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 »  Abstract
 »  Prevalence of Co...
 » Reciprocal Risk
 »  Migraine and Epi...
 »  Neurological Con...
 »  Pathophysiologic...
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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 7  |  Page : 91-97

Borderlands of Migraine and Epilepsy

1 Department of Neurology, Lady Hardinge Medical College, New Delhi, India
2 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission01-Mar-2021
Date of Decision01-Mar-2021
Date of Acceptance15-Mar-2021
Date of Web Publication14-May-2021

Correspondence Address:
Dr. Manjari Tripathi
Room 705, Seventh Floor, CN Center, All India Institute of Medical Sciences, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.315994

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 » Abstract 

Background: The complex relationship between migraine and epilepsy has frequently been described to represent a clinical and electrographic “borderland.” These two conditions share clinical expressions such as paroxysmal and chronic nature, as well as semiology, particularly visual phenomenon.
Objective: We aimed to review the current literature on the overlapping phenomena of migraine and epilepsy.
Materials and Methods: We searched the PubMed for relevant literature and conducted a narrative review on migraine and epilepsy.
Results: Migraine and epilepsy share a complex and pathophysiologically intriguing relationship. The International Classification of Headache Disorders, 3rd edition (ICHD-3) makes diagnostic provisions for migraine aura–triggered seizures (Subchapter 1.4.4) and headache attributed to epileptic seizure (Subchapter 7.6), the latter being further categorized as 7.6.1 Ictal epileptic headache, and 7.6.2  post-ictal headache. Neurological conditions such as certain channelopathies and epilepsy syndromes exhibit both conditions within their phenotypic spectrum, suggesting shared genetic and molecular underpinnings. Diagnostic confusion may arise, particularly between occipital epilepsy and the visual aura of migraine. Antiseizure medications may be effective for the treatment of migraines that occur in concert with epilepsy.
Conclusions: Migraine and epilepsy share several clinical features and have intertwined genetic and molecular underpinnings, which may contribute to common pathogenesis. Electroencephalography may be useful as a diagnostic tool in selected cases.

Keywords: Epilepsy, headache, ictal epileptic headache, migraine, migralepsy, seizure
Key Messages: Migraine and epilepsy share common pathogenesis and semiology. This relationship is recognized by the International Classification of Headache Disorders, 3rd edition (ICHD-3), which classifies the overlap into migraine aura–triggered seizures and headache attributed to epileptic seizures, including ictal epileptic headache and post-ictal headache.

How to cite this article:
Garg D, Tripathi M. Borderlands of Migraine and Epilepsy. Neurol India 2021;69, Suppl S1:91-7

How to cite this URL:
Garg D, Tripathi M. Borderlands of Migraine and Epilepsy. Neurol India [serial online] 2021 [cited 2022 Jun 26];69, Suppl S1:91-7. Available from: https://www.neurologyindia.com/text.asp?2021/69/7/91/315994

Migraine and epilepsy share a complex relationship that has been acknowledged for several centuries. In 1906, Sir William Gowers first described this “borderland” of migraine and epilepsy, reporting that there may be “an actual blending” and that one may lead to the other.[1] Subsequently, in 1960, Lennox and Lennox-Buchthal coined the term “migralepsy” in their textbook, Epilepsy and Related Disorders.[2] In this, they reported a case of “ophthalmic migraine” where the typical symptoms of headache accompanied by nausea and vomiting were succeeded by a seizure. It follows that the term “migralepsy” refers to seizures following typical migraine although the indistinct nature of this term has been challenged because it does not define clearly the exact interrelationship between these two conditions.[3],[4],[5] Certainly, migraine and epilepsy share some similarities – both are paroxysmal neurological disorders that can be distinctly disabling and may, not uncommonly, occur in the same patient, thereby producing a “borderland.”[6]

The International Classification of Headache Disorders, 3rd edition (ICHD-3), highlights the relationship between migraine and epilepsy in two subchapters: 1.4.4 Migraine aura–triggered seizures and 7.6 Headache attributed to epileptic seizure.[7] The latter is further categorized into 7.6.1 Ictal epileptic headache and 7.6.2 post-ictal headache. Subchapter 1.4.4 describes the occurrence of seizures in association with or succeeding an episode of migraine with aura. Subchapter 7.6 is followed by a brief comment on “preictal headache.”

