The Confirming Evidence for Ictal Epileptic Headache

Dr. Fanella et al published in Headache, a possible additional case of “Ictal Epileptic Headache” (IEH), that they classified as a “non convulsive status epilepticus.” They reported a woman experiencing migraine attacks-featuring prolonged, intense, throbbing, left temporal pain associated with ipsilateral visual symptoms (ie, non-colored flashes and photophobia) and nausea or vomiting, unresponsive to painkillers – associated with epileptic activity over the right posterior cerebral regions and responsive to intravenous lacosamide. The first description of a documented isolated headache as a sole ictal manifestation of an epileptic seizure (erroneously reported by Dr. Fanella et al, as first published in 2011) was described and published in Epilepsia in 2007 by Parisi et al. These authors coined and published the “original criteria” for IEH diagnosis in 2012, although they have not yet been recognized by the International League Against Epilepsy classification. Indeed, IEH criteria should be applied to all cases where headache is the sole, or is the earliest and most evident feature, of a seizure, regardless of other possible “subtle” associated manifestations; in fact, the same authors have suggested that, to enable a IEH diagnosis, a careful and detailed neurologic exam must be carried, to rule out other associated ictal signs and symptoms. In particular, the availability of an ictal video-EEG recording confirming the clinical suspect of a headache of epileptic origin as well as the prompt response to anti-seizure therapy is of paramount importance in such cases, which may be challenging even for the most expert of clinicians. Fanella and colleagues’ description confirms that (video)-EEG recording – not routinely recommended in patients with headache – should be considered promptly in individuals reporting prolonged migraine/headache not responsive to analgesics. Moreover, ictal EEG recording does also allow the clinician to differentiate IEH from the misleading “migralepsy” concept that probably does not exist at all (ie, “an isolated ictal headache, immediately followed by other epileptic manifestation”). The pathophysiology of IEH is still a matter of on-going research. Although there is not a specific cortical substrate, the most frequently reported origin of IEH is in the posterior cerebral areas, particularly the occipital lobe, as it is a vulnerable region for the onset of both seizures and headache. Notably, 10 years before the epilepsy onset, the patient reported by Dr. Fanella et al had been hospitalized for eclampsia, followed by focal seizures and prolonged coma. Her brain MRI revealed right parietal-occipital ischemic damage. This clinical and neuroimaging picture is strongly suggestive of posterior reversible encephalopathy syndrome, a usually reversible condition that can sometimes result in death or irreversible neurological deficit, including chronic epilepsy. Therefore, it is likely that the cortical projections of headache pain are widespread projections that involve significantly the autonomic networks (insula, cingulate cortex, prefrontal cortex, amygdala, and other parts of the limbic system) rather than just the primary sensory-sensitive areas, thus supporting the view that IEH is primarily an “autonomic” rather than a “painful” epileptic seizure.