Can Carbon Monoxide Poisoning Cause Seizures?

Carbon monoxide poisoning can absolutely cause seizures, both during the acute exposure itself and weeks or even months afterward. Large population studies have found that people who survive CO poisoning face a substantially elevated risk of developing epilepsy compared to the general population, with one nationwide cohort study reporting roughly two and a half times the overall risk and another estimating it at more than eight times the risk. The relationship between CO and seizures runs deeper than a simple lack of oxygen, involving specific patterns of brain damage that make some survivors prone to recurring seizures long after the initial poisoning event.

How Carbon Monoxide Injures the Brain

Carbon monoxide binds to hemoglobin far more tightly than oxygen does, starving tissues of the oxygen they need. The brain is especially vulnerable because it consumes a disproportionate share of the body’s oxygen supply. But the damage goes beyond simple oxygen deprivation. After CO exposure, a cascade of harmful chemical events unfolds in brain cells. Research in animal models has shown that CO poisoning triggers a flood of glutamate, a chemical messenger that in excess overstimulates brain cells to the point of death. This process, known as excitotoxicity, causes calcium to pour into neurons, eventually killing them. In a mouse study, blocking a specific step in this chain reduced the number of dying brain cells and improved the animals’ memory and learning ability, confirming that excitotoxicity plays a central role in the brain injury that follows CO exposure.¹

This chemical damage is not evenly distributed across the brain. Post-mortem studies and brain imaging consistently point to two areas that take the worst hit: the basal ganglia, a set of deep brain structures involved in movement and other functions, and the hippocampus, a region critical for memory. Selective destruction of the globus pallidus, a part of the basal ganglia, is a characteristic finding in severe CO poisoning cases.² Both of these regions are intimately involved in seizure activity, which helps explain why seizures are such a prominent feature of CO brain injury.

Seizures During Acute Poisoning

Seizures can strike while the poisoning is still happening or shortly after. They tend to signal a more severe exposure. A case report documented a patient who developed focal motor seizures and coma within hours of CO exposure; their brain-wave recording showed sharp electrical discharges and a focal seizure pattern, the kind of activity you would expect in someone with a structural brain injury. That patient eventually made a full recovery, and the abnormal brain-wave pattern resolved within two months.³ Not every patient is so fortunate, but this case illustrates that even dramatic acute seizures do not automatically mean permanent damage.

CO poisoning can also present as something subtler and more deceptive: non-convulsive status epilepticus, a state of continuous seizure activity in the brain without the dramatic shaking most people associate with seizures. In at least one documented case, a CO-poisoned patient showed no outward convulsions but was in continuous electrical seizure on brain monitoring.⁴ This matters because non-convulsive seizures are easy to miss. A patient who appears confused or unresponsive after CO exposure could be actively seizing without anyone realizing it, which delays the right treatment.

The Long-Term Risk of Epilepsy

Perhaps more alarming than seizures during the acute event is the risk of developing epilepsy months or years later. Two large nationwide studies have quantified this, and while their exact numbers differ, both point in the same direction. A Taiwanese population-based cohort study found that people with a history of CO poisoning had about eight times the risk of developing epilepsy compared to matched controls.⁵ A Korean cohort study covering nearly two decades found the overall epilepsy risk was about two and a half times higher, and the risk of status epilepticus, a prolonged seizure emergency, was roughly four times higher.⁶

The gap between these estimates likely reflects differences in how the populations were defined and how strictly epilepsy was diagnosed. Regardless, both studies used hundreds of thousands of patient records and controlled for pre-existing conditions, making the overall finding hard to dismiss. CO poisoning leaves behind structural brain changes that can serve as a lasting trigger for seizures, even in people who seemed to recover well from the initial event.

Why Young Adults May Be Hit Hardest

In the Taiwanese study, age-stratified analysis revealed a striking pattern: adults between 20 and 39 years old who had been poisoned by CO carried the highest relative risk of later epilepsy, with an adjusted hazard ratio above 11.⁵ This does not mean young adults get sicker than older adults in absolute terms; it means the gap between their expected epilepsy rate (which is naturally very low at that age) and their post-poisoning rate is enormous. A 25-year-old with no risk factors for epilepsy who survives CO poisoning suddenly has a seizure risk profile that looks nothing like their peers. The same study found similar elevated risks for both men and women, so sex does not appear to be a major factor in determining who develops seizures afterward.

