine retinal toxicity. Ophthalmic Genet 2020;41:159-70.  Back to cited text no. 107
Siddiqui AK, Huberfeld SI, Weidenheim KM, Einberg KR, Efferen LS. Hydroxychloroquine-induced toxic myopathy causing respiratory failure. Chest 2007;131:588-90.  Back to cited text no. 108
Stein M, Bell MJ, Ang LC. Hydroxychloroquine neuromyotoxicity. J Rheumatol 2000;27:2927-31.  Back to cited text no. 109
Estes ML, Ewing-Wilson D, Chou SM, Mitsumoto H, Hanson M, Shirey E, et al. Chloroquine neuromyotoxicity. Clinical and pathologic perspective. Am J Med 1987;82:447-55.  Back to cited text no. 110
Shukla S, Gultekin SH, Saporta M. Pearls & Oy-sters: Hydroxychloroquine-induced toxic myopathy mimics Pompe disease: Critical role of genetic test. Neurology 2019;92:e742-5.  Back to cited text no. 111
Crawley J, Kokwaro G, Ouma D, Watkins W, Marsh K. Chloroquine is not a risk factor for seizures in childhood cerebral malaria. Trop Med Int Health 2000;5:860-4.  Back to cited text no. 112
Schiemann R, Coulaud JP, Bouchaud O. Seizures after antimalarial medication in previously healthy persons. J Travel Med 2000;7:155-6.  Back to cited text no. 113


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6 Use of poststroke medications and COVID-19-associated mortality
MoonHo Park, Dae-Sung Kyoung
Neurology India. 2022; 70(2): 812
[Pubmed] | [DOI]
7 Medicolegal Priorities for a Neurosurgeon/Neurologist in the COVID Era
GeorgeC Vilanilam, Jaypalsinh Gohil
Neurology India. 2022; 70(3): 845
[Pubmed] | [DOI]
8 Severe Acute Respiratory Syndrome Coronavirus Two (SARS-CoV-2) Associated Guillain-Barre Syndrome
KiranKumar Ramineni, GKrishna Mohan Reddy, UgandharBhattu Chakrahari, SravanKumar Marupaka
Neurology India. 2022; 70(4): 1698
[Pubmed] | [DOI]
9 COVID-19 and Stroke Trends in A Tertiary Care Center from South India -Our Monsoon Experience
Dileep Ramachandran, GithinBenoy George, Praveen Panicker, R Aravind, MK Suresh, Thomas Iype
Neurology India. 2022; 70(5): 1942
[Pubmed] | [DOI]
10 Mental and Psychosocial Health: A Post-COVID Concern in India
Suman Ray
Neurology India. 2022; 70(5): 2116
[Pubmed] | [DOI]
11 Spectrum of Neurological Manifestations of COVID-19 Data from a Tertiary Care Hospital
AkshayLouis Dias, BS Raghavendra, Safwan Ahmed, R Arunachalam
Neurology India. 2022; 70(5): 1901
[Pubmed] | [DOI]
12 COVID-19: Update for Neurosurgeons and Neurologists
Ankit Balani, Chinky Chatur
Neurology India. 2022; 70(5): 2205
[Pubmed] | [DOI]
13 Guillain-Barré Syndrome Following Thrombolysis with Streptokinase for Myocardial Infarction
Ramanathan Venkateswaran, Mehalingam Vadivelan, Abdoul Hamide
Neurology India. 2022; 70(5): 2187
[Pubmed] | [DOI]
14 Cough features during a pandemic
E. N. Popova, L. A. Ponomareva, I. V. Gravel
Academy of medicine and sports. 2022; 2(4): 37
[Pubmed] | [DOI]
15 Guillain—Barre syndrome associated with COVID-19
A.A. Bogdanova, E.S. Kravtsunova, A.I. Raevskaia, An.S. Karpov, R.N. Gadaborshev, A.I. Dzutsev, I.A. Vyshlova, S.M. Karpov
Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova. 2022; 122(9): 132
[Pubmed] | [DOI]
16 Persons with Co-Existing Neurological Disorders: Risk Analysis, Considerations and Management in COVID-19 Pandemic