In this review, we examine the special interaction between these two neurological disorders and the implications of the same.

 » Prevalence of Comorbid Migraine and Epilepsy Top

Assessment of the coprevalent association between migraine and epilepsy is pivotal to an understanding of their relationship. Contradictory reports have emerged from various studies. Whereas some studies have observed an increased prevalence of migraine among persons with epilepsy up to 160%,[8],[9],[10],[11],[12],[13] others have not observed this association.[14],[15],[16] According to the Centers for Disease Control and Prevention (CDC), the presence of active epilepsy increases the prevalence of migraine or severe headache from 16.2% (among patients without epilepsy) to 35.5%.[17]

A systematic review and meta-analysis of population-based studies examined the lifetime relative prevalence of migraine among persons with epilepsy and vice versa.[18] The meta-analysis included 10 studies. It was observed that in comparison with people without epilepsy, patients with epilepsy harbored 52% increased migraine prevalence, with a prevalence ratio of 1.52 (95% confidence interval [CI, 1.29, 1.79]). Among persons with migraine, compared with nonmigraineurs, the prevalence of epilepsy was noted to be increased by 79% with the prevalence ratio being 1.79 (95% CI [1.43, 2.25]). Most of the heterogeneity between studies was attributable to the methodology used to ascertain the presence of migraine and epilepsy among the studies included. For the diagnosis of migraine, the tools used included unvalidated questionnaires (administered by parents to a child migraineur in some studies), semistructured interviews, structured interviews, validated questionnaires, telephone-based questionnaires, as well as International Classification of Diseases (ICD) and the International Classification of Primary Care (ICPC) codes. Similarly, for epilepsy, the tools used for epilepsy diagnosis included unvalidated and validated single-item questionnaires, telephonic single-item questionnaires, and ICD and ICPC codes. Studies that used ICD/ICPC codes and administrative information demonstrated lower prevalence estimates. The lifetime prevalence of migraine among epilepsy patients varied from 1.7% to 33.6% and among migraine patients, the lifetime prevalence of epilepsy was 0.7% to 2.3%. Several studies lacked clear definitions of epilepsy and migraine in this meta-analysis.

From India, a study from Kolkata reported the occurrence of seizures among 1,000 migraineurs (800 adults and 200 children) and their first-degree relatives.[19] One or more seizures were reported to occur in only nine of these patients. However, this was a single-center clinic-based study. Further population-based studies are required to assess the incidence and coprevalence of epilepsy and migraine among Indian patients.

 » Reciprocal Risk Top

A few studies have assessed the risk factors for coprevalence among different patient cohorts.

In a telephonic interview–based study among patients with epilepsy, their parents, and their siblings, the rate ratio for migraine was increased in both epilepsy patients and their relatives.[20] The highest risk was found to occur among female patients and among patients with epilepsy due to head trauma.

In a study among 50 children, most children with comorbid migraine and epilepsy were above 10 years of age and had idiopathic epilepsy.[21] Baldin et al., in a study from Iceland, found that children who had migraine with aura demonstrated 3.7 times increased risk of developing epilepsy, and this increase was across different types of seizures and across both genders.[10] However, the increased risk did not extend to children with migraine without aura.

