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Keywords:

  • Migraine;
  • Headache;
  • Epilepsy;
  • Migralepsy;
  • Photosensitivity;
  • Gowers;
  • Classification;
  • Diagnosis

Summary

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Gowers gave migraine a place in the borderland of epilepsy, justified by many relations and the fact that distinction of these two diseases is difficult. Gowers based his ideas on clinical histories from his patients, and he concluded that in extremely rare instances one may develop while the other goes on. In modern times, patient testimonies of the problem of differentiating migraine from epilepsy are given in health-chat Websites. It shows clearly that distinction between the two conditions is still problematic and that migralepsy is either nonexisting or extremely rare as Gowers noticed.

Sir William R. Gowers kept a list of “all cases, which seemed to be in the border-land of epilepsy – near it, but not of it.” As he wrote: “many were so placed by their features and character; others because they had given rise to an erroneous diagnosis” (Gowers, 1907).

Migraine is Number V of the six subjects listed in “The Border-land of Epilepsy.” Gowers starts by expressing the surprise one feels that migraine is at the borderland of epilepsy. However, he recognizes that migraine (“hemicrania”) is difficult to distinguish from epilepsy: “In extremely rare instances one affection may develop while the other goes on.” It is not entirely clear what he means by this. Most likely he refers to the parallel occurrence of both diseases but with differing times of onset; he does not necessarily mean that one provokes the other, either immediately or with a time lag. The question is whether migraine ever causes epilepsy.

He also gives examples of epilepsy and migraine alternating with each other, with “forced normalization” of the migraine attacks by the epileptic seizures. He describes a patient whose tonic–clonic seizures began 8 years after the migraine onset, in whom the migraine attacks often were provoked by a sudden change in light and not accompanied by headache. As he states: “the visual symptoms could thus be mistaken for a visual epileptic seizure (aura).”Figure 1 shows his concept of the co-occurrence of migraine and epilepsy.

image

Figure 1.   Time relationships of migraine (inline image) and epilepsy (inline image) (after Gowers, 1907; Chapter V).

Download figure to PowerPoint

Gowers stresses two symptoms that are particularly discriminative:

  • 1
     visual symptoms are short in epilepsy and long in migraine;
  • 2
     migraine headache is much more severe than postictal headache.

Modern testimonies also highlight the problem of differentiating migraine from epilepsy as follows:

  • Has anyone heard of migralepsy? I’ve had serious migraines for 16 years now and my doc has now said I might have migralepsy. He said it’s a form of epilepsy in the form of a migraine? I’m not sure if it is it until I get results back but was just wondering if anyone on here has heard of it or suffers from it? and can give me some info please. My son has epilepsy and they say it runs in family. I don’t see my doc till next week and would like to know what it is as its doing my head in not knowing. I should of asked him when I was there but I was a bit dumb struck. Thanks Mandy.

Answers:

  • I’m not sure I’ve ever heard of that.... I know that a lot of this neurology stuff is overlapping, though…. I guess my point is that there’s a whole lot of stuff that is open for interpretation and seems to be a bit of a gray area. There’s a lot they don’t know about the brain! And there can be links between migraines and seizures. Anonymous

  • “Migralepsy”? Sounds like a reasonable concept but it could be your headaches are really epilepsy. Headaches following seizures I have had frequently in the past (eyes became sensitive). Not to mention when given massive medications at the hospital they do a number on our senses. Travis

  • When my myoclonic jerks started they were so bad i would drop things or throw them. Sometimes i couldn’t speak or walk i jerked so bad. I do get enough sleep usually, due to my hubby’s schedule, actually my kids and i all lay down at night before 8 pm and then my hubby gets up at 3:30 am. I am however a very light sleeper, and at the least loud noise i do wake up. I do know that without the right amount of sleep, i usually end up with a migraine.

  • I’ve had migraines for almost 20 years. I think part of it is hormonal and well i am light sensitive. If i’m driving down the road and the sun reflects hard off of a car mirror and it goes in my eyes, i will have a migraine almost immediately following it. If i smell gas or a strange strong odor, i will have a migraine. I have a ton of triggers. My 6 day bout started with no vomiting, but i had light sensitivity. It ended the last 2 days with vomiting, diarrhea, and hot and cold flashes.

  • Every time i go to the ER, they treat my migraine with opiates or some type of pain med with phenegran or something for nausea. I try to handle mine at home, but if i can’t stop vomiting i go to the ER.