Delayed Encephalopathy and Seizures That Come Later

One of the most unsettling aspects of CO poisoning is a phenomenon called delayed encephalopathy. A person may seem to recover from the initial exposure, experience a “lucid interval” of days to weeks where they feel relatively normal, and then develop new neurological problems. These delayed symptoms can include memory loss, personality changes, difficulty concentrating, and seizures. In a study that followed patients with delayed encephalopathy after CO poisoning, most symptoms improved over six months, but epileptic seizures were among the complications that persisted.⁷

The underlying brain damage that drives delayed encephalopathy centers on the same vulnerable regions mentioned earlier. The basal ganglia tend to shrink in the months after poisoning, and the hippocampus sustains damage through ongoing inflammation and excitotoxic cell death. Children with seizures after neonatal brain injury from oxygen deprivation commonly show basal ganglia injury on imaging, and a similar mechanism appears to explain seizures in CO survivors.⁸ The hippocampus damage also helps explain why so many CO survivors struggle with depression and anxiety alongside their seizure risk, since the hippocampus is deeply connected to emotional processing.

Seizures as a Red Flag for Worse Outcomes

When seizures occur early in the course of CO poisoning, they are not just a symptom to manage in the moment. They serve as a warning that the patient is at higher risk of developing delayed neurological problems down the road. A retrospective study of CO-poisoned patients found that seizures occurring before or upon arrival at the emergency department were one of several factors associated with developing delayed neuropsychological problems within a month of discharge. Other red flags in that study included prolonged CO exposure lasting more than six hours, a very low level of consciousness, low blood pressure, and elevated muscle-breakdown markers.⁹

This has practical implications for emergency care. A patient who seizes during or shortly after CO exposure should be monitored more closely and may be a stronger candidate for aggressive treatment, including hyperbaric oxygen therapy, to reduce the risk of lasting brain damage.

Children and Infants Face Extra Danger

Children are generally more susceptible to CO poisoning because of their faster breathing rate and higher metabolic demands. Seizures, fainting, and abnormal heart rhythms can all occur depending on the severity of exposure, and poisoning in infants tends to follow a more severe course than in older children or adults.¹⁰

Diagnosing severity in children is also trickier. The standard blood test for CO poisoning measures carboxyhemoglobin, the percentage of hemoglobin bound to CO rather than oxygen. But in children, this number can be misleading. A study of pediatric CO poisoning found that blood lactate levels were actually more useful than carboxyhemoglobin for predicting which children would lose consciousness or have convulsions.¹¹ Another study found that children who developed cognitive problems after CO poisoning actually had lower carboxyhemoglobin levels than those who recovered normally, likely because these children had been transferred from smaller hospitals and their levels had already dropped by the time they were tested.¹² The takeaway for parents and emergency providers is that a “reassuring” carboxyhemoglobin level does not necessarily mean a child is in the clear.

What About Unborn Babies?

Maternal CO exposure creates a particularly grim scenario for the fetus. Fetal hemoglobin binds CO even more avidly than adult hemoglobin, meaning the fetus accumulates CO faster and clears it more slowly than the mother. Research using primate models showed that fetal brain injury follows a threshold pattern: below a certain level of oxygen deprivation, the fetal brain appears resilient, but once a critical level is crossed, the damage is catastrophic. Animals that crossed that threshold showed extensive hemorrhagic destruction of the brain, with the basal ganglia again being a primary site of necrosis.¹³ This “all or nothing” pattern means a pregnant person exposed to CO may feel only mildly affected while their fetus sustains severe brain damage. Seizure disorders in infants exposed to CO in utero are among the possible long-term consequences.

Hyperbaric Oxygen Therapy and Seizure Prevention

The main treatment aimed at preventing long-term brain damage after CO poisoning is hyperbaric oxygen therapy, where the patient breathes pure oxygen inside a pressurized chamber. The high pressure forces more oxygen into the blood and helps displace CO from hemoglobin much faster than breathing normal air. Beyond the simple mechanics of clearing the poison, hyperbaric oxygen may interrupt some of the inflammatory and excitotoxic processes that lead to delayed brain injury.¹⁴

There is an ironic wrinkle here: hyperbaric oxygen therapy itself can occasionally provoke seizures, because breathing oxygen at high pressure can transiently lower the seizure threshold. A case series examining this found that such oxygen-related seizures during treatment are generally brief and self-limiting, and the therapy remains commonly and safely used for CO poisoning.¹⁵ Providers who administer hyperbaric oxygen are accustomed to this possibility, and it is not considered a reason to withhold treatment from someone whose brain is at risk from CO damage.