An increased prevalence of migraine has been reported among children with Rolandic epilepsy than among children with partial epilepsy or without epilepsy.[22]

Migraine frequency has also been reported to be higher among patients with juvenile myoclonic epilepsy.[23],[24]

 » Migraine and Epilepsy within ICHD-3 Top

1.4.4 Migraine aura–triggered seizure

This is defined as a seizure triggered by an episode of migraine with aura. As per the ICHD-3 diagnostic criteria, the patient must have a seizure that fulfills the diagnostic criteria for one type of epileptic attack and must occur during or within 1 hour after an attack of migraine with aura. The condition, additionally, should not be better accounted for by another ICHD-3 diagnosis. True migraine followed by epilepsy termed “migralepsy” is mentioned as a comment in the ICHD-3 in this subsection. True migralepsy is considerably rare.[4] Epilepsy originating from the occipital lobe may be fallaciously considered as migraine aura–triggered seizures because it may occasionally manifest with only visual events and headaches.[25]

7.6 Headache attributed to epileptic seizure

In this condition, the headache is caused by a seizure, and it may occur during and/or after the seizure. The headache may remit within hours but may last up to 3 days. As per the ICHD-3 diagnostic criteria, a headache that occurs in a patient who is having or has had a seizure recently and the causation of the headache by the seizure must be demonstrated by both the following features: headache develops along with or soon after seizure onset and headache remits once the seizure ceases. The headache should not be better accounted for by another ICHD-3 condition.

Based on the temporal association between the headache and the seizure, this entity is further subdivided as ictal epileptic headache and post-ictal headache.

7.6.1 Ictal epileptic headache

This headache is caused by a focal seizure, occurs ipsilateral to the epileptiform discharges, begins during the seizures, and remits with seizure cessation or soon after. The term “ictal epileptic headache” has been included recently in ICHD-3. Diagnosis is based on the presence of headache in a patient with a partial seizure. The causative association needs to fulfill specific features: For example, the headache must begin concomitantly with the seizure. Additionally, at least one of the following two characteristics must be present: headache occurs on the same side as the epileptiform discharges and/or headache shows improvement or resolution with or soon after cessation of the seizure. As emphasized by Parisi et al., underrecognition of this condition may lead to errors in appropriate treatment.[26],[27],[28] Nonconvulsive status epilepticus in a patient with occipital epilepsy manifesting with migraine alone has also been reported in one patient; this was termed status epilepticus migrainosus.[29] An extremely rare variant of ictal epileptic headache is hemicrania epileptica, which requires an ipsilateral relationship between headache and the epileptogenic focus.[7]

7.6.2 post-ictal headache

Post-ictal headaches occur within 3 hours of a seizure and remit within 72 hours of the seizure.

The diagnosis, as per ICHD-3, requires the occurrence of a headache in a patient with recent partial or generalized epilepsy that must also satisfy two criteria for causation: The headache should develop within 3 hours of termination of the seizure, and it should resolve within 72 hours of the termination of the seizure.

Post-ictal headache may manifest in the form of tension-type headache or migraine. The frequency of post-ictal headache ranges from 12% to 52%.[30] Risk factors identified for the development of post-ictal headache include young adults, long duration of epilepsy, severe epilepsy, the occurrence of generalized tonic–clonic seizures, and interictal headaches in a patient with epilepsy.[30] Other risk factors include frequency of seizures and antiseizure medication (ASM) polytherapy.[31]

The diagnostic criteria of the aforementioned conditions as per ICHD-3 are summarized in [Table 1].
Table 1: ICHD-3 diagnostic criteria[7]

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Preictal headache

There are limited data on preictal headache, which receives a brief mention in the ICHD-3 wherein the need for more studies “to establish the existence of preictal headache” is described.[7]

This describes headache that precedes a seizure. In a small study among 11 patients with refractory epilepsy, the preictal headache was established through a standardized questionnaire.[32] The headache was observed to be ipsilateral to the epileptogenic focus in nine patients with temporal lobe epilepsy, contralateral in one patient with temporal lobe epilepsy, and contralateral in one with frontal lobe epilepsy. Among these, the headache was migrainous among four patients. Following epilepsy surgery, all patients who achieved seizure freedom also experienced resolution of headache, and two patients had infrequent seizures postsurgery.

The occurrence of an interval between the headache and the seizure favors true preictal headache. However, if there is no interval, Cianchetti et al. have suggested that to differentiate this from an ictal headache, epileptiform abnormalities on the electroencephalogram (EEG) should be sought.[3] The presence of EEG discharges favors ictal headache, although the absence of the same may not rule out an ictal headache.