  • Since the myoclonic jerks, i’ve had more headaches than ever.

  • hello everyone, i am new here, and was prompted to find this site because well, it all started about 4 months ago. I began what they call myoclonic jerks or seizures, i am also a migraine sufferer, have been for a long time. Lots of my migraines have ended up in the ER. I just got over a 6 day bout, which ended up in the hospital getting a Depakote drip. Prior to this 6 day marathon, about 3 days into it i experienced numbness in parts of my face and arm which lasted for 2 h. And then finally went away. My neuro had me on zonisamide and clonazepam for myoclonic seizures and migraines, as well as Relpax (=eletriptan, a serotonin receptor agonist), which i feel i eat like candy. I have a headache about every day, and of course some days are worse. My seizures changed along with the numbness, which provoked me to research. Instead of some jumps and jerks, well i started to draw up on one side and couldn’t speak with each attack (at least once a day). I heard of migralepsy, i just wonder if my dr. has! After this last bout he blamed numbness on my migraine, which shocked me. He was so unworried about it, while me well, i just thought wow, i’m scared. I’ve never had a migraine do that. He changed my epilepsy medicine, but still on Relpax, and hydrocodone for my unbelievable neck pain. People kill me when they don’t understand migraines. They say oh it’s just a headache get up. Well, i’ve struggled and pushed my way through each headache!…Can anyone relate? Or am i just crazy!

These Web-testimonies of the confusion of epilepsy—and migraine—symptomatology contain the same items as Gowers noted and described.

What Is Migralepsy, Where Does It Come from and Who Uses This Term?

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Migralepsy literally comes from combining the words migraine and epilepsy. Migralepsy was introduced by Lennox & Lennox (1960) to describe a condition wherein “ophthalmic migraine (= migraine with aura) is followed by symptoms characteristic of epilepsy.” Since then, there have been reports of only about 60 cases of migralepsy (Verrotti et al., 2011). A recent Embase search on “migralepsy” found 31 reviews/debates between 1999 and 2012, and 16 of them with case descriptions: 12 were published in epilepsy journals, 9 in headache journals, and 10 in general neurology journals. Overall, many more epilepsy specialists than headache specialists showed interest in migralepsy and debated this subject. Despite this, migralepsy as such appears in the headache classifications and not in the epilepsy classifications (see below).

In the most recent International Classification of Headache Disorders (ICHD-II) of the International Headache Society, migralepsy was defined as migraine-triggered seizures ICHD-II (1.5.5):

  • Official text:

  • 1.5.5 Migraine-triggered seizure

  • Description: A seizure triggered by a migraine aura.

Diagnostic criteria:

  • A. Migraine fulfilling criteria for 1.2 Migraine with aura

  • B. A seizure fulfilling diagnostic criteria for one type of epileptic attack occurs during or within 1 h after a migraine aura

Comment:

Migraine and epilepsy are prototypical examples of paroxysmal brain disorders. Although migraine-like headaches are frequently seen in the postictal period, sometimes a seizure occurs during or following a migraine attack. This phenomenon, sometimes referred to as migralepsy, has been described in patients with migraine with aura.

Migralepsy is not included in the official current International League Against Epilepsy (ILAE) seizure classification from 1981, or in more recent recommendations of the ILAE Commission on Classification and Terminology (Engel, 2001; Berg et al., 2010).

Why Is Migralepsy Being Discussed?

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Migralepsy is discussed for several reasons:

  • It is surprisingly rare and therefore intriguing.

    • Migraine is common (prevalence about 10%) and epilepsy has a prevalence of about 1%; these are two of the most common conditions in pediatric neurology.

    • Nevertheless, there have been only about 60 cases of possible migralepsy described in children and adults (for overviews, see Sances et al., 2009 and Verrotti et al., 2011). By reviewing these cases rigorously—ictal electroencephalography (EEG) data were normal in 4% and not recorded in 68%– and by applying the ICHD-II criteria strictly, these authors reduced them to only one possible migralepsy case.

