Download Prevalence of migralepsy

HEALTH AND WELLNESS 1/2013
HEALTH AND WELLNESS
CHAPTER II
Chair and Department of Neurological Nursing,
Medical University of Lublin
Katedra i Zakład Pielęgniarstwa Neurologicznego,
Uniwersytet Medyczny w Lublinie
BARBARA CHMIELEWSKA, KRZYSZTOF TUROWSKI
Migraine-triggering epileptic seizures – migralepsy
Migrenopochodne napady padaczkowe – migralepsja
The coexistence of migraine and epilepsy has been a subject of interest for more
than a century and has intrigued prominent neurologists. The clinically based hypothesis that there are several links between both conditions dates back to the 19th
century. Jackson discussed the spectrum of these disorders and analyzed their relationship. Conversely, Gowers, after detailed clinical analysis of cases gave a migraine a place in the borderland of epilepsy and concluded that any relationship was
rare, indirect and frequently constituted a source of errors because a distinction of
these two diseases can be a challenge. Furthermore, he stressed two crucial symptoms that are discriminative: 1. visual symptoms (short in epilepsy, long in migraine), and 2. intensity of headache (severe pain in migraine, moderate in epileptic
postictal headache). In the monograph “The border-land of epilepsy. Faints, vagal
attacks, vertigo, migraine, sleep symptoms, and their treatment” published in 1907
Gowers kept a list of cases, which seemed to be in the border-land of epilepsy (“near
it, but not of it”). Gowers stated that: ”many were so placed by their features and
character; others because they had given rise to an erroneous diagnosis”. He concluded that “some surprise may be felt that migraine is given a place in the borderland of epilepsy, but the position is justified by many relations, and among them the
fact that the two maladies are sometimes mistaken, and more often their distinction
is difficult”. His concept of the co-occurrence of migraine and epilepsy within the
life-time includes three possibilities: 1. overlap at some point in life expectancy, 2. in parallel throughout the life, 3. mutually exclusive illnesses occur in
separate periods of life. Migralepsy is an old term deriving from migraine (migra-) and epilepsy (-lepsy) [1]. It has been used for the first time by Lennox and
Lennox to describe in their three patients a condition wherein “ophthalmic migraine
with perhaps nausea and vomiting was followed by symptoms characteristic of epilepsy”. After describing further cases the term migralepsy was reintroduced in the
nineties by Marks and Ehrenberg [2]. Migralepsy represents a concept in which
two separate disorders occur in succession. Recently, migralepsy as such appears in
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the headache classifications and not in the epilepsy classifications. The term migralepsy or migraine-triggered seizures is currently included in the International
Classification of Headache Disorders, Second Edition (ICHD-II) in section 1.5.5
(“Migraine. Complications of migraine. Migraine-triggered seizure”) as a complication of migraine. The description states that migralepsy means a seizure triggered
by a migraine. According to ICHD-II the diagnosis of migralepsy is based on the
fulfillment of two criteria: 1. migraine fulfilling criteria for migraine with aura and
2. a seizure fulfilling diagnostic criteria for one type of epileptic attack (according to
the International League Against Epilepsy (ILAE) classification) occurring during or
within 1 h after a migraine aura. It is worth stressing that migralepsy is not included in the current seizure classification or in the more recent recommendations of
the ILAE Commission on Classification and Treminology of seizures and epilepsies
[3,4].
PREVALENCE OF MIGRALEPSY
Migralepsy is a rare disease. There have been about 60 cases of possible migralepsy described in children and adults. A recent Embase search found 31 reviews
(half of them with case description) in the last thirteen years. The prevalence of
epilepsy is higher in headache patients than in the normal population. However
direct indices of prevalence are not known. Comorbidity studies have shown the
prevalence of migraine in 7-26 % among epilepsy patients, and prevalence of epilepsy between 1 and 17% among migraine patients. About 1.6-2.0% patients with
migraine-like or tension headache simultaneously complain of seizures [5].
CLINICAL CHARACTERISTICS
Migralepsy is usually under diagnosed due to its clinical rarity. Clinical
diagnosis of migralepsy requires that there is a temporal relationship between the
migraine aura and a seizure event within an hour; epileptic seizure arise during a
pre-established migraine attack. However most reported cases of migralepsy are
complicated. Both disorders can present with episodic, overlapping constellations of
headaches, sensory, motor and cognition symptoms. Both are phenotypically
heterogenous. The diagnosis in the majority of previously published cases is
uncertain and debatable. Most common complains, signs and symptoms of
migralepsy are presented in cited below clinical descriptions.
