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The Migraine- Epilepsy SyndromeArch Neurocien (Mex)Vol 11, No. 4: 282-287, 2006

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The migraine-epilepsy syndrome

Enrique Otero Siliceo, Fernando Zermeo

Arch Neurocien (Mex)Vol. 11, No. 4: 282-287, 2006

INNN, 2006

Artculo de revisin

de caso

EL SINDROME MIGRAA-EPILEPSIA

RESUMEN

La migraa y la epilepsia tienen varios puntos en comnsintomtica clnica y genticamente lo que ha sidopostulado por ms de cien aos. El fenmeno referidocomo migraa-epilepsia sugiere que exista unapatofisiologa comn. El sndrome de migraa oepilepsia tiene fenmenos comunes de dolor adominal jaqueca anormalidades del EE y respuesta a drogaantiepilpticas. En ocasiones el paciente puede tenerun ataque migraoso o una convulsin o en otrasambas. La comorbilidad puede explicarse por estados

de hiperrexcitabilidad neural. Alteraciones electroen-cefalogrficas son comunes en estos estados. Enapariencia el glutamato tiene un papel importante tantoen la migraa como en la epilepsia. Segn el lbuloafectado los sntomas premtorios pueden variar dealteraciones visuales a gstricas, por lo que no debenusarse divisiones artificiales.

Palabras clave: migraa, epilepsia, alteraciones comu-nes, electroencefalograma.

ABSTRACT

Migrane and epilepsy have common points from theclinic symptomatic and genetic view and this has beingnoticed for more than hundred years. The migrainepilpetic syndrom sugest a common pathophysiologywith simptoms as abdominal pain, headacheabnormalities at the spiral fluid and good response toantieplieptic drugs some times the patient might haveboth symptoms headache and convultions and both

Recibido: 13 enero 2006. Aceptado: 30 enero 2006.

Subdireccin de Neurologa. Instituto Nacional de Neurologa y

Neurociruga. Correspondencia: Fernando Zermeo Polhs.

Subdireccin de Neurologa. Instituto Nacional de Neurologa y

Neurociruga. Insurgentes Sur # 3877. Col. La Fama, 14269, Mxico,

D.F.

represent a neural exitation. Since that the glutamatehas in important rol in both patologys depending of

the part of the brain more affected the symptoms mightvary from visual to abdominal phemomena.

Key words: migraine epilepsy, EEG abnormalities,glutamate, diagnosis.

he first steps of a practical, approach byphysicians in recognizing and treating neuro-logic diseases are to recognithat there are

various overlaps between migraine and epilepsy.Epileptic seizures and classic migraine episodes mayoccur in the same patient. Migraine and epilepsy shareseveral genetic, clinical, evolutive and neurophysio-

logic features. A relationship between epilepsy andmigraine has been postulated for over a hundred yearsand the syndrome of Migraine-Epilepsy illustrates thiscomplex relationship between both.

Clinically, the diagnosis of epilepsy is supportedby additional positive motor phenomena or by atransition into a complex partial seizure, e.g. whenepileptic activity secondarily spreads into a temporallobe. Secondarily generalized seizures, however, mayalso occur in patients with migraine. The complexrelationship between migraine and epilepsy ishighlighted by the occurrence of a seizure during amigraine attack without aura. This phenomenon,

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Enrique Otero SiliceoArch Neurocien (Mex)

Vol 11, No. 4: 282-287, 2006

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referred to as Migralepsy, suggests an inherentoverlap in the underlying pathophysiology of theseevents17.

A general pathogenetic model of migraine andseizures may be characterized by a given predis-

position, various co-factors which enhance thetendency, and finally, trigger mechanisms, which indu-ce an attack. In assessing the importance of variousfactors thought to be related to idiopathic migraine-epilepsy syndrome, it is necessary to differentiatebetween causal relation, unspecific association, andcoincidence.