Why CO Poisoning Gets Misdiagnosed

One of the persistent clinical problems with CO poisoning is that it mimics many other conditions. Headache, nausea, confusion, and dizziness are its most common symptoms, and none of them point specifically to CO. When seizures are the presenting complaint, the initial workup may focus on stroke, a primary seizure disorder, drug overdose, or infection, especially if no one thinks to ask about CO exposure. The non-convulsive status epilepticus case mentioned earlier is a perfect example: a patient who appears altered or unresponsive could easily be worked up for a dozen other conditions before anyone checks a carboxyhemoglobin level.

This diagnostic delay matters because treatment is time-sensitive. The sooner high-flow or hyperbaric oxygen is started, the faster CO is cleared and the lower the risk of lasting damage. Emergency physicians in many countries now check CO levels more routinely in patients with unexplained altered mental status, especially during winter months when heating-related exposures spike, but cases still slip through. If you or someone you know develops unexplained seizures, confusion, or persistent headache and there is any possibility of CO exposure, from a malfunctioning furnace, a gas appliance, or a running car in an enclosed space, mention it. A simple blood test can confirm or rule it out.

Home CO Detectors and the Prevention Side

Since treatment can only do so much once the brain has been injured, prevention remains the most effective strategy. Residential CO detectors are widely available and inexpensive. They should be installed on every level of a home, especially near sleeping areas and attached garages. Sources of CO include gas furnaces, water heaters, stoves, fireplaces, generators, and car exhaust. Generators deserve special mention because they produce enormous amounts of CO and are often used during power outages in enclosed or semi-enclosed spaces, a setup responsible for a large share of accidental CO deaths each year.

Low-level chronic exposure is another scenario that sometimes flies under the radar. A slightly malfunctioning appliance can produce CO at levels too low to trigger an alarm but high enough to cause headaches, fatigue, and cognitive problems over weeks or months. At least one case report documented seizures and a cystic brain lesion from chronic, non-fatal CO exposure at levels that never caused the acute crisis most people associate with the poison.² If you have recurring, unexplained neurological symptoms that improve when you leave your home and return when you come back, have your home tested for CO even if your detector has not gone off. Detectors have minimum thresholds and may not alarm at the lower concentrations that can still cause harm over time.

1
PubMed. The role of sGC-cGMP-PKG signaling pathway-mediated excitotoxicity in delayed encephalopathy after carbon monoxide poisoning
2
Clinical Radiology Extra. Seizures and Unilateral Cystic Lesion of the Basal Ganglia: an Unusual Clinical and Radiological Manifestation of Chronic Non-fatal Carbon Monoxide (CO) Poisoning
3
JAMA Neurology. Localized EEG Abnormalities in Acute Carbon Monoxide Poisoning
4
PubMed Central. Carbon Monoxide Poisoning Presenting as Non-Convulsive Status Epilepticus Treated with Hyperbaric Oxygen Therapy
5
Annals of Emergency Medicine. Effect of Carbon Monoxide Poisoning on Epilepsy Development: A Nationwide Population-Based Cohort Study
6
Taylor & Francis Online (Clin Toxicol (Phila)). Carbon monoxide poisoning is associated with an increased risk of epilepsy and status epilepticus: a nationwide population-based cohort study conducted in the Republic of Korea between 2002-2021
7
PubMed Central. Clinical and Imaging Prognosis in Patients with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning
8
Annals of Emergency Medicine. Effect of Carbon Monoxide Poisoning on Epilepsy Development: A Nationwide Population-Based Cohort Study – Section: Discussion
9
PubMed Central. Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the Emergency Department. A retrospective study
10
PubMed Central. Epidemiology, pathophysiology, clinical evaluation, and treatment of carbon monoxide poisoning in child, infant, and fetus
11
Pediatric Emergency Care. Lactate Level Is More Significant Than Carboxihemoglobin Level in Determining Prognosis of Carbon Monoxide Intoxication of Childhood
12
Scientific Reports. Analysis of prognosis of neurological sequelae in children with carbon monoxide poisoning
13
PubMed. Fetal brain injury after maternal carbon monoxide intoxication. Clinical and neuropathologic aspects
14
Indoor Environment. Neurological Sequelae of Carbon Monoxide Poisoning: Role of Hyperbaric Oxygen
15
The Journal of Emergency Medicine. Seizure During Hyperbaric Oxygen Therapy for Carbon Monoxide Toxicity: A Case Series and Five-year Experience