Case 1. 22 year-old woman, at the age 12 began having 2-3 min episodes of
fluorescent-colored flashing, black spots and squiggly lines. At the age 13, visual
symptoms began to be followed by bi-frontal headaches. At the age 15 she
experienced the first convulsion in context of worsened headache after left visual
field scintillations. This latter phenomenon was followed by loss of vision. Over
next four years, she had 1-2 seizures per year preceded by identical visual aura.
Seizures were in relation with menses. She has not had family history of epilepsy
but many maternal relatives suffered from migraine [6].
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Barbara Chmielewska, Krzysztof Turowski
Migraine-triggering epileptic seizures - migralepsy
Case 2. 23-year-old women with a history of migraine attacks but not epilepsy
referred to the epilepsy out-patients clinic because of reappearance of generalized
tonic-clonic seizures. She also had either family history of epilepsy or migraine. At
13 years of age she began having very rare episodes of headaches preceded by
visual aura lasting no longer than an hour with clinical features of migraine with
aura. At 15 years she began having episodes of myoclonic jerks sometimes with
generalized tonic-clonic seizures or absence. Her disorder was diagnosed as juvenile
myoclonic epilepsy. The interictal EEG showed generalized, synchronous polispikeand-waves discharges (typical for juvenile myoclonic epilepsy) with a
photoparoxysmal response. Treatment with valproate reduced seizures, so she
decided to finish it. Three years after drug withdrawal seizures reappeared. Her
neurological examination was normal, as well as routine laboratory analyses,
cerebrospinal fluid examination and brain magnetic resonance imaging with FLAIR
and post-gadolinium sequences. Continuous video EEG recorded one typical
episode of her migraine attack lasting several minutes followed by tonic-clonic
seizure lasting 60 s. Ictal EEG showed bilateral 2-3 Hz delta waves over the frontotemporal regions lasting 6 s and followed by a generalized spike and polyspikes (34 Hz) lasting 10 s, with return to the slow background activity. She was started with
topiramate and she obtained freedom both from seizures and migraine [7].
Case 3. A 20-year female with history of migraine for 7 years and epilepsy for 4
years was presented in epilepsy center with complaints of exacerbation of migraine
with 4-5 seizures attacks per week. She had been given increasing doses of drugs
combination but no relief was achieved. She had no family history of migraines and
seizures; birth and development had been normal. At the age of 13 years she began
to have regular attacks of migraine with aura as well as without aura and without
associated precipitating or exacerbating factors. Headache was severe, throbbing, bifrontal and temporal with nausea, lasting for several hours and occasionally it was
triggered by catamenial component. During and between attacks treatment with
different symptomatic analgesic and anti-migraineous drugs was unsuccessful. At
the age of 16 years she developed her first convulsion attack. CT scan of brain was
normal. EEG showed diffuse fast beta rhythm without abnormal activity. At time of
exacerbation MRI scanning was found to be normal. She has been instructed to
withdraw all her pervious medications and prescribed topiramate at low dose of 25
mg and carbamazepine 200 mg. Patient had migraine and epileptic relief in one
weeks time and there after continued for 3 months. Patient was reported to be
absolutely free from migralepsy [8].
Sances, at al reviewed all potential migralepsy cases published up to 2008.
Assessing clinical and diagnostic characteristics they found as much as 62% of
patients with migraine with aura, while 26% who presented basiliar or without aura
type of migraine. A half of patients suffered from generalized tonic-clonic seizures,
24% had partial and 20% mixed-partial and generalized tonic-clonic seizures.
Interictal EEG showed localized and generalized abnormalities, respectively in 34
and 28% of patients but it was often normal - in one third of patients. Unfortunately,
ictal EEG was rarely available in 32% of cases and was mostly abnormal - in 28% of
these registrations. Any type of brain imaging was performed in two third of cases
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and was normal in a half but shown structural or transient alterations in 20%. In
conclusion the analysis stressed that only 4% of these cases actually met current
ICHD-II criteria for migraine-triggered seizures, while 28% were questionable for
the nature of epileptic seizures and 38% were uncertain [9]. Verotti, et al. reviewed
the records of 4600 children with epilepsy and selected 16 cases (0,3%) of migraine
with or without aura- triggering seizures within 1 hour of the migraine attacks; 75%
were female [10]. 31% of patients had primary generalized epilepsy and among
them 80% had tonic-clonic seizures. 69% had complex partial seizures with occipital
or temporo-parieto-occipital lobe focus in about three quarters of cases. Symptoms
during migraine consisted of nausea, vomiting, abdominal pain, dizziness and
photophobia in 50% of patients. In addition, 56% of patients felt other visual
symptoms during migraine, e.g. scotoma, loss of visual field and elementary or
complex visual hallucinations. The interictal EEG revealed epileptiform complexes
in 87% patients with partial seizures during migraine. Ictal EEG recordings during
migraine revealed spike-and-wave complexes in 56% of patients, while only a
quarter of them had generalized epilepsy (and generalized interictal EEG
discharges). The MRI was nonspecifically abnormal in 25% of patients including
differentiated organic lesions (gliosis, altered neuronal migration or hydrocephalus)
[10].