Sumit Sharma, Sonali Batra, Saurabh Gupta, Vivek K. Sharma, Md. Habibur Rahman, Mohammad Amjad Kamal
CNS & Neurological Disorders - Drug Targets. 2022; 21(3): 228
[Pubmed] | [DOI]
17 Evaluation of Stroke Frequency in COVID-19 Patients
Online Türk Saglik Bilimleri Dergisi. 2022;
[Pubmed] | [DOI]
18 The Wide Variety of Acute Disseminated Encephalomyelitis in Children: A Clinical Perspective
Hyunsuk Lim, Su-Kyeong Hwang, Yun-Jeong Lee, Soonhak Kwon
Annals of Child Neurology. 2022; 30(4): 155
[Pubmed] | [DOI]
19 A Review: The Manifestations, Mechanisms, and Treatments of Musculoskeletal Pain in Patients With COVID-19
Lijuan Wang, Na Yang, Jinfeng Yang, Shuwu Zhao, Chen Su
Frontiers in Pain Research. 2022; 3
[Pubmed] | [DOI]
20 Peripheral Neuropathies Derived from COVID-19: New Perspectives for Treatment
Alfredo Córdova-Martínez, Alberto Caballero-García, Daniel Pérez-Valdecantos, Enrique Roche, David César Noriega-González
Biomedicines. 2022; 10(5): 1051
[Pubmed] | [DOI]
21 Neurological Manifestations in Pediatric Patients Hospitalized for COVID-19: Experiences of the National Medical Center “20 de Noviembre” in Mexico City
Brian Javier López-Pérez, Diana Alejandra Cruz-Chávez, Elsa Solórzano-Gómez, José Antonio Venta-Sobero, Iván Alejandro Tapia-García, Christian Gabriel Toledo-Lozano, Andrea Torres-Vallejo, Gabriela Vianney Castro-Loza, Yazmín Evelyn Flores-Jurado, Cristal Lucero Hernández-Soriano, Sofía Lizeth Alcaraz-Estrada, Paul Mondragón-Terán, Juan Antonio Suárez-Cuenca, Silvia Garcia
Children. 2022; 9(5): 746
[Pubmed] | [DOI]
22 Epilepsy and COVID-19: Recent Findings and Considerations
Hyun Kyung Kim
Epilia: Epilepsy and Community. 2022;
[Pubmed] | [DOI]
23 A prediction model for major adverse cardiovascular events (MACE) in patients with coronavirus disease 2019 (COVID-19)
Dong Huang, Huan Yang, He Yu, Ting Wang, Zhu Chen, Rong Yao, Zongan Liang
BMC Pulmonary Medicine. 2022; 22(1)
[Pubmed] | [DOI]
24 Assessment of Guillain-Barre Syndrome Cases in Brazil in the COVID-19 Era
Lorena D. Aquino Ferraz, Nelson P. Marques, Denise M.M. Silveira, Marcelo J.S. de Magalhães, Eduardo A. Oliveira, Hercílio Martelli Júnior
The Neurologist. 2022; Publish Ah
[Pubmed] | [DOI]
25 Acute-onset chronic inflammatory demyelinating polyneuropathy complicating SARS-CoV-2 infection and Ad26.COV2.S vaccination: report of two cases
Aggeliki Fotiadou, Dimitrios Tsiptsios, Stella Karatzetzou, Sofia Kitmeridou, Ioannis Iliopoulos
The Egyptian Journal of Neurology, Psychiatry and Neurosurgery. 2022; 58(1)
[Pubmed] | [DOI]
26 An overview of the neurological aspects in COVID-19 infection
Divyanshi Singh, Ekta Singh
Journal of Chemical Neuroanatomy. 2022; : 102101
[Pubmed] | [DOI]
Vrish Dhwaj Ashwlayan, Chanchal Antlash, Mohd. Imran, Syed Mohammed Basheeruddin Asdaq, Mohammed Kanan Alshammari, Marwa Alomani, Eman alzahrani, Divya Sharma, Ritu Tomar, Abida
Saudi Journal of Biological Sciences. 2022;
[Pubmed] | [DOI]
28 Long COVID, neuropsychiatric disorders, psychotropics, present and future
Siu Wa Tang, Brian E. Leonard, Daiga Maret Helmeste
Acta Neuropsychiatrica. 2022; : 1