  • The diagnosis is difficult

    • It is difficult to make a definite diagnosis of migraine (phenotypically heterogeneous), since there are no objective tests and markers. It is therefore not surprising that prevalence studies thus show a wide variability: 1-year prevalence ranging between 1.0% and 15.3% and lifetime prevalence between 2.6% and 27.5% (Breslau & Rasmussen, 2001). Similarly, there is a wide range of comorbidity of migraine and epilepsy: among epilepsy patients, the prevalence of migraine is 7–26% and in migraine patients, the prevalence of epilepsy is 1–17%. Lance and Anthony performed a strict and detailed study in Sydney, Australia, with standardized history-taking in 1,152 headache clinic patients: they compared the first 500 patients with clear migraine complaints only, with 100 patients who had tension headache only. Although the prevalence of epilepsy was higher in both groups than in the normal population, there was no statistically significant difference in epilepsy prevalence between the two groups (1.6% for migraine, 2.0% for tension headache), and no excess positive family histories of epilepsy (Lance & Anthony, 1966).

A diagnosis of migralepsy requires that there is a temporal relationship between the migraine aura and a seizure event (within an hour). However, the apparent “migraine” aura could be just part of the seizure itself; thus a visual epileptic aura is simply followed by the second phase of the seizure (secondarily generalization of the focal epileptiform discharges). Gastaut recognized occipital epilepsies in 1982 and described their corresponding clinical and EEG symptoms in about 5% of epilepsy patients. Since then, Panayiotopoulos (1987, 1999) and others have stressed the difficulties in distinguishing epileptic occipital aura from migraine aura, particularly if there is no precise history about the color, shape, and development of the visual disturbance:

  • a
    Migraine visual aura starts as a flickering, uncolored, zigzag line in the center of the visual field, progressing over 4–30 min toward the periphery of one hemifield, and a scotoma often follows. The total duration of the migraine aura is about 60 min.
  • b
    Ictal elementary visual hallucinations of occipital lobe epilepsies are mainly colored and circular, develop rapidly (within seconds) and are relatively brief (2–3 min). They often appear in the periphery of a temporal hemifield, widen and multiply during the seizure, and frequently move horizontally toward the contralateral side.

In clinical practice, however, such a distinction is not always easy. Visual symptoms may be restricted to blurred vision or be more of a mixed type (Walker et al., 1995; Dainese et al., 2011). Brief visual seizures may be followed by headache and vomiting, thus making them indistinguishable from migraine (Panayiotopoulos, 1987, 1999). Furthermore, headache itself may even be ictal, as in the following two examples:

  • 1
    An epileptic“aura”of a seizure. Patients with focal epilepsies but no migraine may have so-called preictal headache, which disappears when the patient becomes seizure-free, for example, after epilepsy surgery (Yankovsky et al., 2005)
  • 2
    An ictal epileptic manifestation itself. A 37-year-old woman with idiopathic generalized epilepsy reported headache symptoms that were synchronous with bursts of generalized epileptiform discharges (Fanella et al., 2012).

Headache can therefore be an epileptic phenomenon (“ictal headache”) (Piccioli et al., 2009; Parisi & Kasteleijn-Nolst Trenité, 2010).

EEG abnormalities can be similar in migraine and occipital epilepsy

Both interictal and ictal EEG abnormalities in patients with migraine comprise mainly (a)symmetrical (high voltage) theta bursts, located over the temporooccipital areas (Walker et al., 1995; Bjørk et al., 2011). Patients with epileptic visual symptoms may show similar EEG abnormalities (Holzbach, 1975; Gastaut, 1982; Piccioli et al., 2009). Patients with ictal autonomic manifestations, as in Panayiotopoulos syndrome or from a deep epileptic focus in the orbitomesial frontal zone, may not show clear epileptiform spikes and spike and wave activity (Parisi et al., 2005; Koutroumanidis, 2007). Scalp EEG recordings might therefore record only theta or delta waves, reflecting the subcortical abnormalities.

Influence of Bright Lights and Computer Screens; Photosensitivity

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Most migraineurs (50–70%) have photophobia (Kelman, 2006; Choi et al., 2009). In 13–57%, this includes migraine provocation by visual stimuli such as bright sunlight, TV screens, and patterns (Choi et al., 2009).

Photophobia is mentioned sporadically in epilepsy. However, only about 5% of patients—mainly children and adolescents—have seizures triggered by visual stimuli, such as flickering sunlight, TV, and patterns (Kasteleijn-Nolst Trenite, 1989).