The syndrome of migraine-epilepsy is infrequentphenomena with paroxystic episodes of headache orabdominal pain, awareness, EEG abnormalities andpositive results with the introduction of antiepilepticdrugs. The most constant characteristic is the

paroxysmal occurrence of the symptoms, frequentlytriggered by emotional stress, fatigue or flashing light,heralded by prodromal signs and symptoms such aspallor, flushing, sweating, languor, irritability anddizziness and on occasions sensory disturbances ortransient hemiparesis, followed by sleep. A individualmay have a seizure on one occasion and a classicattack of migraine on another. Histories of children withepilepsy occasionally disclose that the seizures havebeen preceded for several years by attacks ofmigraine. However, epilepsy is more likely to becomemigraine than migraine to become epilepsy. A familialhistory of the syndrome is present in 70 to 85 per cent

of children with migraine and in 3 to 8 per cent of thosewith epilepsy. The history of migraine is more commonin the families of epileptic patients than in the normalpopulation.

The syndrome has been elaborated with basesin his clinical features and in the EEG contributions andlong-term video/EEG that has allowed improveddifferentiation between epileptic syndromes and non-epileptic disorders that may mimic epilepsy clinicallyor migraine disorders; recognition of its relativelybenign course may prevent unnecessary investigationand undue alarm.

A critical review of the data indicative of arelationship between migraine and epilepsy show thatthe pathogenesis point towards their combinedoccurrence are frequent.These data are consideredunder five major headings: genetic, epidemiological,clinical, electroneurophysiological and neurochemical.

Besides purely coincidental combinations, avariety of reasons is held responsible for this side-by-side occurrence.

The relation of migraine and epilepsy

The two conditions were thought to be closelyrelated by Liveing and Vining, while others held that theoccurrence of migraine and epilepsy in the same

patient is probably coincidental, for example Bramwell,Alvarez and Brain. In discussing the relation of migraineand epilepsy, Gowers in 1907, began with alterationwhere one replaces the other in the same subject butalso observed that epileptic attack and paroxysmalheadaches may coexist.

Dealing with the premonitory symptoms ofmigraine and their distinction from epilepsy, heemphasized the difference in duration and also pointedout that when isolated prodromas occur, they are oftenvery much briefer than when followed by headacheand might easily be thought to be minor epilepticseizures but the identity of character with those that

preceded the headaches made their nature certain.

Risk for migraine and epilepsy

In adults, Marks and Ehrenberg studied therelationship between migraine and epilepsy in 395seizure patients, 20% also had migraine syndrome and3% of these patients experienced seizures during orimmediately following a migraine aura. Patients withcatamenial epilepsy and patients with migraine withaura were at an increased risk for an associationbetween these two disorders.

Lees and Watkins found only 2.1 per cent of ilieircases of migraine showed features of epilepsy, and

Lance and Anthony found the same incidence ofepilepsy, 2 per cent, both in their series of migraineand tension headaches. Ely in 1930, from the ancestralhistories, concluded that migraine is possibly themorbid ancestor of both migraine and epilepsy.

Classical investigations have shown that epilepsyoccurs more commonly in patients with migraine thatwould be expected by chance (Slatter 1968,Hockaday and Whitty 1969) although the frequency ofthe association varies from study to study. By the otherhand, the incidence of migraine studied in severalgroups of patients show that migraines were present in62% of the patients with centro-temporal epilepsy, 34%of the patients with absence of epilepsy, 8% of thepatients with partial epilepsy and 6% of the patientswith cranial trauma. These results suggest that theassociation of centro-temporal epilepsy and migraineis non-fortuitous as well as, to a lesser degree,absence of epilepsy and migraine and that centro-tem-poral epilepsy together might be a feature for thediagnosis of migraine.


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Migraine in childhood and adolescence seemsto be definitively associated with vegetative dysfunction,abdominal symptoms and hormonal factors andpossibly with allergic reactions, whereas a relation toepilepsy can be excluded.

Pathogenic models of the syndrome of migraine-epilepsy

Electroencephalographic abnormalities

The comorbidity of migraine and epilepsy maybe explained by a state of neuronal hyperexcitabilitythat increases the risk of both disorders. Individuals withepilepsy are 2.4 times more likely to develop migrainethan their relatives without epilepsy. Risk of migraine iselevated in patients with partial-onset and generalized-onset seizures. There are rare seizures, either focal orgeneralized, usually followed a migrainous aura thatseemed to be readily controlled with anticonvulsantmedication. Whether the syndrome is migrainous orepileptic has yet to be elucidated.