[Pubmed] | [DOI]
29 Neurological and Neuroradiological Patterns with COVID-19 Infection in Children: A Single Institutional Study
Sanchi Rastogi, Foram Gala, Shilpa Kulkarni, Vrushabh Gavali
Indian Journal of Radiology and Imaging. 2022;
[Pubmed] | [DOI]
30 Delirium in COVID-19 and post-liver transplant patients: an observational study
Gianluca Fiore, Silvia Ferrari, Anna Cutino, Claudia Giorgino, Laura Valeo, Gian M. Galeazzi, Mattia Marchi
International Journal of Psychiatry in Clinical Practice. 2022; : 1
[Pubmed] | [DOI]
31 Gait analysis in people with COVID-19 history: A cross sectional study to identify the intensive care impact on musculoskeletal system
Z. Sawacha, A. Ruggiero, M. Asmaa, C. Spagnuolo, P. Serafini, M. Romanato, G. Squartini
Gait & Posture. 2022; 97: S339
[Pubmed] | [DOI]
32 The relationship between the serotonergic system and COVID-19 disease: A review
Tahereh Eteraf-Oskouei, Moslem Najafi
Heliyon. 2022; 8(5): e09544
[Pubmed] | [DOI]
33 Serum Brain-Derived Neurotrophic Factor (BDNF) in COVID-19 Patients and its Association with the COVID-19 Manifestations
Ali Asgarzadeh, Nasrin Fouladi, Vahid Asghariazar, Shahnaz Fooladi Sarabi, Hamid Afzoun Khiavi, Mahsa Mahmoudi, Elham Safarzadeh
Journal of Molecular Neuroscience. 2022;
[Pubmed] | [DOI]
34 COVID-19 Encephalopathy: Delayed Onset in Unvaccinated Patients
Dana Heller, Ramesh Pandit, Trupti Pandit, Gregory P Morris
Cureus. 2022;
[Pubmed] | [DOI]
35 Divulging the Intricacies of Crosstalk Between NF-Kb and Nrf2-Keap1 Pathway in Neurological Complications of COVID-19
Ranjana Bhandari, Garima Khanna, Dhriti Kaushik, Anurag Kuhad
Molecular Neurobiology. 2021; 58(7): 3347
[Pubmed] | [DOI]
36 A Review on SARS-CoV-2-Induced Neuroinflammation, Neurodevelopmental Complications, and Recent Updates on the Vaccine Development
Medha Karnik, Narasimha M. Beeraka, Chinnappa A. Uthaiah, Suma M. Nataraj, Anjali Devi S. Bettadapura, Gjumrakch Aliev, SubbaRao V. Madhunapantula
Molecular Neurobiology. 2021; 58(9): 4535
[Pubmed] | [DOI]
37 Emerging COVID-19 Neurological Manifestations: Present Outlook and Potential Neurological Challenges in COVID-19 Pandemic
Saikat Dewanjee, Jayalakshmi Vallamkondu, Rajkumar Singh Kalra, Nagaprasad Puvvada, Ramesh Kandimalla, P. Hemachandra Reddy
Molecular Neurobiology. 2021; 58(9): 4694
[Pubmed] | [DOI]
38 SARS-CoV-2 new variants: Characteristic features and impact on the efficacy of different vaccines
Abbas Khan, Taimoor Khan, Shughla Ali, Summiya Aftab, Yanjing Wang, Wang Qiankun, Mazhar Khan, Muhammad Suleman, Shahid Ali, Wang Heng, Syed Shujait Ali, Dong-Qing Wei, Anwar Mohammad
Biomedicine & Pharmacotherapy. 2021; 143: 112176
[Pubmed] | [DOI]
39 Coronavirus Disease 2019
Sophie Lin, Rachael Kantor, Elizabeth Clark
Clinics in Geriatric Medicine. 2021; 37(4): 509
[Pubmed] | [DOI]
40 Central nervous system manifestations in COVID-19 patients: A systematic review and meta-analysis
Shahrzad Nazari, Amirhossein Azari Jafari, Seyyedmohammadsadeq Mirmoeeni, Saeid Sadeghian, Mohammad Eghbal Heidari, Siavash Sadeghian, Farhad Assarzadegan, Seyed Mahmoud Puormand, Hamid Ebadi, Davood Fathi, Sahar Dalvand