Wendorff & Juchniewicz (2005) studied the prevalence of a photoparoxysmal response (PPR) in 263 migraine patients aged 7–18 years: this was most common in patients younger than 12 years and in people with migraine with aura (17.6%); 7 of these 12 patients had headache exclusively provoked by visual stimuli. Similarly, Piccinelli et al. (2006) in a somewhat younger age group found a PPR in 30% of children with migraine with aura (median age 10 years), far higher than in a healthy population of children (PPR prevalence 1.4%) or epilepsy patients in general (5%).

Patients with photosensitive epilepsy report pain in their eyes significantly more often during intermittent photic stimulation (and PPRs) than nonphotosensitive patients (18% compared to 2%) (Kasteleijn-Nolst Trenite, 1989). Pain in the eyes also occurs in migraineurs, but the prevalence is not known, since it is considered part of photophobia. Recent positron emission tomography studies have shown lack of habituation and/or cortical hyperexcitability to light in migraineurs. The studies also demonstrated multisensory integration, confirming the abnormal interrelationship between light perception and trigeminal nociception (Boulloche et al., 2010). Ictal photophobia was also linked with visual cortical hyperexcitability (Denuelle et al., 2011). Visual evoked potential studies also showed a lack of habituation in visual processing in patients with photosensitive epilepsy (Brazzo et al., 2011).

Light as a consistent trigger for migraine is especially likely in migraine with aura; 47% of Danish adults recognized that light—especially reflected sunlight—caused at least 50% of their migraine attacks (only hormonal changes were a more frequent cause) and that the time between the triggering light and the attack was the shortest for any triggers (Hauge et al., 2011).

When visual stimuli evoke occipital seizures, the type of epilepsy is photosensitive occipital epilepsy; in these patients, PPRs can be evoked with intermittent photic stimulation. This subtype of epilepsy comprises 0.7% of epilepsy patients (Guerrini et al., 1995). This photosensitive occipital epilepsy has several features in common with migraine with aura:

  • 1
     high prevalence in women (female-to-male ratio 2:1) with an earlier onset in male than female patients
  • 2
     sensitivity to light stimuli and striped patterns, with provocation of attacks
  • 3
     visual aura with positive and negative ictal features
  • 4
     autonomic disturbances, such as pallor and vomiting
  • 5
     slow spreading of ictal EEG abnormalities, originating in the occipital area.

A proper differential diagnosis is only possible with an ictal EEG. This is illustrated by the following three cases:

  • 1
     A 14-year-old photosensitive girl had status migrainosus for 3 days. Standard analgesic therapy had not helped, and the headache resolved only after diazepam 10 mg intravenously. Continuous EEG recording during the headache showed epileptiform discharges over the right occipital region, which disappeared 7 min after the diazepam injection, with the headache resolving 3 min later. Of interest, the migraine status was provoked by prolonged TV viewing (a new, large-screen TV) and by visiting an exhibition with much color and contrast (Parisi et al., 2007). This relatively long delay of epileptic phenomena after visual stimulation is rather typical for occipital photosensitive epilepsies. In this case, the headache was a photosensitive occipital seizure.
  • 2
     A 25-year-old computer systems analyst had headaches with photophobia and nausea starting 2 min after working on a computer; he consulted a headache specialist. He worked out that changing the screen frequency from 60 to 75 Hz abolished his headaches (Kowacs et al., 2004). Perhaps he had photosensitive occipital epilepsy, but there was no EEG recording.
  • 3
     A 23-year-old woman with a history of migraine with aura (onset at 13 years) and epilepsy (juvenile myoclonic) since age 15 years, had a “migralepsy” attack captured on an EEG. After a typical visual aura with slow waves over the frontotemporal regions, she went into a generalized tonic–clonic seizure with generalized epileptiform discharges (Labate et al., 2011). Her EEGs had shown PPRs.

Are Children Different from Adults?

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Children are more likely to have autonomic symptoms, especially during seizures, and to have isolated long-lasting ictal autonomic manifestations. By contrast, in adults, ictal autonomic manifestations are usually associated, simultaneously or sequentially, with other motor or sensory ictal features (Foldvary-Schaefer & Unnwongse, 2011). Evaluation of (presurgical) temporal lobe seizures recorded on video-EEG has indeed shown that abdominal epilepsy, characterized by episodic abdominal pain, nausea, vomiting and confusion, is a common autonomic manifestation of temporal lobe epilepsy in children (Fogarasi et al., 2006). The tendency for rapid propagation of occipital seizures, especially to the temporal lobes, might explain why parietooccipital seizures have predominant autonomic symptoms and can be mistakenly diagnosed as migraine.