Electroencephalographic abnormalities are seenin 50 to 70 per cent of children with migraine and 80to 90 per cent of those with epilepsy as compared to15 to 20 per cent in the normal population. A positivespike pattern of 14 and 6 cycles per second wasdemonstrated by Whitehouse and his co-workers in 46per cent of children with migraine as compared to18 per cent in normal controls. Chao, et alfind that50 per cent of children with convulsive-equivalentepilepsy also has this spike abnormality in their elec-

troencephalograms. This EEG pattern disturbance isthe primary factor in migraine, vascular and humoralfactors being secondary manifestations.

Electroencephalographic abnormalities withtemporo-parieto occipital or temporo-occipital spikesor spike-wave complexes suppressed by eye openingshow different neurological syndromes: migraine withaura, vertebrobasilar migraine, visual phenomena,epilepsy, psychomotor retardation and syndrome ofmigraine-epilepsy. All of the EEG finding of occipitalspike-wave complexes seems to extend to differentneurological syndromes.

The high incidence of EEG abnormalities was first

noted in patients with migraine by Dow and Whitty andsubsequently by Selby and lance, Lees and Watkins,Barolin, Otero, et al and Townsend, the latterquestioning their diagnostic importance. Ziegler andWong found a high percentage of paroxysmaldisorders in children with migraine and to a less extentin their siblings. Smyth and Winter described a photicdriving response to high frequencies in patients withmigraine, and Towle found the most significant thing

was an exaggerated and prolonged response tohyperventilation. Slatter concluded that the response tophotic stimulation reflected a constitutional predispo-sition to migraine and suggested that permanentcerebral damage resulting from migraine may produ-

ce abnormal electroencephalographic findings andrarely cause local epileptic changes. This suggestionis very difficult to substantiate simply based on atemporal sequence of events in successive elec-troencephalograms. The generally dysrhythmicelectroencephalograms of some migraine patientscould not be distinguished from certain of theepilepsies and that the aura in migraine is associatedwith cortical firing, differing only in degree but not inkind from other paroxysmal cortical discharges.

Spreading depression of activity of the cerebral cortex

The higher speed of trans-synaptic propagationof epileptic discharges and postictal inactivation cau-ses a more rapid time-course of the epileptic aura ascompared to a migraine aura resulting from adepolarization spreading by diffusion. Records of theentire sequence from migraine aura to partial seizureshow distinctive changes on the EEG during themigraine aura that preceded the onset of anelectrographic complex partial seizure.

Leaos first paper on Spreading Depression ofActivity of the Cerebral Cortex appeared in 1944. Thestudy originated in an attempt to secure more data forthe understanding of the electrocorticogram which

occurs in experimental epilepsy and of the conditionsin which it is brought forth by electrical stimulation.Early in the development of the study, an interestingresponse elicited by electrical stimulation was noticedin 1he cortex of rabbits. The distinctive feature of thisresponse was a marked enduring reduction of thespontaneous electrical activity of the cortex. Thedepression slowly spread in all directions, succe-ssively affecting adjacent areas.

Spontaneous activity at the stimulated regionwas often well recovered at a time when the depressionwas just starting in distant parts. Specific activitydifferent from the spontaneous often developed during

the period of depression of a region. The mostcommon type of this activity was composed of largeslow localized potential waves during which oneelectrode became negative with respect to others 1-3mm. distant. Fast components might also appear andthe activity, when intense, closely resembled theseizure pattern of experimental epilepsy. Milner notedcorrespondence between the scotomas of migraineand the spreading depression of Leao. He drew his


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ESTE DOCUMENTO ES ELABORADO POR MEDI-

GRAPHIC

evidence from Lashleys paper from 1941, on patternsof cerebral integration indicated by scotomas ofmigraine.

Interictal and ictal EEG recordings can beimportant to prove an epileptic origin, but their

sensitivity is low if ictal discharges remain limited to asmall brain area. In rare cases, measurements of ictalcerebral perfusion can contribute to the differential diag-nosis.

There is a possible connection between scotomain migraine and epileptic discharge It is proposed thatspreading depression, as the basis of the migraineprodromata, is preceded by a moment of intenseneuronal excitation which change the epilepticintercritical activity into a critical one10. In some casesthe EEG show an epileptogenic occipito-temporalfocus that correspond to the region of the scotomaorigin.