Brain and Behavior. 2021; 11(5)
[Pubmed] | [DOI]
41 Prevalence and characteristics of new-onset pain in COVID-19 survivours, a controlled study
Felipe Henriques Carvalho Soares, Gabriel Taricani Kubota, Ana Mércia Fernandes, Bruno Hojo, Catarina Couras, Bárbara Venturoti Costa, Jorge Dornellys da Silva Lapa, Luíza Mansur Braga, Matheus Merula de Almeida, Pedro Henrique Martins da Cunha, Vítor Hugo Honorato Pereira, Adriano Donizeth Silva de Morais, Manoel Jacobsen Teixeira, Daniel Ciampi de Andrade
European Journal of Pain. 2021; 25(6): 1342
[Pubmed] | [DOI]
42 Update on neurological symptoms in patients infected with severe acute respiratory syndrome coronavirus-2
Mei-Fang Xiao, Zhi-Jian You, Chang Zeng, Ze-Bing Huang, Liang Dong
Ibrain. 2021;
[Pubmed] | [DOI]
43 Neuroinvasion of SARS-CoV-2 may play a role in the breakdown of the respiratory center of the brain
Jhilik Dey, Md T. Alam, Sreyashi Chandra, Jalaj Gupta, Upasana Ray, Amit K. Srivastava, Prem P. Tripathi
Journal of Medical Virology. 2021; 93(3): 1296
[Pubmed] | [DOI]
44 Aneurismal subarachnoid hemorrhage during the COVID-19 outbreak in a Hub and Spoke system: observational multicenter cohort study in Lombardy, Italy
Alessandro Fiorindi, Marika Vezzoli, Francesco Doglietto, Luca Zanin, Giorgio Saraceno, Edoardo Agosti, Antonio Barbieri, Silvio Bellocchi, Claudio Bernucci, Daniele Bongetta, Andrea Cardia, Emanuele Costi, Marcello Egidi, Antonio Fioravanti, Roberto Gasparotti, Carlo Giussani, Gianluca Grimod, Nicola Latronico, Davide Locatelli, Dikran Mardighian, Giovanni Nodari, Jacopo Carlo Poli, Frank Rasulo, Elena Roca, Giovanni Marco Sicuri, Giannantonio Spena, Roberto Stefini, Oscar Vivaldi, Cesare Zoia, Stefano Calza, Marco Maria Fontanella, Marco Cenzato
Acta Neurochirurgica. 2021;
[Pubmed] | [DOI]
45 Development and External Validation of a Delirium Prediction Model for Hospitalized Patients With Coronavirus Disease 2019
Victor M. Castro, Chana A. Sacks, Roy H. Perlis, Thomas H. McCoy
Journal of the Academy of Consultation-Liaison Psychiatry. 2021; 62(3): 298
[Pubmed] | [DOI]
46 COVID-19: a new emerging respiratory disease from the neurological perspective
Amr El-Sayed, Lotfi Aleya, Mohamed Kamel
Environmental Science and Pollution Research. 2021; 28(30): 40445
[Pubmed] | [DOI]
47 Encephalitis as a neurological manifestation of COVID-19
Herminia Lozano Gómez, Ana Pascual Bielsa, Paula Abansés Moreno, María Pilar Luque Gómez, Almudena Matute Guerrero, Juan José Araiz Burdio
Medicina Clínica (English Edition). 2021; 157(3): 141
[Pubmed] | [DOI]
48 Encefalitis como manifestación neurológica del COVID-19
Herminia Lozano Gómez, Ana Pascual Bielsa, Paula Abansés Moreno, María Pilar Luque Gómez, Almudena Matute Guerrero, Juan José Araiz Burdio
Medicina Clínica. 2021; 157(3): 141
[Pubmed] | [DOI]
49 Síndrome de Guillain-Barré de presentación inusual y ataxia cerebelosa asociado a COVID-19 en paciente pediátrico
Adolfo Álvarez, Mónica Alonso, Delusca Ospino, Verónica Escamilla
Neurología Argentina. 2021;
[Pubmed] | [DOI]
50 Delirium in hospitalized COVID-19 patients: A case series
Alonso-Sánchez M, Delgado-Parada E, Ayuso-Mateos JL