Preictal migraine with aura may precede a seizure. The differential includes occipital epilepsy in which visual symptoms may occasionally occur in concomitance with migraine. The occurrence of a time interval would aid in the differentiation between the two as mentioned above. Additionally, characteristics of the visual aura may also help discern between the two conditions.[33] In occipital epilepsy, the visual hallucinations are elementary, colored circles develop rapidly and occur over short durations of time, that is, 2 to 3 minutes, and progress in size and number, moving from the temporal visual field to the opposite side. In migraine, the visual aura is composed of flashing zigzag lines that occur in the central visual field and have a gradual onset and longer duration up to 1 hour. However, an EEG may definitively demonstrate the epileptic nature of the visual aura. Preictal migraine without aura preceding seizures has also been reported.

[Table 2] summarizes some similarities, differences, and borderlands between migraine and epilepsy.
Table 2: Similarities, differences, and borderlands of migraine and epilepsy

Click here to view

 » Neurological Conditions that Manifest both Migraine and Epilepsy Top

Although migraine is known to be one of the comorbidities among epilepsy patients, certain neurological conditions may demonstrate both epilepsy and migraine as prominent clinical features [Table 3].
Table 3: Neurological disorders sharing migraine and epilepsy and pathophysiological basis

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The foremost among these are mitochondrial disorders. Among the spectrum of mitochondrial disorders, epilepsy and migraine may be prominent in mitochondrial encephalopathy, lactic acidosis, and stroke-like symptoms (MELAS), and POLG1 mutations. Both of these conditions demonstrate occipital predilection: In MELAS, strokes tend to affect the posterior circulation, and in POLG1 mutations, epilepsy emanating from the occipital lobes is frequent. This occipital preference in both these mitochondrial disorders points toward shared underlying pathogenetic mechanisms with migraine. Defective neuronal mitochondrial phosphorylation may provoke cortical spreading depression (CSD) leading to migraine.[34]

Certain channelopathies may also exhibit epilepsy as well as migraine among their gamut of clinical features. Mutations in channels CACNA1A, SCN1A, and ATP1A2 that lead to familial hemiplegic migraine (FHM) are also known to be associated with epilepsy. Abnormal function in these channels may provoke neuronal hyperexcitability and CSD.[35] In CACNA1-related conditions (CACNA1 codes for a voltage-gated calcium channel subunit), absence of epilepsy may occur along with FHM type 1, apart from episodic ataxia type 2 and spinocerebellar ataxia type 6. Mutations in ATP1A2 may lead to FHM type as well as benign familial infantile convulsions. Mutations in SCN1A are associated with several epilepsy syndromes, including Dravet syndrome, generalized epilepsy with febrile seizures plus (GEFS+), and FHM type 2.

In Sturge– Weber syndrome More Details (SWS), which is a rare phakomatosis, abnormal and asymmetric cerebral microvasculature development occurs, in association with port-wine stain. It is a multisystemic disorder in which up to 90% of patients may experience drug-refractory epilepsy and up to 60% may experience migrainous headaches. The association of hemiplegic migraine and SWS have also been reported.[36],[37],[38] Post-ictal headaches have also been reported, with the possible explanation being that neuronal hypersynchrony during the seizure activates CSD.

Mutations in the proline-rich transmembrane protein (PRRT2) gene lead to paroxysmal kinesigenic dyskinesia (PKD), which is a paroxysmal disorder triggered predominantly by movements. It may be associated with migraine, epilepsy, hemiplegic migraine, and a range of episodic neurological conditions.[39]

 » Pathophysiological Considerations Top

Although the pathogenetic shared underpinnings of migraine and epilepsy are not entirely understood, the following potential mechanisms have been described.