Glutamate metabolic actions in neuronal excita-

tory modulation

It has become increasingly apparent thatglutamate occupies a central position in the deve-lopment of epilepsy or in the onset of a migraineincident. The importance of glutamate is explained bya variety of functions in the CNS: as a dominantconstituent of many proteins, by its intermediary rolein linking energy metabolism to that of many otheramino acids, and as the virtually exclusive precursor ofGABA.

Moreover, glutamate serves as the primarysubstrate in ammonia detoxification and the product,glutamine, actively participates in CSF waterhomeostasis.

Glutamate occupies by its direct electrophysio-logical and metabolic actions on neurons and glia, viaat least four distinct types of receptor proteins, and isimplicated in a number of critical mechanisms ofinformation. These include neuronal excitatorymodulation, intracellular Ca2+ redistribution, and keymetabolic (phosphorylation) mechanisms. Thephenomena, when exaggerated due to excessiveextracellular glutamate levels, may cause pathological

effects such as hypersynchrony-epilepsy, SpreadingDepression- Migraine, high intemal Ca (2+)-damage,impaired phosphorylation/dephosphorylation-necrosis,among others. Not surprising therefore that severeepilepsy may eventually cause CNS cytoarchitecturaland metabolic damage, or conversely, that neural tissuetrauma not infrequently gives rise to epilepsy manyyears later. Both conditions are associated with apersistent, excessive leakage or release of glutamate

into the extracellular milieu. An electrophysiological andneurochemical commonality between migraine andepilepsy has also been noted.

Mg (2+) deficiencies and disordered energy metabolism

It is hypothesized that disturbances in mag-nesium ion homeostasis may contribute to brain cortexhyperexcitability and the pathogenesis of migrainesyndromes associated with neurologic symptoms.

Studies by multipleslice spectroscopic imagingof patients with migraine with a neurologic aura havesuggested that disordered energy metabolism or Mg(2+) deficiencies may be responsible for hyperex-citability of neuronal tissue in migraine patients. Whenthese studies are extended to include multiple brainregions and larger numbers of patients thosedisordered energy metabolism or Mg (2+) deficiencieshas a tendency to be significantly lower in the poste-rior brain regions. In contrast, migraine patients withouta neurologic aura may exhibit compensatory changesin [Mg (2+)] and membrane phospholipids thatcounteract cortical excitability .Cerebral blood flowmeasured by radionuclide tracing in migraine-freeinterval tend to speeding up. By disintegration ofcerebrovascular regulation and vascular supply oftheneuron, migraine may promote secondary epilepto-genesis.

Distinguishing epileptic events from nonepilepticnot be paroxysmal neurologic events represents acommon diagnostic challenge. Studies carried out on

large population samples have shown that therelationships between migraine and epilepsy may be ofthe following type:1. Associated attacks, with migraine and seizures

occurring quite independently of one another;2. Combined attacks, with the two types of attacks

succeeding one another in time;3. Basilar artery migraine with seizures and marked EEG

abnormalities;4. Benign epilepsies with occipital discharges end5. Migraine and intercalated seizures.

There is an increasing body of evidence tosuggest that benign rolandic epilepsy and benign

occipital epilepsy of childhood are frequentlyassociated with migraine, two conditions whichprobably have different pathophysiology, although tobe related to idiopathic migraine-epilepsy syndrome.

A detailed analysis of the aura does providesufficient information for classifying the disorder as anaura in migraine or as a simple partial epileptic seizurein most cases. Visual phenomena as if lightnings,disturbed contours of objects, or skotoma, can be due


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to ophthalmological diseases, but can also occur assymptoms generated by the central nervous system(aura) in migraine or epilepsy. A subsequenthemicrania is considered as a hallmark of migraine, butin many cases does not allow for a certain distinction

from postictal headaches in patients with focalepilepsy.

