Epilepsy is a neurological disorder defined by recurrent, unprovoked seizures, which are sudden, abnormal bursts of electrical activity in the brain. Migraine is a separate neurological condition characterized by severe, recurring headaches, often accompanied by nausea and heightened sensitivity to light and sound. While epilepsy is not considered the direct cause of a migraine attack, these two disorders frequently affect the same individuals. The clinical and biological pathways linking seizure activity and severe headaches reveal a deep connection.
Defining the Clinical Relationship
Epilepsy is not typically considered the direct cause of an independent migraine attack, but the two conditions exhibit strong comorbidity. This connection is recognized as a bidirectional association, where the presence of one disorder significantly increases the likelihood of the other. Epidemiological studies consistently show that people diagnosed with epilepsy have a substantially higher prevalence of migraine than the general population.
Individuals with epilepsy are estimated to have an approximately 80% increased lifetime prevalence of migraine compared to those without epilepsy. Similarly, people who suffer from migraine also have a notably increased risk of developing epilepsy. This close clinical relationship suggests that the two conditions may share underlying biological vulnerabilities.
The prevalence of migraine in the epilepsy population is often cited between 8% and 23%, figures significantly higher than in the general public. This frequent co-occurrence has led researchers to investigate shared genetic and neurophysiological factors. These shared risk factors point toward a common neurological foundation that makes the brain susceptible to both seizures and severe headaches.
Shared Mechanisms of Neuronal Hyperexcitability
The core scientific explanation for the link between epilepsy and migraine lies in neuronal hyperexcitability, a state where neurons are overly prone to firing. Both seizures and migraine attacks are episodic disorders resulting from transient disturbances in brain electrical activity. This shared tendency toward excessive electrical activity is thought to arise from similar molecular and cellular dysfunctions.
A central mechanism in migraine, particularly those with aura, is Cortical Spreading Depression (CSD). CSD is a slow-moving wave of intense neuronal and glial depolarization that sweeps across the brain cortex. This significant electrical event is characterized by a massive redistribution of ions, which is believed to be the neurophysiological correlate of migraine aura.
CSD is highly relevant to epilepsy because this intense depolarization can lower the threshold for seizure activity. An epileptic focus, an area of the brain prone to generating seizures, can facilitate the initiation of CSD. This process further links the two conditions at the cellular level by contributing to the brain’s hyperexcitable state.
The genetic overlap between the disorders is often described through channelopathies, which are diseases caused by defects in ion channels. Ion channels are proteins that regulate the flow of charged particles across neuronal membranes, fundamental to electrical signaling. Mutations in genes coding for these channels can compromise the brain’s ability to maintain a stable electrical environment.
Specific genetic mutations in ion channel genes, such as SCN1A (a sodium channel) and CACNA1A (a calcium channel), have been identified in rare forms of both epilepsy and migraine, including Familial Hemiplegic Migraine (FHM). Certain mutations in the SCN1A gene can cause a gain-of-function in inhibitory neurons, making them hyperactive and increasing susceptibility to CSD in migraine. Conversely, other mutations in the same gene can lead to a loss-of-function, causing decreased inhibition and increasing the risk of seizures.
This molecular evidence demonstrates that a fault in a single type of ion channel can result in either or both disorders, depending on the mutation’s nature. The dysfunction affects the balance of excitatory and inhibitory signals, which are partly regulated by neurotransmitters like glutamate and GABA. This shared molecular fragility in the electrical infrastructure of the brain provides a compelling reason for the clinical co-occurrence.
Distinguishing Seizure-Related Headaches from Migraines
When a person with epilepsy experiences a headache, physicians must determine if it is an independent migraine or a headache directly related to the seizure event. Headaches temporally related to a seizure are classified as peri-ictal, including those occurring before, during, or immediately after the event. The timing of the pain relative to the seizure is the most important diagnostic clue.
The most common type is the post-ictal headache (PIH), which develops within three hours following a seizure and typically resolves within 72 hours. PIH often shares features with migraine, such as a throbbing quality and sensitivity to light (photophobia) and sound (phonophobia). They are particularly common after generalized tonic-clonic seizures.
Far less common is the ictal headache, which occurs during the seizure itself. In rare cases, a headache can be the sole manifestation of an epileptic seizure, sometimes termed “ictal epileptic headache.” Confirming this diagnosis requires an electroencephalogram (EEG) to document simultaneous epileptic activity occurring alongside the pain.
A separate, rare diagnostic category is Migraine aura-triggered seizure, which describes a seizure that happens during or shortly after a migraine aura. This is distinct from a true comorbid migraine, which occurs independently of any seizure activity. Accurate differentiation of these headache types is important because the treatment strategy for a seizure-related headache may differ from that for an independent migraine disorder.