An epileptic headache refers to a headache that is temporally related to a seizure event, and it is a common condition in people with epilepsy. The association between these two disorders is complex and bidirectional. Headaches occur in a higher percentage of people with epilepsy compared to the general population, with estimates ranging from 8% to over 50%.
Classification of Peri-ictal Headaches
Headaches that occur close to a seizure are classified based on their timing relative to the event, known as peri-ictal headaches. These are divided into three categories: pre-ictal, ictal, and post-ictal.
Pre-ictal headaches occur before a seizure, sometimes serving as a warning sign or aura. These headaches may be migrainous, preceding the epileptic event by hours or days. In some cases, a true migraine attack with aura can directly trigger a seizure, sometimes referred to as migralepsy.
Ictal headaches happen during the seizure itself. In rare instances, the headache may be the sole manifestation of the seizure, known as Ictal Epileptic Headache and classified as a type of autonomic seizure. The pain is typically severe, brief, and often localized to one side of the head, resolving almost immediately after the seizure terminates.
Post-ictal headache is the most frequent type, occurring within three hours after a seizure and typically resolving spontaneously within 72 hours. These headaches often have features resembling a migraine, including throbbing pain, sensitivity to light, and nausea. Post-ictal headache is particularly common after generalized tonic-clonic seizures.
The Shared Neurological Basis
The frequent co-occurrence of epilepsy and migraine suggests a shared neurological foundation. Both disorders are paroxysmal brain conditions characterized by neuronal hyperexcitability.
A key unifying mechanism is Cortical Spreading Depression (CSD), the neurophysiological event underlying the migraine aura. CSD is a slow-moving wave of intense neuronal and glial depolarization that sweeps across the gray matter, followed by a suppression of electrical activity. This depolarization leads to a massive redistribution of ions, including the release of the excitatory neurotransmitter glutamate.
The surge of extracellular glutamate and subsequent ionic shifts associated with CSD can trigger a seizure in an excitable brain. Conversely, an epileptic discharge can also initiate CSD, explaining the bidirectional relationship. Dysfunction in ion channels (channelopathies), involving genes like \(CACNA1A\) and \(SCN1A\), further supports this shared basis by contributing to impaired ion homeostasis in both disorders.
The balance between excitatory signals (glutamate) and inhibitory signals (Gamma-aminobutyric acid, or GABA) is disrupted in both conditions. Many Anti-Epileptic Drugs (AEDs) are effective in preventing migraines because they restore this balance. They achieve this either by blocking sodium and calcium ion channels or by enhancing the inhibitory effects of GABA.
Evaluation and Treatment Approaches
The clinical evaluation of epileptic headaches begins with a patient history and the use of a headache diary. A prospective diary accurately records the timing, severity, and associated symptoms of headache attacks relative to the seizure events, which helps reduce recall bias. This information is essential for distinguishing between the different peri-ictal types and for identifying potential triggers.
Diagnostic tools like the electroencephalogram (EEG) are utilized to confirm the presence of an epileptic focus and to determine if a headache is truly ictal. Neuroimaging, such as MRI, may also be performed to rule out any underlying structural brain causes responsible for both the seizures and the headaches. The challenge in management is treating both conditions simultaneously, often requiring a single prophylactic medication to serve a dual purpose.
Prophylactic treatment involves selecting an Anti-Epileptic Drug (AED) effective in preventing both seizures and migraines. Topiramate and valproate are two such agents, as they modulate neurotransmitters and ion channels implicated in both pathologies. Topiramate, for example, blocks sodium channels and enhances GABA activity, providing both seizure control and migraine prevention.
Acute treatment for peri-ictal headaches, particularly the post-ictal, migraine-like pain, may involve non-steroidal anti-inflammatory drugs (NSAIDs) or triptans. Triptans, which act on serotonin receptors to constrict blood vessels, are moderately effective for post-seizure headaches. However, acute headache medications must be used judiciously to mitigate the risk of developing a Medication Overuse Headache (MOH), a concern in patients with frequent headache episodes.