Discussion
Although coronavirus disease 2019 [COVID-19] primarily manifests as a lung infection, with symptoms ranging from those of a mild upper respiratory infection to severe pneumonia and acute respiratory distress syndrome (ARDS), other multisystemic manifestations of this disease and related complications are becoming more commonly recognized (4).
With respect to the neurological manifestations of COVID-19,such as ischaemic stroke, myelitis, seizure, encephalitis and virus isolation from cerebrospinal fluid, it is understood that SARS-CoV-2 has a neurotropic and neuroinvasive nature [5].The initial report from Rothsteinet al.demonstrated the occurrence of ischaemic stroke, subarachnoid haemorrhage and intracerebral haemorrhage associated with SARS-CoV-2 in individuals with COVID-19, which was described as relatively uncommon [5]. Gogiaet al.r eported the first case of COVID-19-associated hyperacute SDH along with extensive intra-cerebral haemorrhage and sub-arachnoid haemorrhage in a 75-year-old patient. This individual was on double antiplatelet (aspirinand clopidogrel) treatment [6]; however, our case had no history of antiplatelet or anticoagulant therapy. Different types of intracranial haemorrhage and their risk factors in patients with COVID-19 were described by Altschulet al.in November2020 [7]. In their study, among 5227 individuals with COVID-19, 35 were found to have haemorrhage of some kind and 17of the 35 had acute SDH. Based on the characteristics of thesepatients, 70.6% (n= 12) had a head trauma before the haemorrhage and five were on anticoagulant drugs [7]. However,such predisposing factors were not observed in our case. Intracranial haemorrhage in individuals with COVID-19 were systematically assessed in a review by Cheruiyotet al.According to that study, out of 148 individuals with a diagnosis of intracranial haemorrhage, extracted from 23 studies, only 19 had a diagnosis of SDH and none of them were diagnosed withthe subacute type of SDH [8].Some mechanisms can be considered in the tendency of these patients to develop SDH. The point of entry for SARS-CoV-2 into human tissue is mediated primarily by a specific cellular receptor, angiotensin-converting enzyme 2 (ACE-2),which is expressed in various organs including brain parenchyma. In addition, ACE-2 receptors play an important role invascular autoregulation and cerebral blood flow. Sharifi-Razaviet al. Hypothesized that ACE-2 receptor dysfunction caused by direct invasion by SARS-CoV-2 may result in disruption of autoregulation and make the patient prone to vascular wall rupture in the presence of hypertension spikes [9]. In fact,systemic viraemia and subsequent endothelial dysfunction may make the bridging veins of the subdural space more vulnerable to bleeding following a minor trauma even to the point of sneezing, coughing or a Valsalva manoeuvre. Vascular damage can also happen during viral infections that result in vasculitis, such as varicella zoster virus or human immunodeficiency virus.(10)