Neocortical hyperexcitability

Neocortical hyperexcitability, in association with genetic and molecular links, is a largely accepted hypothesis underlying both conditions.[40],[41] Neocortical hyperexcitability leads to a paroxysmal depolarizing shift in epilepsy. In patients with migraine, it is believed that neocortical hyperexcitability progressed into CSD. This spreading depolarization through the cortex also provokes fluctuations in neurotransmitter and calcium levels. This is succeeded by cortical suppression. These changes induced by CSD are believed to activate the trigeminal–vascular nociceptive system triggering pain. CSD, believed to be a shared event between migraine and epilepsy, also has a particular predilection for the occipital cortex. Other features supporting the role of CSD as a shared pathogenetic pathway include observations that post-ictal headaches are more frequent in persons with occipital epilepsy and response of migraine to ASM prophylaxis.

Channelopathies and shared genes

As discussed above, in FHM, mutations may occur in calcium channel 1A (CACN1A), ATP1A2, and sodium channel 1A (SCN1A). These channels are also associated with certain epilepsy syndromes, such as childhood absence epilepsy, Dravet syndrome (SCN1A), and generalized epilepsy with febrile seizures plus (GEFS+) [Table 3].

Mitochondrial dysfunction

Mutations in the POLG gene, which encodes for a subdomain of mitochondrial DNA polymerase, and C10orF2, which encoded for mitochondrial DNA helicase Twinkle have also been reported to play a role in the pathogenesis of both conditions. Putatively, mitochondrial phosphorylation dysfunction triggers neocortical hyperexcitability, provoking CSD.[42],[43]

“Migralepsy”: To be or not to be

The term “migralepsy,” coined by Douglas Davidson but mainly attributed to and as originally used by Lennox and Lennox-Buchthal, was based on the clinical sequence of migraine followed by an epileptic seizure.[2] After their description of three cases, the term was largely forgotten until it was revived in 1993 by Marks and Ehrenberg.[44] Despite the dubiousness surrounding the term, it was included in the ICHD-II.

As per the diagnostic criteria stated in the 2004 ICHD-II, migralepsy could be diagnosed if the patient had migraine fulfilling the criteria for a migraine with aura and a seizure fulfilling the criteria for one type of epileptic attack that should occur during or within 1 hour after the migraine aura.[45] However, the fallacies of this description were underscored in a study by Sances et al. who found that among the 50 cases of migralepsy reported in the literature up to that point in time, only two satisfied the definition as per ICHD-II.[4] Moreover, they reported a high prevalence of solely epileptic disorders among the so-called migralepsy reports.

In a multicentric retrospective study published by Verrotti et al. in 2011, all cases of migralepsy reported in the literature were revisited and 16 probable cases were identified. None of the remaining cases could satisfy the ICHD-II diagnostic criteria.[5] Many authors called for a revision of the then definition of migralepsy.[5],[46] There was wide consensus that many visual seizures and ictal headaches were mistaken for migraine and that the epilepsy–migraine sequence was more common than the migraine–epilepsy sequence (referred to as “migralepsy”).

Many discouraged the use of the term “migralepsy” to describe the sequence of visual aura followed by seizure because the former may be either epileptic or migrainous in origin.[47],[48] To confound matters further, there have been reports of both epileptic and migrainous visual aura occurring in the same patient.[49] A plethora of case reports of the so-called migralepsy preceded the diagnostic criteria put forth by ICHD-II.[50] Subsequently, the term was encompassed within Subchapter 1.4.4 in ICHD-3. However, this term does not find a place in the classification of seizures put forth by the International League Against Epilepsy.[51],[52]

Therapeutic implications

Migraine prophylaxis armamentarium in adults includes several ASMs. Most robust evidence among adults is available for valproate and topiramate. Among patients who have epilepsy in conjunction with migraine, antiepileptic therapy would be naturally preferred for antimigraine prophylaxis as well.