DIFFERENTIATION
The mentioned reviews have shown that there is the high prevalence of purely
epileptic disorders among cases reported as migralepsy. Detailed analysis of Lennox and Lennox cases of migralepsy also revealed that two of three were in fact
symptomatic and idiopathic occipital epilepsies with visual hallucinations [9]. Occipital epilepsies represent 5% of partial epilepsies. Headache or visual symptoms
can be the epileptic aura of a seizure in occipital lobe epilepsy. Distinction between
migraine visual auras and occipital lobe seizures aura must be kept in mind when
evaluating attacks suggestive of migralepsy. According to Panayiotopoulos 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 hemi-field. It is often
followed by scotoma. Total duration of aura is about 60 min. Contrary, ictal elementary visual hallucinations of occipital lobe epilepsies develop rapidly (seconds),
and they are colored, circular and brief (2 min). They appear in the periphery of a
temporal hemi-field, widen during seizure and move horizontally toward the contralateral side (tab.1)[11]. However visual symptoms may be mixed or simply blurred
vision, followed by headache and vomiting as in migraine attack. Furthermore
headache itself can be exclusive ictal epileptic phenomenon. Some epilepsy syndromes such as childhood benign epilepsy with occipital paroxysms (focal cryptogenic or symptomatic epilepsies) and childhood benign epilepsy with centrotemporal spikes (benign rolandic epilepsy) ought to be differentiated from migralepsy in which seizures are triggered by migraine aura. Both are primary migraineepilepsy syndromes with features of both migraine and epilepsy without a specific
underlying cause. Benign rolandic epilepsy is characterized by unilateral somatosen26
Barbara Chmielewska, Krzysztof Turowski
Migraine-triggering epileptic seizures - migralepsy
sory or motor seizures and centro-temporal spikes. Among symptoms are speech
arrest, pooling of saliva with preservation of consciousness; secondary generalization may also occur. The seizures respond well to anticonvulsant medication and
disappear by age 15. An association with migraine has been reported; migraine was
presented much higher in patients with centro-temporal epilepsy and higher in patients with absence epilepsy than in patients with any other partial epilepsy or in
cases without epilepsy. The association may be a part of the co-morbidity of migraine with all forms of epilepsy [12]. Benign epilepsy of childhood with occipital
paroxysm is a rare disorder characterized by a partial seizure with visual symptoms,
followed by postictal migraine and occipital spikes on EEG. It has features of both
epilepsy and migraine. The visual symptoms include amaurosis, elementary or complex visual hallucinations or illusions often followed by colonic, complex partial or
secondary generalized tonic-clonic seizures, following by migraine-like headaches
in about 40% of patients. The interictal EEG is characterized by normal background
activity and occipital biphasic spike high-voltage discharges. They disappear with
eye opening and reappear after eye closure. Occipital spikes are not specific for
occipital epilepsies; they have been reported in people with migraine, in myoclonic,
absence and photosensitive epilepsies and in healthy children under 4 years [13].
EEG AND NEUROIMAGING CONTRIBUTION TO STUDY
THE ASSOCIATION BETWEEN MIGRAINE AND EPILEPSY
EEG abnormalities can be similar in migraine and occipital epilepsy. Both interictal and ictal EEG abnormalities in patients with migraine comprise symmetrical
high voltage theta bursts over the temporo-occipital areas. Patients with epileptic
visual symptoms may show similar abnormalities. However patients with ictal autonomic manifestation or from a deep epileptic focus may not show epileptiform
spikes or spike and wave activity and scalp EEG might only record theta/delta
waves, reflecting the subcortical abnormalities. Prolonged 24-h video EEG recordings seems to be more useful in assessment headache/epilepsy patients. It was
shown in migralepsy subjects that during migraine aura, burnst of spike activity may
resemble the ictal EEG during an epileptic seizure although their sequence may be
different. EEG does not show the usual temporal evolution with progressive increase
and declines in the frequency and amplitude of rhythmic, repetitive epileptiform
activity, typical of ictal EEG during epileptic fit. EEG during migraine aura shows
variable course with both disturbed and completely normal activity despite the persistence of clinical symptoms [2, 14]. The interictal EEG in published migralepsy
cases was rarely normal in one third of patients but displayed localized (34%) or
generalized (28%) abnormalities in majority of them. They were characterized by
spikes, sharp waves or spike-wave complexes in the temporal or occipital lobe.
