Tang et al. Persistent inflammatory status in COVID patients acts as an important stimulus for a coagulation cascade. Certain cytokines, including IL-6, activates the coagulation cascade and suppresses the fibrinolytic system. Endothelial damage to the pulmonary and peripheral arteries due to a direct viral attack may be an equally important factor in increasing blood clotting.
Endothelial cell damage can activate the coagulation system. Moreover, the immune response can be increased by coagulation disorders. These two processes may act as a vicious cycle to worsen this situation. In addition, the appearance of antiphospholipid antibodies may impair blood coagulation as well [38] , [39] , [40] , [41]. Post-ischemic and stroke seizure is one of the causes of epilepsy [42].
When a stroke occurs, a seizure may be caused by a variety of factors, including hypoxia, metabolic disorders, and decreased or increased blood perfusion. Acute ischemia may also generate early seizures by increasing extracellular glutamate concentrations, impaired ion channel function, and BBB damage. The mechanisms involved in late seizures vary and include gliosis, chronic inflammation, angiogenesis, apoptosis and neuronal death, neurogenesis, synaptogenesis, and loss of synaptic plasticity [ 43 , 44 ].
In hemorrhagic stroke, hemosiderin deposits lead to neuronal hyper-excitability and seizures. Subsequently, downregulation of potassium channels Kir4.
The result of this event is increasing the potassium and glutamate in the synaptic cleft. An increase in extracellular K leads to seizures.
This cycle can amplify epilepsy after a stroke [46] , [47] , [48]. High levels of glutamate released from ischemic or hypoxic cells into the extracellular spaces may activate AMPA and NMDA receptors leading to neuronal apoptosis or death [49]. GABA is a major neurotransmitter in the nervous system. Decreased inhibition of this neurotransmitter after stroke leads to excessive neuronal excitability. Animal studies have demonstrated post ischemic encephalopathy in forebrain ischemia which can cause damage to the GABAergic system.
The striatum is specifically vulnerable to transient forebrain ischemia. The dorsolateral striatum has profound neuronal necrosis associated with a marked decrease in GABA synthesis after global ischemia [50].
Decreased GABA receptors may also lead to hyper-excitability of neural networks and seizure [51]. Studies also show that hypoxia, induced by brain ischemia, may play an important role in the onset of epilepsy, depending on how long it lasts. The AMPA receptor antagonist prevents long-term epilepsy after hypoxia [ 52 , 53 ]. Oxidative stress is closely related to mitochondria dysfunction, and the role of mitochondria in the pathology of COVID disease has been confirmed [54] , [55] , [56] , [57].
There is an interplay between mitochondria, oxidative stress, and inflammation during Covid infection. Inflammatory cytokines increase reactive oxygen species ROS production in mitochondria [58].
Mitochondria are intracellular organs with two inner and outer membranes that play an important role in energy homeostasis. In addition to energy production, mitochondria have a variety of functions, including calcium homeostasis, the production of reactive oxygen species ROS , the modulation of neurotransmitters in the central nervous system, and the regulation of cell apoptosis [59] , [60] , [61].
There is a reciprocal, cause or consequence relationship between mitochondrial dysfunction and epilepsy. In most types of epilepsy, there is secondary damage to the mitochondria. Mitochondrial dysfunction plays an important role in developing epilepsy. These organelles are responsible for generating energy in the cells, which is important for the normal electrical activity of neuronal and synaptic transmission.
Any disturbance in mitochondrial function may lead to abnormal electrical activity of neurons and produce seizures. Studies have reported various electrolyte abnormalities in patients with coronavirus infection COVID [ 62 , 63 ]. The COVID infection is associated with decreased serum concentrations of sodium, potassium, magnesium, and calcium, leading to hyponatremia, hypokalemia, hypocalcemia, and hypomagnesemia.
These disorders, especially hypokalemia, may have severe clinical consequences for the infected patient. Hypokalemia leads to exacerbation of ARDS and acute heart damage [ 10 , 64 , 65 ].
Potential factors that exacerbate electrolyte imbalance in COVID patients may include gastrointestinal symptoms such as diarrhea and nausea [66] , [67] , [68].
Seizures are the most important clinical symptoms of electrolyte disturbances and are more common in patients with hyponatremia, hypocalcemia, and hypomagnesemia. In these individuals, successful treatment of seizures begins with an accurate diagnosis of the underlying electrolyte disturbances [ 69 , 70 ]. Early detection and correction of these disorders are essential to control seizures and prevent permanent brain damage.
If the electrolyte disorder persists, anti-epileptic drugs AED alone is ineffective and inadequate for controlling seizures. The treatment of seizures induced by electrolyte imbalance is determined by the underlying cause and in most cases, AED administration is not necessary until the disturbance is rectified [71] , [72] , [73]. The impact of the new coronavirus on various organs is not fully understood. The virus can cause complicated disorders in the nervous system, such as seizures and epilepsy.
The destructive effects of Covid in the central nervous system are mainly caused by a cytokine storm produced by either the entry of pro-inflammatory cytokines from the periphery into the CNS or the production of these cytokines by activated microglia.
Secondary seizures may be initiated after strokes, electrolyte imbalance, increased oxidative stress, and mitochondrial dysfunction in Covid patients.
More research is needed to prove the exact mechanism of seizures in Covid patients. National Center for Biotechnology Information , U. Mult Scler Relat Disord. Published online Sep Author information Article notes Copyright and License information Disclaimer. All rights reserved. Elsevier hereby grants permission to make all its COVIDrelated research that is available on the COVID resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source.
This article has been cited by other articles in PMC. Abstract The new coronavirus has spread throughout the world in a very short time and now has become a pandemic. Keywords: Covid, Seizure, Epilepsy, Pandemic. Introduction Coronavirus or COVID has affected many people around the world and is now a major global health threat. COVID, Epilepsy and central nervous system inflammation cytokine storm Like all six previous beta-coronaviruses, COVID has the ability to enter the nervous system and causes neurological symptoms.
Conclusion The impact of the new coronavirus on various organs is not fully understood. Declaration of Competing Interest The authors declare that there is no conflict of interest. References 1. Thompson R. Pandemic potential of nCoV. Lancet Infect Dis. This system is more biologically active in younger patients, and the combination of hyperactive endothelial and blood-clotting systems puts these patients at a major risk for developing blood clots.
That said, it would be premature to conclude from available data that COVID preferentially causes strokes in younger patients. However, it can be challenging to get these studies. Our patients with COVID can be extremely weak and even confused, so we need to balance treating their immediate medical needs with information gathering to better understand how we can help fight the virus in others who may develop this condition in the future.
How Does Coronavirus Affect the Brain? Stevens explains some of the prevailing scientific theories. Q: In what ways does the coronavirus affect the brain?
Patel H, et al. Long-term sequelae of West Nile virus-related illness: A systematic review. The Lancet Infections Diseases. Acute viral encephalitis in children: Treatment and prevention. Daroff RB, et al. Viral encephalitis and meningitis. In: Bradley's Neurology in Clinical Practice. Zachary KC. Acyclovir: An overview. Breisch N. Prevention of arthropod and insect bites: Repellents and other measures. Centers for Disease Control and Prevention.
Riggin EA. Allscripts EPSi. Mayo Clinic, Rochester, Minn. Howe CL, et al. Neuroprotection mediated by inhibition of calpain during acute viral encephalitis. Scientific Reports. Singh TD, et al.
Predictors of outcome in HSV encephalitis. Journal of Neurology. Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Research has shown that, among other things, delirium and risk of stroke are both possible symptoms that come with COVID infections.
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