Epilepsy is a neurological condition defined by recurring, unprovoked seizures, which are episodes of abnormal, synchronized electrical activity in the brain. Sleep apnea is a common sleep disorder characterized by repeated interruptions in breathing during sleep, categorized primarily as Obstructive Sleep Apnea (OSA) or Central Sleep Apnea (CSA). OSA involves a physical blockage of the upper airway, while CSA involves a lack of effort from the brain to initiate a breath. These two disorders frequently coexist, and the relationship between them is complex, often involving a two-way street where each condition can influence the other’s severity and presentation.
Seizures Impact on Respiratory Control
A seizure can directly disrupt the brain’s control over breathing, causing an apneic event. This occurs when seizure activity originates in or spreads to specific brain regions that regulate respiratory function, such as the amygdala, insula, and parts of the brainstem.
Seizure activity in these areas can inhibit the pre-Bötzinger complex, the rhythm-generating center for breathing located in the brainstem. This inhibition leads to a temporary cessation of respiratory drive, known as central apnea. During a generalized tonic-clonic seizure, intense muscle contraction can also paralyze the respiratory muscles, contributing to hypoventilation or temporary cessation of breathing.
The breathing abnormalities that occur during or immediately following a seizure are referred to as ictal or post-ictal respiratory changes. These acute events can lead to significant oxygen desaturation and are a major mechanism implicated in Sudden Unexpected Death in Epilepsy (SUDEP). While some focal seizures may mimic Obstructive Sleep Apnea due to muscle contraction causing airway obstruction, this respiratory disruption is typically a transient effect of the acute seizure, not a chronic sleep apnea disorder.
How Sleep Apnea Can Increase Seizure Risk
The relationship is more commonly observed in the reverse direction, where chronic sleep apnea increases the frequency and severity of seizures in individuals with epilepsy. Untreated Obstructive Sleep Apnea is problematic because it fragments sleep and causes repeated drops in blood oxygen levels. Sleep deprivation resulting from constant arousals is a well-established trigger for seizures, lowering the brain’s seizure threshold and increasing neuronal excitability.
Chronic intermittent hypoxia, the cycle of low oxygen and normal oxygen levels during apneic events, stresses brain cells. These chemical changes, along with increased carbon dioxide levels (hypercapnia), alter the brain’s chemical environment, making neurons more susceptible to abnormal firing. Sleep apnea also causes a reduction in Rapid Eye Movement (REM) sleep, which is thought to have an anti-epileptic influence.
The combination of fragmented sleep, chronic oxygen deprivation, and loss of REM sleep creates a highly pro-epileptic state. Studies show that patients with epilepsy and untreated OSA experience higher rates of nocturnal seizures and drug-resistant epilepsy. Treating the underlying sleep disorder often leads to improvement in seizure control, highlighting the direct influence of sleep apnea on seizure burden.
Factors Contributing to Co-occurrence
The high rate of co-occurrence between sleep apnea and epilepsy suggests shared underlying vulnerabilities and exacerbating factors. Obesity, for instance, is a risk factor for OSA and is common in the epilepsy population due to lifestyle factors and certain medications. Older age and male gender are also independently associated with a higher risk for both conditions.
Certain anti-epileptic drugs (AEDs) can inadvertently worsen or contribute to sleep apnea. Some AEDs cause weight gain, directly increasing the risk of OSA due to increased tissue around the airway. Other medications may have a sedative effect, which reduces muscle tone in the upper airway, making it more prone to collapse during sleep.
The Vagus Nerve Stimulator (VNS), a common device-based treatment for refractory epilepsy, can sometimes cause or worsen sleep apnea. VNS stimulation activates motor nerves that supply the upper airway muscles, potentially leading to airway narrowing and obstruction. These shared physiological vulnerabilities and treatment side effects contribute to the frequent co-diagnosis of these two disorders.
Treatment Approaches for Both Conditions
Given the strong bidirectional link, effective management of one condition requires addressing the other. Clinicians should proactively screen all epilepsy patients for symptoms of sleep apnea, such as excessive daytime sleepiness, snoring, or morning headaches. A formal sleep study, or polysomnography, is necessary to confirm the diagnosis and determine the severity of sleep apnea.
Treating sleep apnea, particularly with Continuous Positive Airway Pressure (CPAP) therapy, can lead to reductions in seizure frequency. One study found that patients with co-occurring OSA and epilepsy who were compliant with CPAP therapy had a greater reduction in seizures compared to those with untreated OSA. CPAP works by splinting the airway open with pressurized air, preventing the intermittent hypoxia and sleep fragmentation that contribute to seizure risk.
Careful selection of anti-epileptic medications is also important for patients with coexisting sleep apnea. Physicians should aim to use AEDs that are less likely to cause weight gain or excessive sedation, avoiding exacerbation of the underlying breathing disorder. Coordinated care between an epileptologist and a sleep specialist is necessary to manage these two conditions effectively, leading to better seizure control and improved patient quality of life.