Mis diagnosis of visual seizures as visual aura ofmigraine is common; but the analysis of differentialdiagnosis between migraine and the occipitalepilepsies conclude that elementary visual hallucina-tions, blindness or both, alone or followed byheadache and vomiting of symptomatic occipitalepilepsy are identical to those of idiopathic occipi-tal epilepsy. Progress to temporal lobe structures isdifferent and consistent with symptomatic occipitallobe epilepsy. The clinical diagnosis of visual seizures

is easy if individual elements of duration, colour, shape,size, location, movement, speed of development andprogress are identified. They are markedly differentfrom visual aura of migraine, although they often triggermigrainous headache, probably by activating trigeminovascular or brain stem mechanisms.

Benign occipital epilepsy of childhood is anidiopathic partial epilepsy syndrome with elementaryvisual symptomatology, frequently associated withother ictal phenomena. Seizures are usually followedby postictal headache and are often associated withinterictal occipital rhythmic paroxysmal EEG activitythat appears only after eye closure. It has been defined

by Panayiotopoulos as consisting of brief, infrequentattacks or prolonged status epilepticus and charac-terized by ictal deviation of the eyes and/or head andvomiting, occurring in children usually between theages of 3 and 7 years.

Migraine and benign focal spikes of childhood(BFSDC) may be genetically linked. In migraine withBFSDC, frequently interictal EEGs records are interpret89% normal and 9% with benign focal epileptiformdischarges (BFEDC), independent of history. OtherEEGs records have temporal spikes, and few have bac-kground slowing. The patients with BFEDC did not

differ from others with migraine. None has epilepsy. Thisincidence of 9% is higher (p less than 0.0001) than theincidence of BFEDC in the normal population (1.9%).The significance of this finding is not clear, but migraineand benign focal epilepsy of childhood may begenetically linked, or the vascular abnormality ofmigraine may cause brain injury to produce sharpwaves of low epileptogenicity. Those do not suggestthat headaches are epileptic. Patients with occipital

epileptiform abnormalities present with ictal vomitingare often diagnosed as having Vague Migraine-Epilepsy Syndromes. By the other hand, Parietal andoccipital seizures have been investigated relatively little.The most prominent clinical manifestations of parietal

epilepsy are elementary sensory phenomena at thebeginning of seizures and elementary visualhallucinations in occipital epilepsy. Because of thesecontroversial symptoms, diagnostic criteria may bedifficult to define. The wide difference in clinical andEEG manifestations between reported series of parietaland occipital epilepsy also reflects a considerableproblem with patient sampling. Classification ofepilepsy according to the anatomic division of the brainmay be arbitrary, and it may be appropriate to defineepileptic syndromes such as sensorimotor seizures oroccipito-temporal seizures that cross such artificial di-

vides.From the existing literature, we can conclude

that precise incidence and prevalence of the epilepticsyndromes such as sensorimotor seizures or occipito-temporal seizures are largely unknown. A recentcommunity-based study of 252 subjects with partialepileptic seizures in an epileptic population of 594showed that parietal seizures and seizures of posteriororigin each comprised 6.3% and central or sensory-motor seizures comprised 32.5% of focal seizures in the160 cases in which seizures could be sub classified(Manford, et al, 1992). This incidence seems low foroccipital seizures as compared with the 1953 study by

Gibbs and Gibbs, who observed occipital epileptiformactivity in 8% of subjects with focal epilepsy.

The benign childhood epilepsy with occipitalparoxysms (BCEOP) with early onset has a benigncourse despite of initial attacks of partial statusepilepticus and/or migraine attacks. Since occipitalseizures differ depending on age, an age-dependentepilepsy with occipital paroxysms exists; a preferentialage for the association between epilepsy and basilarmigraine also exists.

In all of benign childhood epilepsy with occipitalparoxysms, photic stimulation induce seizures in the

right occipital lobe followed by clinical and EEG signssuggesting infra-sylvian spreading to ipsilateralmesiotemporal limbic structures and by vomiting,appearing at late stages of the attacks. Seizure spreadis very slow last 16 and 25 minutes. Vomit can be alate ictal phenomenon resulting from temporal lobespread of seizures originating in the occipital lobe.Scalp EEG is frequently negative or maybe misleading.Hence, role played by maturational processes in these


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various aspects of epilepsy, migraine and occipitalseizures in children is important; furthermore, spread ofepileptic discharges from the parietal and occipitallobes to frontal and temporal regions may obscureseizure origin.

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