Background Patients suffering from migraine with aura (MWA) and migraine without aura (MWoA) show abnormalities in visual motion perception during and between attacks. Whether this represents the consequences of structural changes in motion-processing networks in migraineurs is unknown. Moreover, the diagnosis of migraine relies on patient’s history, and finding differences in the brain of migraineurs might help to contribute to basic research aimed at better understanding the pathophysiology of migraine.

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Anatomical Alterations of the Visual Motion Processing Network in Migraine with and without Aura

Headache is one of the most common neurological symptom reported in childhood and adolescence, leading to high levels of school absences and being associated with several comorbid conditions, particularly in neurological, psychiatric and cardiovascular systems. Neurological and psychiatric disorders, that are associated with migraine, are mainly depression, anxiety disorders, epilepsy and sleep disorders, ADHD and Tourette syndrome. It also has been shown an association with atopic disease and cardiovascular disease, especially ischemic stroke and patent foramen ovale (PFO).

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Headache and comorbidity in children and adolescents

Abnormal brain excitability may provide the susceptibility for triggering migraine attacks. Antiepileptic drugs may diminish neuronal excitability and consequently reduce the frequency of migraine. Because migraine aura is predominantly visual, hyperexcitability of the occipital cortex has been the focus of investigations. Functional magnetic resonance imaging of the brain and magnetoencephalography provide the most consistent evidence for the role of brain hyperexcitability in migraine and confirm that triggering an abnormal electric and metabolic event consistent with the cortical spreading depression (CSD) of Leao is anatomically and functionally linked with migraine aura symptoms. Future drug discovery should focus on the interface between the excitable cell and the earliest events of CSD.

Brain Hyperexcitability: The Basis for Antiepileptic Drugs in Migraine Prevention

Epilepsy and migraine.

Migraine-like features sometimes characterize the headache that follows epileptic seizure (postictal headache, PIH). We compared patients with different types of epilepsy to investigate the association between migraine-like PIH and seizure type. Subjects comprised 364 patients with partial epilepsy. Epilepsy types were temporal lobe epilepsy (TLE, n = 177), frontal lobe epilepsy (FLE, n = 116), and occipital lobe epilepsy (OLE, n = 71). Patients participated in a structured interview pertaining to PIH as well as interictal headache and family history of migraine. Headaches were classified according to the International Headache Society criteria, which was modified for this study. Forty percent had PIH and 26% of these patients had migraine-like PIH. Migraine-like PIH occurred significantly more often in cases of TLE and OLE than in cases of FLE. In addition, the incidence of interictal migraine headache was significantly higher in patients with migraine-like PIH. These results suggest that migraine-like PIH is related to particular regions of epileptogenic focus and that susceptibility to migraine headache predisposes to migraine-like PIH.

Characteristics of Postictal Headache in Patients with Partial Epilepsy

Summary:  Purpose: Headache is often ignored as a symptom of epileptic seizures. The purpose of this prospective study was to analyze frequency, classification, and characteristics of seizure-associated headache (SH) according to the criteria of the International Headache Society.



Methods: Over a period of 15 months, 341 patients with epilepsy, consecutively evaluated at our outpatient clinic for SH, completed a standardized questionnaire.



Results: Of the 341 epilepsy patients, 115 (34%) experienced SH with a pain intensity of 6.1 ± 1.6 (SD) on the visual analogue scale and a duration of 12.8 ± 15.7 (SD) h. Seizures were always accompanied by headache in 69 (60%) of these 115 patients. SH occurred in four (3%) of 115 patients only preictally, in 31 (27%) of 115 patients periictally, and in 80 (70%) of 115 patients only postictally. In the majority of the 115 patients (55.7%), SH could be classified as migraine headache, whereas in 36.5%, as tension-type headache. The type of SH was not correlated with sex, an epilepsy syndrome, or a seizure type. Migraine-like SH was significantly associated with a history of migraine (p < 0.001). In 20 (77%) of the 26 patients experiencing migraine-like SH with a history of migraine, the phenomenology of migraine-like SH and migraine attacks was identical.



Conclusions: SH is a frequent, long-lasting, and severe symptom of epileptic seizures, causing major impairment of daily living. A history of migraine significantly increases the risk for developing migraine-like SH.

Seizure‐Associated Headache in Epilepsy

Objective.—Neuronal hyperexcitability might explain the comorbidity of migraine and epilepsy. Spreading depression, a postulated pathophysiological mechanism of epileptic seizures and migraine with aura, may hypothetically be the link between the disorders in these comorbid conditions. The aim of the present study was to determine whether certain clinical characteristics associated with spreading depression are overrepresented in patients with comorbidity.



Methods.—In an outpatient clinic-based series, clinical characteristics of 61 patients with a comorbidity of migraine and epilepsy were compared to those of 280 patients with epilepsy alone and 248 patients with migraine alone. Patients were interviewed with a standardized questionnaire.



Results.—The proportion of females was significantly higher in patients with comorbidity and patients with migraine as compared to patients with epilepsy (P  <  .001). Comparing patients with epilepsy and comorbidity, the frequency of epilepsy syndromes and seizure types was not significantly different. Comparing patients with migraine and comorbidity, migraine with aura was significantly more frequent in patients with comorbidity (P  =  .019). Other migraine features such as moderate to severe pain intensity, worsening of pain on activity, phonophobia, and photophobia were significantly more frequent in patients with comorbidity as compared to patients with migraine (P  ≤  .001).



Conclusion.—No specific epileptic characteristics could be found in patients with comorbidity. Altered cerebral excitability resulting in an increased occurrence of spreading depression may explain the differences in migraine attacks in patients with comorbidity as compared to patients with migraine alone.

Katrin Isbruch

Papers

Seizure‐Associated Headache in Epilepsy

Clinical characteristics of patients with comorbidity of migraine and epilepsy.