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)