Topiramate may be preferred for glutamate antagonism, which may inhibit neuronal hyperexcitability responsible for both the seizure and cortical spreading depression of migraine.[6]

Lamotrigine has been described to be effective in managing migraine in patients with SWS, including hemiplegic migraine. The efficacy of lamotrigine in this condition is attributed to sodium channel blockade, leading to suppression of glutamate release, thereby negating the development of CSD.[38],[53]

 » Conclusions Top

Migraine and epilepsy share several clinical manifestations and have linked genetic and molecular underpinnings that may contribute to common pathogenesis. Therapeutically, ASMs may be effective when both are clinically expressed in a patient. Diagnostic guidelines for some of the conditions have been provided within the ICHD-3. Diagnosis may need EEG in certain selected cases where the suspicion of epilepsy masquerading as or in combination with migraine is high. Further and extensive research is necessary on pathophysiological mechanisms as well as optimum effective therapeutic strategies among patients harboring both migraine and epilepsy.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 » References Top

Gowers WR. Clinical lectures on the borderland of epilepsy. III.—Migraine. Br Med J 1906;2:1617-22.  Back to cited text no. 1
Lennox WG, Lennox-Buchthal MA. Epilepsy and Related Disorders. Vol 1. Boston: Little, Brown; 1960.  Back to cited text no. 2
Cianchetti C, Avanzini G, Dainese F, Guidetti V. The complex interrelations between two paroxysmal disorders: Headache and epilepsy. Neurol Sci 2017;38:941-8.  Back to cited text no. 3
Sances G, Guaschino E, Perucca P, Allena M, Ghiotto N, Manni R. Migralepsy: A call for a revision of the definition. Epilepsia 2009;50:2487-96.  Back to cited text no. 4
Verrotti A, Coppola G, Di Fonzo A, Tozzi E, Spalice A, Aloisi P, et al. Should “migralepsy” be considered an obsolete concept? A multicenter retrospective clinical/EEG study and review of the literature. Epilepsy Behav 2011;2:52-59.  Back to cited text no. 5
Crepeau AZ. Migralepsy: A borderland of wavy lines. Curr Neurol Neurosci Rep 2014;14:427.  Back to cited text no. 6
Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38:1-211.  Back to cited text no. 7
Gaitatzis A, Sisodiya SM, Sander JW. The somatic comorbidity of epilepsy: A weighty but often unrecognized burden. Epilepsia 2012;53:1282-93.  Back to cited text no. 8
Nuyen J, Schellevis FG, Satariano WA, Spreeuwenberg PM, Birkner MD, van den Bos GAM, et al. Comorbidity was associated with neurologic and psychiatric diseases: A general practice-based controlled study. J Clin Epidemiol 2006;59:1274-84.  Back to cited text no. 9
Baldin E, Ludvigsson P, Mixa O, Hesdorffer DC. Prevalence of recurrent symptoms and their association with epilepsy and febrile seizure in school-aged children: A community-based survey in Iceland. Epilepsy Behav 2012;23:315-9.  Back to cited text no. 10
Le H, Tfelt-Hansen P, Russell MB, Skytthe A, Kyvik KO, Olesen J. Co-morbidity of migraine with somatic disease in a large population-based study. Cephalalgia 2011;31:43-64.  Back to cited text no. 11
Téllez-Zenteno JF, Matijevic S, Wiebe S. Somatic comorbidity of epilepsy in the general population in Canada. Epilepsia 2005;46:1955-62.  Back to cited text no. 12
Hesdorffer DC, Lúðvígsson P, Hauser WA, Ólafsson E, Kjartansson Ó. Co-occurrence of major depression or suicide attempt with migraine with aura and risk for unprovoked seizure. Epilepsy Res 2007;75:220-3.  Back to cited text no. 13