Psychiatry Research. 2021; 305: 114245
[Pubmed] | [DOI]
51 Critical neurological features of COVID-19: Role of imaging methods and biosensors for effective diagnosis
Vishakha Singh, Prince Allawadhi, Amit Khurana, Anil Kumar Banothu, Kala Kumar Bharani
Sensors International. 2021; 2: 100098
[Pubmed] | [DOI]
52 Acute Necrotizing Rhombencephalitis and Disemminated Thrombosis After SARS-CoV-2 Infection
Priyanka Samal, Heramba N. Praharaj, Biswajit Mishra, Sharmistha Sarangi
Infectious Diseases in Clinical Practice. 2021; 29(4): e260
[Pubmed] | [DOI]
53 Spike protein multiorgan tropism suppressed by antibodies targeting SARS-CoV-2
Molly Brady, Conor McQuaid, Alexander Solorzano, Angelique Johnson, Abigail Combs, Chethana Venkatraman, Akib Rahman, Hannah Leyva, Wing-Chi Edmund Kwok, Ronald W. Wood, Rashid Deane
Communications Biology. 2021; 4(1)
[Pubmed] | [DOI]
54 Central nervous system outcomes of COVID-19
Margaret F. Doyle
Translational Research. 2021;
[Pubmed] | [DOI]
55 Inflammatory neuropsychiatric disorders and COVID-19 neuroinflammation
Siu Wa Tang, Daiga Helmeste, Brian Leonard
Acta Neuropsychiatrica. 2021; 33(4): 165
[Pubmed] | [DOI]
56 Case Report and Literature Review: COVID-19 and status epilepticus in Dyke-Davidoff-Masson syndrome
Lourdes de Fátima Ibañez Valdés, Jerry Geroge, Sibi Joseph, Mohamed Alshmandi, Wendy Makaleni, Humberto Foyaca Sibat
F1000Research. 2021; 10: 9
[Pubmed] | [DOI]
57 COVID-19 and Its Symptoms’ Panoply: A Case-Control Study of 919 Suspected Cases in Locked-Down Ovar, Portugal
Regina Sá, Tiago Pinho-Bandeira, Guilherme Queiroz, Joana Matos, João Duarte Ferreira, Pedro Pereira Rodrigues
Portuguese Journal of Public Health. 2021; : 1
[Pubmed] | [DOI]
58 SARS-CoV-2: is there neuroinvasion?
Conor McQuaid, Molly Brady, Rashid Deane
Fluids and Barriers of the CNS. 2021; 18(1)
[Pubmed] | [DOI]
59 Guillain–Barré syndrome with bilateral facial diplegia secondary to severe acute respiratory syndrome coronavirus-2 infection: a case report
Natalia Ramirez, David Ujueta, Luis Felipe Diaz, Lucila Emilse Folleco, Andrea Rodríguez, Ivan Gaona, Mauricio O. Nava-Mesa
Journal of Medical Case Reports. 2021; 15(1)
[Pubmed] | [DOI]
M. Thangaraj, R. Amirtha Lakshmi, P. Lenin Shankar
[Pubmed] | [DOI]
61 Interplay between nuclear factor erythroid 2-related factor 2 and inflammatory mediators in COVID-19-related liver injury
Dan-Dan Zhu, Xue-Mei Tan, Li-Qing Lu, Si-Jia Yu, Ru-Li Jian, Xin-Fang Liang, Yi-Xuan Liao, Wei Fan, Lucíia Barbier-Torres, Austin Yang, He-Ping Yang, Ting Liu
World Journal of Gastroenterology. 2021; 27(22): 2944
[Pubmed] | [DOI]
62 Lived Experiences of Hospitalized COVID-19 Patients: A Qualitative Study
Montserrat Venturas, Judith Prats, Elena Querol, Adelaida Zabalegui, Núria Fabrellas, Paula Rivera, Claudia Casafont, Cecilia Cuzco, Cindy E. Frías, Maria Carmen Olivé, Silvia Pérez-Ortega
International Journal of Environmental Research and Public Health. 2021; 18(20): 10958
[Pubmed] | [DOI]
63 Neurological and neuropsychiatric disorders associated with COVID-19. Part I: overview and neurological disorders
