Annals of Indian Academy of Neurology
: 2020  |  Volume : 23  |  Issue : 3  |  Page : 361--362

Neurological manifestations of COVID-19 - continually evolving and perplexing

Pranav Ish1, Kirti Sachdev2, Sumita Agrawal3, Nitesh Gupta1,  
1 Department of Pulmonary, Critical Care and Sleep Medicine, VMMC and Safdarjung Hospital, New Delhi, India
2 Consultant Neurology, Medipulse Hospital, Jodhpur, Rajasthan, India
3 Department of Pulmonary Medicine, Medipulse Hospital, Jodhpur, Rajasthan, India

Correspondence Address:
Dr. Nitesh Gupta
Department of Pulmonary, Critical Care and Sleep Medicine, VMMC and Safdarjung Hospital, New Delhi - 110 029

How to cite this article:
Ish P, Sachdev K, Agrawal S, Gupta N. Neurological manifestations of COVID-19 - continually evolving and perplexing.Ann Indian Acad Neurol 2020;23:361-362

How to cite this URL:
Ish P, Sachdev K, Agrawal S, Gupta N. Neurological manifestations of COVID-19 - continually evolving and perplexing. Ann Indian Acad Neurol [serial online] 2020 [cited 2020 Aug 6 ];23:361-362
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The article '2019-NCoV: What Every Neurologist Should Know?' is a comprehensive summary of the various neurological manifestations of Novel coronavirus 2019 (NCoV-2019). It reviews in detail the published studies on the frequency of these manifestations.[1] However, the underlying pathophysiology though yet unproven remains an area of interest. Treatment of the neurological manifestations also demands attention as the article itself claims that such manifestations lead to increased morbidity and mortality.


There are various theories proposed: ACE2 is present in the human brain in glial cells and neurons and can serve as a potential target; Bloodborne dissemination along with sluggish movement within the microcirculation can facilitate penetration through the blood-brain barrier; migration of the virus anterograde or retrograde through olfactory nerve, thereby producing anosmia also; hypoxia leading to cerebral vasodilation, interstitial edema and raised intracranial pressure; and the massive inflammatory response leading to demyelinating disorders, seizures and stroke.[2]

The literature has documented ischemic and hemorrhagic stroke. The incidence is more eminent in patients with comorbidities (hypertension, diabetes, and dyslipidemia). There is a reduced expression of ACE2 in patients of hypertension. New infection by SARS-CoV-2, the binding of the virus to ACE2, further reduces the ability to lower blood pressure causing sustained hypertension and predisposing to intracranial bleed. Additionally, thrombocytopenia is a risk factor for hemorrhagic stroke. Ischemic stroke occurs secondary to elevated D-Dimer level causing microthrombi and septic shock causing watershed infarcts.[3]

Headache is a common symptom reported by patients. This can occur as a result of infectious or hypoxic encephalopathy. Skeletal muscle injury is reflected by muscle pain, muscle tenderness, and serum creatinine kinase level above 200 U/L. It is usually secondary to massive inflammatory reaction or direct muscle damage by the virus. GBS has also been diagnosed in a 61-year-old lady with travel history to Wuhan and COVID-19 positive, suggesting parainfectious etiology. Acute necrotizing encephalopathy has been attributed as a complication of COVID-19 primarily as a result of a massive inflammatory storm rather than direct invasion or demyelination. MRI of the reported case revealed hemorrhagic rim enhancing lesion in bilateral thalami, medial temporal and subinsular region.[4],[5],[6]

An attractive hypothesis is that hypoxic respiratory failure that occurs in some COVID-19 patients is due to the infiltration of the respiratory center in medulla due to the neuroinvasive nature of the virus. Based on an epidemiological study, the median time for the first symptom to dyspnoea was 5 days, to hospital admission was 7 days, and to intensive care was 8 days. This latency period was thought to be enough for the virus to enter and destroy medullary neurons.[7],[8]


Neurological manifestations are to be treated with the usual therapy for the same. The patient who developed GBS attributed to coronavirus infection was managed by intravenous immunoglobulin along with antivirals (arbidol, lopinavir, and ritonavir).[5]

Specific consideration to evaluate for features of raised intracranial pressure such as headache, vomiting, confusion and lateral rectus palsy. The treatment protocol comprises decongestants like mannitol, hypertonic saline and hyperventilation to maintain target PCO2 around 30mmHg. In ischemic stroke, with a high D-Dimer level, preventive anticoagulation is recommended. In the chinese database, a COVID-19 patient with limb ischemia and bilateral infarcts in the brain, had raised Antiphospholipid antibodies; thereby requiring anticoagulation.[9] In patients of intracranial hemorrhage, optimal blood pressure control is targeted using calcium channel blockers and diuretics.

Facing a global pandemic, it is only with further large-scale studies, that more insight into pathophysiology, manifestations, and options for COVID-19 can be deciphered; especially for the less frequent but more severe neurological manifestations.

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Conflicts of interest

There are no conflicts of interest.


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