In children, migraine without aura is five times more common than migraine with aura (compared to adults, where it is 3–4 times more common). In addition, there is not such an overwhelming female preponderance in children as in adults (1.8:1 in children vs. 2.8:1 in adults) (Schürks et al., 2009; Toldo et al., 2010). A recent study of children with headache showed that 56 (3%) of 1,795 had both headache and epilepsy; most often this was migraine. In 44%, the onset of epilepsy preceded that of the headache; in 27% headache started first and in 29% both started in the same year. There were no cases of “migralepsy” (Toldo et al., 2010). It is interesting to note that the vast majority of the 56 cases with both headache and epilepsy had cryptogenic or idiopathic focal epilepsy; yet 12.5% showed a PPR (much higher than in a general epilepsy population).

Genetics and Family Studies

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

To date, there are no causative genes or probability loci in “migralepsy.” Some studies have analyzed families with both epilepsy and migraine. Familial occipitotemporal lobe epilepsy and migraine was linked to chromosome 9q (Deprez et al., 2007) in a five-generation family, where epilepsy and migraine co-segregated nicely. The affected family members had migraine and epilepsy and were photosensitive (Deprez et al., 2007). The apparent association between migraine and epilepsy might be because the migraine was an epileptic aura of occipital seizures; thus the locus may relate to occipital epilepsy.

Another five-generational family with febrile seizures, epilepsy (generalized tonic–clonic seizures), migraine either with (22%) or without aura (33%), and a PPR in some patients, showed linkage to chromosomes 14q and 12q (Polvi et al., 2012). Both loci are linked to epilepsy and migraine. All but one patient became seizure-free during adolescence.

Photosensitivity was shown to be important in four families with both headache and epilepsy: the first-degree relatives of probands with both photosensitivity and headache underwent a routine EEG and extensive standardized intermittent photic stimulation; 9 of the 12 subjects (10 female and 2 male, mean age 30 years, range 14–46 years) were photosensitive, with either focal (n = 5) or generalized (n = 4) epileptiform discharges. Two subjects had an ictal recording of headache after visual stimulation (Piccioli et al., 2009).

Does Migralepsy Exist?

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Diagnosing “migralepsy” has a lot to do with the inability to discriminate visual aura from migraine and epilepsy; most likely there is an overlap in both disorders in the expression of visual disturbances (not just colored vs. black and white). In addition, interictal scalp EEG studies are often not conclusive.

Most reported cases of migralepsy are complicated and do not have an unequivocal migraine–epilepsy sequence; thus they may be considered as genuine (photosensitive) epileptic occipital seizures that resemble migraine with aura, the seizures being characterized by visual aura, headache and other autonomic symptoms. Migraine patients with aura often find it difficult to distinguish between triggering of the migraine by bright lights and the visual aura itself. EEG studies with standardized photic stimulation (Kasteleijn-Nolst Trenité et al., 2012) are recommended in “headache and migralepsy” patients who have a family history of epilepsy and migraine, to distinguish photosensitive occipital epilepsy from migraine.

Headache can even be a sole ictal epileptic event. Children especially may have a lower threshold for triggering cortical spreading depression (CSD) than that required for an epileptic focus. In other words, an epileptic seizure may facilitate the onset of CSD to a greater degree than CSD facilitates the onset of epileptic seizure. Thus headache develops frequently after an epileptic seizure but it is rare indeed for a migraine attack to trigger an epileptic seizure (Parisi et al., 2008).

Thus migralepsy most likely does not exist.

What About Gowers?

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

Gowers, being an excellent clinician and not having the chance to record scalp or depth-electrode EEG studies, was most likely right: “The most frequent relation of migraine to epilepsy is as source of error.” In extremely rare instances one affection may develop while the other goes on—meaning that one can have both migraine and epilepsy in parallel without being “migraleptic,” a diagnosis he actually never made.

Migraine is indeed in the borderland of epilepsy.

Disclosure

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References

The authors have no conflicts of interest to disclose. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

References

  1. Top of page
  2. Summary
  3. What Is Migralepsy, Where Does It Come from and Who Uses This Term?
  4. Why Is Migralepsy Being Discussed?
  5. Influence of Bright Lights and Computer Screens; Photosensitivity
  6. Are Children Different from Adults?
  7. Genetics and Family Studies
  8. Does Migralepsy Exist?
  9. What About Gowers?
  10. Disclosure
  11. References