Neurological Complication in Covid-19

1. Karaganda medical university
 Department of
neurology and mental
health
Topic :- Covid-19 neurological complication
Name :- kasana mayank

2. Introduction
Pathogenesis and route of transmission
Clinical feature
How virus reach in our brain
Neurological complication
Brief content

3. Introduction
 Coronavirus disease 2019 (COVID-19), the highly
contagious viral illness caused by severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2)
 SARS-CoV-2 is a single-stranded RNA virus which
belongs to genus Coronavirus and
family Coronaviridae.

4. Structure of SARS-CoV-2. SARS-
CoV-2 has surface viral proteins,
namely, spike glycoprotein (S), The
viral membrane glycoprotein (M)
and envelope (E) of SARS-CoV-2
are embedded in host membrane-
derived lipid bilayer encapsulating
the helical ,the nucleocapsid
comprising viral RNA

5. Pathogenesis and route of transmission
 The virus is transmitted via respiratory droplets and aerosols
from person to person.
 Once inside the body, the virus binds to host receptors and
enters host cells through endocytosis or membrane fusion.
 The coronaviruses are made up of four structural proteins,
namely, the spike (S), membrane (M), envelop (E) and
nucleocapsid (N) proteins.The S protein is seen to be
protruding from the viral surface and is the most important
one for host attachment and penetration. This protein is
composed of two functional subunits (S1 and S2), among
which S1 is responsible for binding to the host cell receptor
and S2 subunit plays a role in the fusion of viral and host
cellular membranes

6. Covid 19.
Ace-2

7. ACE-2 has been
identified as a
functional
receptor for
SARS-CoV and
is highly
expressed on the
pulmonary
epithelial cells.

9. Clinical feature
 Most common symptoms:
• fever
• dry cough
• Tiredness
 Less common symptoms:
• aches and pains
• sore throat
• diarrhoea
• conjunctivitis
• headache
• loss of taste or smell
• a rash on skin, or discolouration of fingers or toes
 Serious symptoms:
• difficulty breathing or shortness of breath
• chest pain or pressure
• loss of speech or movement

10. Clinical
feature

11. How virus reach in our brain
 As we know from our previous section that ACE2 receptor are
main role in viral penetration so ACE 2 receptors are also found in
glial cells in brain and spinal neurons. Hence it can attach,
multiply and damage the neuronal tissue.
 Virus also retrograde transfer via the olfactory epithelium or
through the cribriform bone and reaches the brain secondly,
during the viremia phase of illness, disruption of blood brain
barrier causes the virus to enter the brain directly.

13. Neurological
complication
 Anosmia and Ageusia
 Meningitis
 Encephalitis
 Acute cerebrovascular disease
 Guillain Barre syndrome
(GBS)
 Epilepsy
 If the chance severe neurological manifestation occurs in covid 19 is related to
immnocompromise , severe HTN and uncontrolled diabetes ,some one had organ trnsplant
etc..

14. Anosmia and Ageusia
 These are initially occurring mild symptoms which is totally
reversible if person survive. A complete or partial loss of
smell sensation (anosmia) and taste sensation (ageusia)
 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,and replicate there
and damage the pathway of smell.

15. Meningitis

Meningitis is the inflammation of the coverings (duramater, Arachnoid
mater pia mater) of the brain and spinal cord
 As others viral meningitis SARSCOV2 also enter brain trough retrograde
nervous pathway which is olfactory bulb and hematogenous route.
 Symptoms
1. Headaches
2. Vomitting
3. Nuchal rigidity
4. Fever
5. Meningeal symptoms positive

16. Diagnosis
 CSF finding
o Increased opening pressure
o Increased pleocytosis lymphocytes
o Normal glucose
o Clear CSF
o RT-PCR positive SARSCOV2 if high viral load in csf
We can do CT or MRI of haed

18.  Encephalitis
Covid 19 Encephalitis is the inflammation of brain tissue by
 virus itself
 post infection autoimmunity which is induced in cytokine strom
 Symptoms of patient is according to area damage by virus we
can clearly see
 focal neurological features
 fever
 headaches
 nuchal rigidity,
 meningeal symptoms some time.
 Till now there was no specific area that mainly dominant for covid 19 virus
encephalitis