Martina Giacalone, Marcos Roberto Tovani-Palone, Luca Marin, Massimiliano Febbi, Tommaso Russano, Andrea Giacalone
Einstein (São Paulo). 2021; 19
[Pubmed] | [DOI]
64 Neuroinflammation and Its Impact on the Pathogenesis of COVID-19
Mohammed M. Almutairi, Farzane Sivandzade, Thamer H. Albekairi, Faleh Alqahtani, Luca Cucullo
Frontiers in Medicine. 2021; 8
[Pubmed] | [DOI]
65 Treatment of neurological complications in patients with type 2 diabetes mellitus at the stage ofrehabilitation after COVID-19
V.I. Pankiv
[Pubmed] | [DOI]
66 Immunological aspects of SARS-CoV-2 coronavirus damage
Timur I. Minnullin, Alexander V. Stepanov, Sergey V. Chepur, Evgeny V. Ivchenko, Ivan V. Fateev, Evgeniy V. Kryukov, Vasily N. Tsygan
Bulletin of the Russian Military Medical Academy. 2021; 23(2): 187
[Pubmed] | [DOI]
67 COVID-19-associated acute disseminated encephalomyelitis: A systematic review
KiranSunil Mahapure, AnaghaSudhakar Prabhune, AradhanaVijaysinh Chouvhan
Asian Journal of Neurosurgery. 2021; 16(3): 457
[Pubmed] | [DOI]
68 Síndrome de Guillain-Barré de presentación inusual y ataxia cerebelosa en paciente pediátrico asociado a COVID-19
Adolfo Alvarez, Mónica Alonso, Delusca Ospino, Verónica Escamilla
Neurología, Neurocirugía y Psiquiatría. 2021; 49(2): 66
[Pubmed] | [DOI]
69 Occupational Therapy Management of a Moderate COVID-19 Disease Process in a Skilled Nursing Facility: A Case Report
Jaime L. Smiley, Stacey Reynolds
The American Journal of Occupational Therapy. 2021; 75(Supplement)
[Pubmed] | [DOI]
70 In-silico Immunomodelling of SARS-CoV-2
Amirhosein Maali, Hossein Teimouri, Mehdi Azad, Shahin Amiri, Setare Adibzadeh
Journal of Medical Microbiology and Infectious Diseases. 2021; 9(2): 88
[Pubmed] | [DOI]
71 Demyelinating Disease of the Central Nervous System Concurrent With COVID-19
Sibel Karsidag, Sevki Sahin, Miruna F Ates, Nilgun Cinar, Sude Kendirli
Cureus. 2021;
[Pubmed] | [DOI]
72 Multiple Sclerosis Following SARS-CoV-2 Infection: A Case Report and Literature Review
Sobia Sarwar, Sylvette Rogers, Alaa S Mohamed, Enitare Ogula, Rihanat A Ayantayo, Ahmed Ahmed, Iram Shahzadi, Saurabh Kataria, Romil Singh
Cureus. 2021;
[Pubmed] | [DOI]
73 Clinical and Laboratory Factors in Predicting Mortality Among COVID-19 RT-PCR Positive Patients: A Retrospective Observational Study From a Tertiary Care Center
Raja Sundaramurthy, Suryakumar Balasubramanian, Vithiya Ganesan, Pearl Aggarwal, Tarun Parvataneni, Devi Parvathy Jyothi Ramachandran Nair, Raja Prahadeesh Saravanan
Cureus. 2021;
[Pubmed] | [DOI]
74 COVID-19: What lies ahead for Homoeopathy?
Anil Khurana
Indian Journal of Research in Homoeopathy. 2020; 14(3): 169
[Pubmed] | [DOI]
75 Aneurysm surgery during the COVID-19 pandemic: Ecstasy, agony and dilemma
Daljit Singh
Journal of Cerebrovascular Sciences. 2020; 8(2): 73
[Pubmed] | [DOI]
76 The Need to Change and the Necessity to Evolve During the COVID-19 Pandemic
Randeep Guleria
Neurology India. 2020; 68(4): 726
[Pubmed] | [DOI]
77 Involvement of the nervous system in COVID-19: The bell should toll in the brain
Sairaj Satarker, Madhavan Nampoothiri
Life Sciences. 2020; 262: 118568
[Pubmed] | [DOI]


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