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Advanced Neurology COVID-19 and neurodegenerative diseases

BBB. Neuroimaging revealed multifocal cortical indicates an underlying neurodegenerative process. It
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infarcts in some patients, representing the evidence for is, however, imperative to consider that neuropsychiatric
arterial microvascular thrombosis along with hyperdense symptoms, such as post-traumatic stress disorder and
veins, which feature sluggish venous outflow. Detection depression, might also be a result of the taxing treatment
of multifocal petechial bleeding and eventual massive that the patient had to go through in an intensive care unit;
hemorrhage has led to the belief that microangiopathy and these symptoms represent the after-effects of being isolated
microthrombosis might play a role in the pathogenesis for a long time or dealing with the stigma that comes with
of cerebrovascular symptoms of COVID-19. Roldán- contracting contagious diseases such as COVID-19. 5
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Santiago et al. showed that the brain does possess some
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lymphatic vessels which could constitute a proper route 5. PD
for the dissemination of the virus. Endotheliitis could PD is a neurodegenerative disorder caused by the loss of
also facilitate the dissemination of the virus through the dopaminergic neurons in the striatal system (especially
lymphatics, resulting in meningitis/encephalitis. The virus the substantia nigra). The classic motor symptoms seen
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could also reach the brain tissue through circumventricular in PD include bradykinesia, tremors, rigidity, and a lack
organs which have unavailable junctional proteins, usually of postural reflexes. Neuropsychiatric conditions such as
expressed in the BBB. On the other hand, SARS-CoV-2 was depression and anxiety may be seen in people with PD as
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not detected in the CSF of most of the patients afflicted with well as COVID-19. 23
COVID-19, and this can be explained by two possibilities:
(i) The virus may be cell-bound and spread from cell to cell, 5.1. Prevalence and etiology
or (ii) the viral load might not be sufficient to be detected by The incidence of PD increases with increasing age, although
conventional testing algorithms. The cerebrum has almost the age of peak incidence varies with sex. According to
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four times as many neuroglial cells as the cerebellum, Hirsch et al. for ages 40 and above, the overall incidence
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and the predominant presence of the SARS-CoV-1 in rate of PD in females was 37.55/100,000 person years
the cerebrum indicates that on infection the neuroglia while the same for men was 61.21. In females, it seems to
becomes activated and causes neuroinflammation. increase steadily with time, peaking around the ages of
Therefore, within the infected brains, the viral load may 70 – 79, while, in males, the incidence continues to rise
trigger reactive astrogliosis and activation of microglia. even after the age of 80 years. The authors further found
Studies indicate that systemic inflammation regardless of that males have a higher incidence rate in other age groups
origin (bacterial, viral, or toxic) compromises the BBB and as well; however, the difference is not as significant. A study
actuates the Toll-like receptors present in microglia and conducted by Ascherio and Schwarzschild showed an
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astrocytes, promoting neuroinflammation, and disturbing incidence male-to-female ratio of 0.95 in Asia, perhaps due
the brain homeostasis. Even with moderate SARS-CoV-2 to differences in smoking habits, which has a purported
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infection, elevated levels of glial fibrillary acidic protein protective effect on reducing PD risk, between the two
and neurofilament light chain protein were detected which genders. PD is a global public health issue, but a higher
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are indicative of astrocytic reaction and axonal injury. number of cases are detected in certain geographical areas
Acute respiratory distress syndrome is considered the (Americas, Europe, and Asia) compared to others (Africa).
most serious clinical presentation of COVID-19 and the The relation of PD with race is inconsistent and varied,
resultant hypoxemia has been shown to cause damage to as the Hispanic population and black population seem to
neuronal cells. bear a higher risk of developing the disease, as reported in
certain studies, while the white population seems to have a
4. Neuropsychiatric effects of SARS-CoV-2 higher number of cases, as reported in other studies. 25
The acute effects of SARS-CoV-2 include headache, Classically, PD is associated with degeneration of the
dizziness, anosmia, ageusia, and encephalopathy. Rogers substantia nigra in the midbrain, which causes a deficiency
et al. summarized that during the acute phase of this of dopamine, causing the majority of the symptoms. The
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infectious disease, approximately 27 – 41% of cases presence of Lewy bodies (intracytoplasmic bodies made
experienced neuropsychiatric symptoms such as confusion, up of α-synuclein neurofilaments) is common, but not
altered mood, anxiety, diminished memory, and insomnia. pathognomonic. Pathophysiology of PD is associated with
The capability of neural and immune cells of hosting certain genes, environmental toxins (MPTP has been
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latent CoV can result in delayed neuronal and psychiatric implicated), and chronic inflammation (associated with
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manifestations. Patients suffering from autoimmune a “cytokine storm”), but the exact mechanism remains
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sclerotic lesions showed alterations in their non-motor unknown, although a possible viral etiology cannot be
symptoms after being infected with COVID-19, which ruled out. The theory concerning neurotropism of certain

Volume 3 Issue 1 (2024) 4 https://doi.org/10.36922/an.2200