A seizure is an abnormal electrical disturbance in the brain, causing temporary changes in movement, behavior, sensation, or awareness. Infection with the SARS-CoV-2 virus, which causes COVID-19, is associated with seizure activity in some individuals. This neurological symptom can manifest during the acute phase of the illness or emerge later as a persistent complication.
Acute Seizure Risk During COVID-19 Infection
Seizures occurring during the acute phase of COVID-19 are often classified as acute symptomatic seizures, meaning they are a direct consequence of the systemic illness rather than a new diagnosis of epilepsy. These events are typically triggered by severe physiological stress. A common driver, particularly in children, is a high fever, which can lead to febrile seizures, a well-recognized reaction to various infections.
In more severe cases, two major factors contribute to electrical instability in the brain: hypoxia and metabolic disturbances. Hypoxia, or a lack of oxygen, results from the severe respiratory distress and lung damage often seen in critical COVID-19 patients. When brain cells are deprived of sufficient oxygen, they become electrically unstable, increasing the likelihood of a seizure.
Metabolic changes, such as severe electrolyte imbalances including low potassium (hypokalemia), are also common in critically ill patients and can lower the seizure threshold. Furthermore, a widespread inflammatory response, often called a cytokine storm, releases high levels of pro-inflammatory chemicals that can directly excite neurons and trigger seizure onset. These seizures are closely tied to the overall severity of the infection and organ failure.
Underlying Neurological Mechanisms
The mechanisms by which SARS-CoV-2 affects the brain’s electrical stability are complex, extending beyond simple fever or oxygen deprivation. One central pathway involves neuroinflammation, where the body’s immune response directly impacts the central nervous system. The virus prompts the release of pro-inflammatory cytokines, which are signaling molecules that can breach the blood-brain barrier (BBB).
The BBB normally acts as a protective shield, but its disruption allows inflammatory molecules to enter the brain tissue, where they can directly excite neurons and initiate seizure activity. This neuroinflammation can alter the balance of neurotransmitters, such as increasing excitatory glutamate and decreasing inhibitory GABA, leading to neuronal hyperexcitability.
Although direct viral invasion of the brain is possible, it appears to be rare in most cases. The virus uses the Angiotensin-Converting Enzyme 2 (ACE2) receptor to enter host cells, and these receptors are present on cells within the brain, including neurons and glial cells. When the virus binds to ACE2, it can disrupt the receptor’s normal function, potentially contributing to inflammation and neurotoxicity. Additionally, the infection can cause blood clots, leading to cerebral vasculitis or stroke, and the resulting brain damage can serve as a focus for seizure generation.
Impact on Existing Epilepsy and Long-Term Effects
The infection can have a measurable impact on individuals already diagnosed with epilepsy, often causing an exacerbation of their condition. Patients with pre-existing epilepsy frequently experience a temporary increase in seizures following the infection. This is likely due to the generalized stress, sleep deprivation, and inflammatory state caused by the illness, all of which lower the seizure threshold.
Beyond the acute phase, COVID-19 is associated with an increased long-term risk of developing new-onset epilepsy or seizures. Compared to other respiratory illnesses like influenza, COVID-19 infection is associated with a greater likelihood of a new seizure or epilepsy diagnosis in the six months following infection. Although the absolute risk remains low, affecting less than one percent of all patients, the relative risk is notably higher.
This increased risk is pronounced in children under the age of 16 and in individuals whose initial infection did not require hospitalization. Long-term neurological symptoms linked to Long COVID, such as cognitive fog, fatigue, and persistent insomnia, can also indirectly affect seizure control. These persistent issues disrupt medication adherence, sleep cycles, and overall well-being, which are factors that influence seizure susceptibility.
COVID-19 Vaccines and Seizure Risk
Concerns about the safety of COVID-19 vaccines regarding neurological side effects have been addressed through extensive global monitoring and epidemiological studies. Large-scale data from millions of vaccinated individuals generally show no increased risk of developing new-onset seizures or epilepsy following authorized vaccines. The incidence of seizures following vaccination is low, consistent with background rates in the general population.
Researchers have specifically looked for an association with different vaccine types, including mRNA and viral vector formulations, and have found no evidence of a widespread increased risk in adults. While some surveillance systems have detected a slight statistical signal for febrile seizures in very young children (ages 2 to 5) shortly after vaccination, this type of seizure is a known, transient response to the fever that can accompany any vaccine. The risk of a seizure or new epilepsy diagnosis following a COVID-19 infection remains significantly higher than any risk associated with the vaccine.