COPD does not directly cause seizures in the way epilepsy does, but it creates several conditions that can trigger them. Low blood oxygen, high carbon dioxide levels, acid-base imbalances, and even some medications used to treat COPD can all lower the brain’s seizure threshold. In a study of hospitalized patients with respiratory diseases who experienced seizures, over half had symptomatic seizures (meaning no prior epilepsy history), and the dominant trigger was metabolic changes tied to impaired breathing.
How Low Oxygen and High CO2 Affect the Brain
The most direct link between COPD and seizures runs through blood gas abnormalities. When your lungs can’t move enough air, two things happen simultaneously: oxygen levels drop (hypoxemia) and carbon dioxide builds up (hypercapnia). Both of these shift the chemical environment of the brain in ways that make neurons more excitable and more likely to fire abnormally.
In a retrospective study of 705 patients with respiratory diseases who were evaluated for seizures, rates of hypoxemia and respiratory acidosis were significantly higher among those experiencing first-time symptomatic seizures compared to those with a known history of epilepsy. The patients with symptomatic seizures had lower average blood oxygen levels and lower blood pH values, meaning their blood was more acidic. Researchers identified the drop in oxygen and pH as the most influential factors pushing these patients past the seizure threshold.
Prolonged episodes of low oxygen also cause cumulative damage. Experimental studies have shown that sustained drops in oxygen saturation increase the rate and severity of brain injury from reduced blood flow, which can further predispose someone to seizures over time. In more than half of the seizure patients studied, multiple overlapping factors contributed rather than a single cause.
Hypercapnic Encephalopathy
When carbon dioxide retention becomes severe enough, it produces a condition called hypercapnic encephalopathy, a state of brain dysfunction driven by excess CO2. Early signs include lethargy, confusion, and memory problems. At moderate levels, CO2 causes arousal and excitability in the nervous system. At very high concentrations, it becomes sedating. That middle zone of elevated but not extreme CO2, where the brain is overstimulated, is where seizure risk climbs.
This is particularly relevant during COPD exacerbations, when breathing worsens suddenly and CO2 can spike. People with chronic CO2 retention may tolerate higher levels than a healthy person would, but acute increases on top of an already elevated baseline can still push the brain into dangerous territory.
COPD as a Risk Factor for Stroke-Related Seizures
COPD also increases seizure risk through an indirect route: it raises the likelihood of stroke, and strokes themselves are a leading cause of seizures in older adults. A study of 237 stroke patients who developed seizures, compared to 939 stroke patients who did not, found that COPD emerged as an independent risk factor for seizure development after stroke. This held true regardless of COPD severity or the type of treatment used for it.
The most plausible explanation researchers identified was nocturnal oxygen desaturation. People with COPD commonly experience drops in blood oxygen during sleep, when breathing naturally becomes shallower. These repeated overnight dips may damage brain tissue in ways that make it more vulnerable to abnormal electrical activity, especially after a stroke has already injured part of the brain.
COPD Medications That Lower Seizure Threshold
Some of the drugs used to manage COPD carry their own seizure risks, which compounds the problem.
Theophylline, an older bronchodilator still used in some cases, is the most well-documented offender. Seizures have been reported at blood levels between 14 and 35 mg/l, a range that overlaps with what’s considered therapeutic. For patients with additional risk factors, keeping blood levels below 10 to 15 mg/l is recommended to reduce seizure risk.
Short-acting bronchodilators like salbutamol (albuterol) have also been implicated, though the evidence is less clear-cut. Salbutamol crosses into the brain after entering the bloodstream, reaching concentrations of about 5% of plasma levels. Case reports describe tonic-clonic seizures that resolved after stopping excessive salbutamol use. In one published case, a 65-year-old man with COPD who was being treated with a combination of ipratropium and salbutamol experienced a seizure after nebulization. A survey found that about a third of patients who had been prescribed salbutamol were not using it because of a personal history of seizures associated with the medication. That said, hypoxia from the underlying lung disease may have contributed in many of these cases, making it hard to isolate the drug as the sole cause.
Seizures vs. Fainting Spells in COPD
Not every episode of sudden collapse or loss of consciousness in someone with COPD is a seizure. Syncope, or fainting, can look remarkably similar and is also common in people with impaired breathing. The distinction matters because the causes and treatments differ.
Syncope results from a temporary drop in blood flow to the brain rather than abnormal electrical discharges. It typically resolves quickly and completely, with no prolonged confusion afterward. A seizure, by contrast, often involves sustained rhythmic jerking of the limbs (not just brief twitches) and is followed by a postictal period of grogginess, confusion, or fatigue that can last minutes to hours. Brief myoclonic jerks can happen during a fainting spell too, which is one reason the two get confused. An EEG showing abnormal electrical patterns in the brain is the definitive way to confirm a true seizure.
For someone with COPD, both possibilities should be on the table. A sudden drop in oxygen can cause either one, and in some cases a person may experience fainting episodes that progress to seizures if the oxygen deprivation is severe or prolonged enough.
Why Nighttime Is Especially Risky
Sleep is when COPD patients are most vulnerable to oxygen drops. During sleep, the muscles that assist breathing relax, the drive to breathe decreases, and the body’s normal response to rising CO2 is blunted. For someone whose respiratory system is already compromised, this can produce significant overnight desaturation. These repeated dips in oxygen are thought to be one reason COPD independently predicts seizure development in stroke patients, and they may also contribute to seizure risk in COPD patients without a stroke history. If you or someone you care for has advanced COPD and has experienced any episode resembling a seizure, overnight oxygen monitoring can help identify whether nocturnal desaturation is a contributing factor.
Managing Oxygen in COPD Patients With Seizure Risk
Oxygen management in COPD is a balancing act. Too little oxygen raises seizure risk, but too much can also be dangerous because some people with COPD rely on low oxygen levels as their primary signal to keep breathing. Clinical guidelines from the American Association for Respiratory Care recommend a target oxygen saturation of 88 to 92% for patients with COPD, compared to 94 to 98% for most other hospitalized patients. This narrower range is specifically designed to correct dangerous hypoxemia without suppressing the breathing drive. For COPD patients who have experienced seizures, maintaining oxygen within this window becomes even more important, since both the seizures themselves and the postictal period can worsen respiratory function and create a dangerous feedback loop.