Jalava M, Sillanpää M. Concurrent illnesses in adults with childhood-onset epilepsy: A population-based 35-year follow-up study. Epilepsia 1996;37:1155-63.  Back to cited text no. 14
Brodtkorb E, Bakken IJ, Sjaastad O. Comorbidity of migraine and epilepsy in a Norwegian community. Eur J Neurol 2008;15:1421-3.  Back to cited text no. 15
Mutlu A. Association between epilepsy and headache. Neurol Sci 2018;39:2129-34.  Back to cited text no. 16
Kobau R, Price PH, Giles HW, Pennell PB, Hargis E. Centers for disease control and prevention managing epilepsy well network. Epilepsy Behav 2010;19:216-7.  Back to cited text no. 17
Keezer MR, Bauer PR, Ferrari MD, Sander JW. The comorbid relationship between migraine and epilepsy: A systematic review and meta-analysis. Eur J Neurol 2015;22:1038-47.  Back to cited text no. 18
Chakravarty A, Mukherjee A, Roy D. Migraine, epileptic seizures and psychogenic non-epileptic seizures: Observations in Indian patients in a clinic-based study. Neurol India 2010;58:631-3.  Back to cited text no. 19
[PUBMED]  [Full text]  
Ottman R, Lipton RB. Comorbidity of migraine and epilepsy. Neurology 1994;44:2105-10.  Back to cited text no. 20
Yamane LE, Montenegro MA, Guerreiro MM. Comorbidity headache and epilepsy in childhood. Neuropediatrics 2004;35:99-102.  Back to cited text no. 21
Giroud M, Couillault G, Arnould S, Dauvergne M, Dumas R, Nivelon JL. Epilepsy with rolandic paroxysms and migraine, a non-fortuitous association. Results of a controlled study. Pediatrie 1989;44:659-64.  Back to cited text no. 22
Dedei Daryan M, Güveli BT, Baslo SA, Mulhan K, Sari H, Balçık ZE, et al. Prevalence and clinical characteristics of headache in juvenile myoclonic epilepsy: Experience from a tertiary epilepsy center. Neurol Sci 2018;39:519-25.  Back to cited text no. 23
Schankin CJ, Rémi J, Klaus I, Sostak P, Reinisch VM, Noachtar S, et al. Headache in juvenile myoclonic epilepsy. J Headache Pain 2011;12:227-33.  Back to cited text no. 24
Kasteleijn-Nolst Trenité D, Parisi P. Migraine in the borderland of epilepsy: “Migralepsy” an overlapping syndrome of children and adults? Epilepsia 2012;53:20-5.  Back to cited text no. 25
Parisi P, Verrotti A, Costa P, Striano P, Zanus C, Carrozzi M, et al. Diagnostic criteria currently proposed for “ictal epileptic headache”: Perspectives on strengths, weaknesses and pitfalls. Seizure 2015;31:56-63.  Back to cited text no. 26
Parisi P, Striano P, Trenité DGAK-N, Verrotti A, Martelletti P, Villa MP, et al. “Ictal epileptic headache”: Recent concepts for new classifications criteria. Cephalalgia 2012;32:723-4.  Back to cited text no. 27
Parisi P, Paolino MC, Raucci U, Della Vecchia N, Belcastro V, Villa MP, et al. Ictal epileptic headache: When terminology is not a moot question. Front Neurol 2019;10. doi: 10.3389/fneur. 2019.00785.  Back to cited text no. 28
Perucca P, Terzaghi M, Manni R. Status epilepticus migrainosus: Clinical, electrophysiologic, and imaging characteristics. Neurology 2010;75:373-4.  Back to cited text no. 29
Ekstein D, Schachter SC. post-ictal headache. Epilepsy Behav 2010;19:151-5.  Back to cited text no. 30
Mainieri G, Cevoli S, Giannini G, Zummo L, Leta C, Broli M, et al. Headache in epilepsy: Prevalence and clinical features. J Headache Pain 2015;16. doi: 10.1186/s10194-015-0556-y.  Back to cited text no. 31
Yankovsky AE, Andermann F, Mercho S, Dubeau F, Bernasconi A. Preictal headache in partial epilepsy. Neurology 2005;65:1979-81.  Back to cited text no. 32
Panayiotopoulos CP. “Migralepsy” and the significance of differentiating occipital seizures from migraine. Epilepsia 2006;47:806-8.  Back to cited text no. 33
