Headache as the Initial Symptom in Focal ImpairedEpilepsy: Case Report

Lawrence Robbins, M.D.

Clinical Case Summary

Description of the spells: The patient is a 58 year old man who suffered a mild to moderate traumatic brain injury (TBI) 4 years earlier. He was struck on the right frontal area in a motor vehicle accident. He experienced loss of consciousness for less than 1 minute. He subsequently had brief retrograde amnesia for the event. Shortly after the TBI, he began experiencing 3 episodes per week (as described below). These spells usually occurred shortly after work. The episodes consisted of a sudden onset of severe parietal-occipital throbbing head pain. The pain was accompanied by confusion and a ‘disconnected’ feeling. At times during the spell he described experiencing a brief (10 to 30 seconds) feeling of depersonalization-derealization. There were no features of a migraine. His wife described a glazed look on his face. The patient would sit and nod, or simply stare, during the spell. His wife stated that he “did not want to talk, or could not talk, during the episodes”.  On occasion he would cry for a brief time during the episode. He was able to walk slowly but required help going to bed. He occasionally had automatisms during the episode, as his right hand repetitively tapped against his leg.

When he awakened the next morning, the patient was fatigued and could not remember the events of the previous night. In between the discrete spells the patient was asymptomatic with no headache or neck pain.

Past medical history:  The patient has mild hypertension, with no history of headache or seizure. There is no FH of epilepsy.  He had no childhood psychological trauma. There was no previous history of significant TBI.

Work-up:  Routine blood tests were normal, as was a brain MRI. A routine one hour EEG (awake and drowsy) was normal.

Clinical course: The spells continued 3 times weekly for 4+ years. He was diagnosed as post traumatic migraine by several neurologists. Amitriptyline, losartan, and OTCs were ineffective. Because focal impaired epilepsy was suspected, therapy with lamotrigine was slowly initiated. After the dose was increased to 200 mg, the seizures stopped and he became asymptomatic. He has been seizure and headache free until the present time (7 months after lamotrigine was instituted).

Discussion:  This 58 y.o. man had a TBI, with subsequent focal impaired seizures for 4+ years. With each seizure his initial symptom was a parietal-occipital headache. The headaches and seizures completely resolved after he was placed on lamotrigine.

Definition and Diagnosis: The relationship between epilepsy and headache is complex and varied.  The definition is controversial and remains in flux. Epileptic headache (EH) may be a more accurate description than IEH, as EH implies that a seizure is occurring.1 The older terms hemicranias epileptic and migralepsy are imprecise. IEH may be focal aware, focal impaired, or generalized.  The diagnosis should be considered when symptoms of headache coincide with those of focal epilepsy.  IEH is probably underdiagnosed. The 2012 criteria for IEH resulted in few patients being diagnosed with the condition. ICHD-3 has not adequately addressed IEH.2 Cianchetti lists criteria for IEH, which state “EH is a headache of any type that is an expression of ictal epileptic activity; therefore, if isolated, its onset and cessation coincide with a scalp or deep EEG pattern of epileptic seizure, which is indispensable for its diagnosis.”  They then define other variants. Other proposals include mention of the need for EEG discharges to be present, but also mention that the EEG may reveal variable patterns. Currently there is no consensus as to definition, and this is a work in progress.3I believe that an abnormal EEG is helpful, but there are exceptions. In our current case, the patient clinically suffered from IEH, but the routine EEG was not revealing. The patient did not wish to undergo a 72 hour EEG. Utilizing response to antiepileptic medicine may be a useful part of the diagnostic criteria.4However, that approach is also problematic, as there may be non-epileptic patients who respond to anticonvulsants.  

Clinical aspects of IEH:  IEH is equally prevalent in men and women. IEH occurs across the entire age spectrum.5The headache may resemble tension or migraine and the location may be anywhere about the head.1 The pain may last from seconds to hours to days. Interictal EEG may or may not reveal the epileptic focus, and even an ictal EEG may be normal if the focus is deep.1 During the headache there may be symptoms of migraine such as nausea, photophobia, or phonophobia.  Focal impaired epilepsy symptoms may be present, such as GI symptoms, staring, difficulty with speech, picking, tapping, and other autonomic gestures. As in the present case, depersonalization-derealization may be present. The headache location does not necessarily correlate with the abnormal EEG location.6

Pathophysiology:  The hyperexcitability of the cortex likely underlies both epilepsy and headache. Cortical Spreading Depression (CSD) is certainly a mechanism in migraine, and probably epilepsy as well. CSD may initiate the inflammatory cascade within the trigeminovascular system. For many patients with IEH the event may originate within the pain processing centers.1,6,7These include the anterior cingulate cortex, the thalamus, the primary and secondary somatosensory cortices, the insula, the amygdala, and the prefrontal cortex. Occipital lobe epilepsy may originate within the calcarine cortex. Both migraine and epilepsy often involve specific genetic loci, some of which may be shared. Migraine and epilepsy both involve abnormal activity within the serotonin, glutamate, ion channel, and dopamine systems.  There is some thought to the concept that IEH may represent an “autonomic seizure”.2

Even if an EEG does not reveal definite epileptic activity epilepsy remains a possibility. The epileptic focus may lie deep within insular or orbitofrontal areas. Invasive EEG with deep electrodes is not usually performed if surgery is not contemplated. There is no specific EEG pattern associated with IEH.1  There have been four cases of IEH where a generalized pattern was revealed on the EEG.1

There have been various brain pathologies that have resulted in IEH. These have included trauma, neoplasms, encephalopathies (including chronic encephalitis), congenital malformations, genetic conditions, and(rarely) idiopathic epilepsy.


IEH is a rare event but is probably underreported.  The most common type of epilepsy associated with IEH is focal impaired epilepsy. The definition of IEH is in flux. Ideally the patient’s headache will respond to anticonvulsant medication that is controlling the seizures. IEH should be considered when a headache coincides with epileptic symptoms.

Lawrence Robbins, M.D. Associate Professor of Neurology, Chicago Medical School  lrobb98@icloud.com


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