Discussion
The primary effect of COVID-19 on the human body is on the respiratory
system but it can inflict certain neurological manifestations as well
[12]. Although the evidence on the neurological manifestations of
COVID-19 is still scarce as it is rare, a study has documented that 36
of the patients having ARDS caused by COVID-19 had some forms of
neurological manifestations [6]. COVID-19 can affect the nervous
system in different ways which are classified into three main
categories, CNSÂ symptoms or diseases (headache, dizziness, impaired
consciousness, ataxia, acute cerebrovascular disease, and epilepsy),
peripheral nervous system (PNS) symptoms (hypogeusia, hyposmia,
hypopsia, and neuralgia), and skeletal muscular symptoms [7].
Interestingly, the occurrence of neurological manifestations in COVID-19
affected patients depends upon the severity of the disease, greater the
severity greater will be the likelihood of having the neurological
manifestations [2].
The target receptor via which the COVID-19 virus attaches to the cells
is the ACE 2 receptor and after internalization of the virus into the
cells, the RNA of the virus is released which then leads to translation
and replication [8]. After entering the cells, the COVID-19 virus
can damage the cells via 2 main mechanisms, either via immune mediated
damage due to cytokine storm or via severe hypoxia as a result of
pneumonia and ARDS [9].
The diagnosis of COVID-19 encephalitis will require the isolation of
virus from the CSF sample and it is generally very difficult because of
the transient dissemination of virus in the CSF and very low titers
which don’t allow virus detection [6]. Similar pattern was also
observed in our case series with only 1 out of 5 patients had a positive
CSF COVID-19 Polymerase Chain Reaction (PCR) and the mainstay of
diagnosis was the exclusion of all other important causes of
encephalitis. MRI brain can also aid in the diagnosis of COVID-19
encephalitis and a wide range of MRI findings can be seen in COVID-19
related encephalopathy and they include leptomeningeal enhancement,
ischemic strokes, and cortical fluid-attenuated inversion recovery
(FLAIR) signals [10]. We also observed similar MRI findings in our
patients.
The main treatment of COVID-19 encephalitis is supportive. However a
variety of treatments like IV immunoglobulins, IV steroids, IV
Tocilizumab and IV rituximab have been tried with variable outcomes
[5]. In our case series the patients received IV Tocilizumab 400 mg
(4-8 mg/kg) and a short course of IV methylprednisolone (0.5-2 mg/kg)
resulted in drastic improvement in the outlook of the patient showing
its efficacy as a treatment option. Neurological dysfunction may be
persistent even after the acute illness has resolved and in a case
series almost one-third of the patients were cognitively impaired ay
discharge and at follow up [11]. In our case series the patients had
improved significantly at discharge and had no residual neurological
damage on follow up after one month.