Cevoli S, Pallotti F, La Morgia C, Valentino ML, Pierangeli G, Cortelli P, et al. High frequency of migraine-only patients negative for the 3243 A>G tRNALeu mtDNA mutation in two MELAS families. Cephalalgia 2010;30:919-27.  Back to cited text no. 34
Crompton DE, Berkovic SF. The borderland of epilepsy: Clinical and molecular features of phenomena that mimic epileptic seizures. Lancet Neurol 2009;8:370-81.  Back to cited text no. 35
Dora B, Balkan S. Sporadic hemiplegic migraine and Sturge-Weber syndrome. Headache 2001;41:209-10.  Back to cited text no. 36
Freilinger T, Peters N, Rémi J, Linn J, Hacker M, Straube A, et al. A case of Sturge-Weber syndrome with symptomatic hemiplegic migraine: Clinical and multimodality imaging data during a prolonged attack. J Neurol Sci 2009;287:271-4.  Back to cited text no. 37
Planche V, Chassin O, Leduc L, Regnier W, Kelly A, Colamarino R. Sturge-Weber syndrome with late onset hemiplegic migraine-like attacks and progressive unilateral cerebral atrophy. Cephalalgia 2014;34:73-7.  Back to cited text no. 38
Gardiner AR, Bhatia KP, Stamelou M, Dale RC, Kurian MA, Schneider SA, et al. PRRT2 gene mutations: From paroxysmal dyskinesia to episodic ataxia and hemiplegic migraine. Neurology 2012;79:2115-21.  Back to cited text no. 39
Berger M, Speckmann E-J, Pape HC, Gorji A. Spreading depression enhances human neocortical excitability in vitro. Cephalalgia 2008;28:558-62.  Back to cited text no. 40
Sowell MK, Youssef PE. The comorbidity of migraine and epilepsy in children and adolescents. Semin Pediatr Neurol 2016;23:83-91.  Back to cited text no. 41
Jancic J, Djuric V, Hencic B, van den Anker JN, Samardzic J. Comorbidity of migraine and epilepsy in pediatrics: A review. J Child Neurol 2018;33:801-8.  Back to cited text no. 42
Liao J, Tian X, Wang H, Xiao Z. Epilepsy and migraine—Are they comorbidity? Genes Dis 2018;5:112-8.  Back to cited text no. 43
Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy, with EEG correlation. Neurology 1993;43:2476-83.  Back to cited text no. 44
The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004;24:9-160.  Back to cited text no. 45
Parisi P, Kasteleijn-Nolst Trenité DGA. “Migralepsy”: A call for revision of the definition. Epilepsia 2010;51:932-3.  Back to cited text no. 46
Belcastro V, Striano P, Parisi P. Is it migralepsy? Still don't know. Headache 2015;55:1446-7.  Back to cited text no. 47
Belcastro V, Striano P, Parisi P. Is it migralepsy? No evidence yet. Neurol Sci 2013;34:1837-8.  Back to cited text no. 48
Hartl E, Rémi J, Noachtar S. Two patients with visual aura – Migraine, epilepsy, or migralepsy? Headache 2015;55:1148-51.  Back to cited text no. 49
Belcastro V, Striano P, Parisi P. From migralepsy to ictal epileptic headache: The story so far. Neurol Sci 2013;34:1805-7.  Back to cited text no. 50
Scheffer IE, Berkovic S, Capovilla G, Connolly MB, French J, Guilhoto L, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for classification and terminology. Epilepsia 2017;58:512-21.  Back to cited text no. 51
Fisher RS, Cross JH, French JA, Higurashi N, Hirsch E, Jansen FE, et al. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for classification and terminology. Epilepsia 2017;58:522-30.  Back to cited text no. 52
Nomura S, Shimakawa S, Fukui M, Tanabe T, Tamai H. Lamotrigine for intractable migraine-like headaches in Sturge-Weber syndrome. Brain Dev 2014;36:399-401.  Back to cited text no. 53


  [Table 1], [Table 2], [Table 3]


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