19. Diagnosis by Lumbar puncture
CSF finding
I. Increase protein level
II. Normal glucose level
III. Increase cell count which is lymphocytes
IV. Increase CSF opening pressure
And we can do CSF RT-PCR FOR SARSCOv2
 CT scan and MRI of brain

20. Like here we can se
area involved is
parietooccipital
and manifestation
in patient is
wernickes
aphasia,short term
memory loss,

21. Differentiate
diagnosis
 Different type of viral encephalitis:– but we
have specific history of particular virus
infection and have Positive PCR test for
them
 Meningitis:– we don’t have focal
neurological symptoms there.
 Brain absess :- there periodically fever
persistent

22. In COVID-19, coagulopathy enhance the risk of cerebral
arterial and venous thrombosis. SARS-CoV-2 causes a
global inflammatory response and a hypercoagulable
state increased D-dimers, prolonged prothrombin time,
and disseminated intravascular coagulation When
microthrombi form in vessel they travel to the brain and
occlusion of major artery of brain and cause stroke of
specific area
Acute ischemic stroke is main occurs in covid 19 patients
then acute hemorrhagic stroke
Acute cerebrovascular disease

23. Symptoms
 All these symptoms must with covid 19 positive
test or history of contact.
 Confusion ,trouble with speaking and
understanding
 Numbness of face arm or leg particularly one
side of body
 Trouble in seeing
 Lack of coordination

25.  CT scan :- we can differentiate acute ischemic stroke from
hemorrhagic stroke
 MRI
 D-dimer test in blood
 Treatment according patient condition we will do endovascular
management thrombectomy but never do thrombolysis.
 Because of this we use UFH or LMWH like enoxaparin To
prevent risk of formation of thrombosis before stroke
Diagnosis and treatment

26. By this finding we
estimate that
artery involve
here is MCA ,area
involvement is
temporoparietal.

27.  GBS is a symmetric, ascending flaccid paralysis, often
preceded by respiratory or gastrointestinal infections from
a virus or bacteria in covid 19 after infection the
autoimmune reaction of body causes damage of neurons
and causes clinical feature like
Ascending symmetrical muscle weakness
Starting with leg paralysis
Face and oropharygeal weakness
Oculomotor weakness
Guillain Barre syndrome (GBS)

29. Diagnosis
NERVE CONDUCTION VELOCITY:– LATENCY INCREASED
MRI OF SPINE:- DEMYELINATION
AUTOANTIBODIES LIKE GM1 ANTIBODY
CSF finding
Opening pressure normal
Cell normal
Sugar normal
Color normal
Protein increased due to albumin
cytological dissociation
Doc is iv immunoglobulin
We can also do plasmapheresis for
removal of autoantibodies

30. Epilepsy
 A seizure represents the uncontrolled, abnormal electrical activity of the brain that may
cause changes in the level of consciousness, behavior, memory, or feelings. Convulsive
concussion, convulsive syncope, movement disorders, rigors, sleep-related events.In covid
19 that etiology is following….
 Encephalitis
 Hypoxic brain injury due to lungs involvement
 Ischemic or hemorrhagic stroke
 Fever
 Metabolic electrolytes disbalance

31. Epilepsy
 Epilepsy occurs because of a predisposition to a chronic pathologic process, unprovoked
seizures occur in the absence of provocative causes or more than seven days after an acute
injury or insult such as stroke or brain hemorrhage. Recurrent unprovoked seizures define
epilepsy.

32. Management
 We can give anti epilepsy drug but we must know that patient already
taken many type of drug and also respiratory and cardio unstable because
this ,
 drugs with significant respiratory/cardiac adverse effects (e.g., Phenytoin,
Phenobarbital, etc.) should be prescribed cautiously, with clinical
monitoring.
 In addition, drugs with significant drug interactions (e.g., Carbamazepine,
Phenytoin, Phenobarbital, and Valproic acid) should be prescribed
cautiously

33. Conclusion
 Tll now we don’t have any specific treatment
against covid 19 so our primary aim is prevention
of neurological complication like prevent
microthrobi formation decreased viral load ect.but
it neurological manifestation already occurs we will
do treatment according specific disease and
pathogenesis like in GBS damage of neuron by
autoimmune reactions so we give iv immunoglobin
, in stroke we can dothrombectomy.

34. Reference
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7273036/
https://www.uptodate.com/contents/covid-19-
neurologic-complications-and-management-of-
neurologic-conditions#H4153922458