Simultaneously an EEG during the migraine attack was not available in the majority
of cases (15). In cases of migralepsy, most EEG recordings showed a diffuse, irregular, high voltage, theta-delta activity during the episodes. These abnormalities were
transient and disappeared at the long-term follow-up. Although an EEG abnormalities are expected, they would be irrelevant in the differential diagnosis. Only ictal
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EEG recordings performed in migraine-epileptic patients to demonstrate the underlying pathogenic mechanism of these episodes have the meanings. Sporadically, in
about 6% of patients with migralepsy neuroimaging studies showed transient reversible brain abnormalities in MRI. These alterations were explained as a consequence of blood-brain damage resulting in brain edema persisting for days while
disappeared [16].
PATHOPHYSIOLOGY
Migraine and epilepsy share similar pathophysiological mechanisms. However,
the exact phenomenon of migraine-induced seizures are still undefined. The hypothesis of excessive paroxysmal hyperexcitability of neocortical cells as a triggering
pathological process underlying the onset of both disease have been extensively
studied. It is associated with the phenomenon of cortical spreading depression during headache and hypersynchronous activity during epileptic fit. Cortical spreading
depression (CSD) is believed to be the connecting point between migraine and epilepsy. CSD, a mechanisms of profound cellular depolarization is responsible for
migraine aura and is a trigger for the headache pain in migraine. In turn, cellular
hyperexcitability is associated with localized epileptiform discharges. Hyperexcitability is an initial event preceding cortical spreading depression. CSD is characterized by a slowly propagating neuronal depolarization followed by neural suppression. This initial phase means transient loss of membrane ionic gradients and surge
of extracellular potassium, neurotransmitters and intracellular calcium and it is associated with an increase in regional cerebral blood flow, contrary to the reduced
circulatory during the next phase [15]. The CSD causes the activation of the trigeminovascular system (TVS) at the cortical level and initiates release of inflammatory
mediators and neurotransmitters, which result in pain during the migraine attack.
The threshold required for the onset of CSD seems to be lower than that of hyperexcitation required for the epileptic seizures onset and propagation. Independently,
the cortical excitation treshold in migraineurs is lower than in healthy subjects,
thereby favoring the occurrence of seizures. This lower cortical excitation threshold
might be due to several condition, such as disturbances in electrolyte metabolism,
mitochondrial defects or ion channelopathies. The onset of CSD and that of the
epileptic seizure may facilitate each other. The triggering causes may be environmental or individual, and among others also some of them are genetically determined. Also, recurrent seizures might predispose to CSD, thereby increasing the
occurrence of peri-ictal migraine-like headache. Changes in the composition of
extracellular fluid such as an elevation of glutamate and potassium ions during CSD
results in hyperexcitability and in lowering threshold for seizures. Altered metabolisms of such neurotransmitters as glutamate, serotonine and dopamine as well as
impaired ion channels play an importand role in both disorders [17,18]. Glutamate is
a critical mediator of the hyperexcitability in both focal seizures and migraine.
Ionotropic glutamate receptors play roles in both migraine and epilepsy with NMDA
receptors critical to cortical spreading depression of particular importance on migraine. Candidates for drug therapy include NMDA, GluK1 and GluR5 antagonists.
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Barbara Chmielewska, Krzysztof Turowski
Migraine-triggering epileptic seizures - migralepsy
In experiments memantine inhibited CSD and was effective in migraine prophylaxis.
In focal epilepsy, seizure generation and spread is mediated by synaptically released
glutamate acting on AMPA receptors. Triggering of CSD depends on NMDA receptors and spread does not require synaptic transmission [18].
GENETIC ASPECTS
To date, there is no causative genes in migralepsy. Numerous studies have analysed families with both epilepsies and migraines. Familiar occipito-temporal lobe
epilepsy and migraine was linked to chromosome 9q in the five-generation family.
The affected members had both diseases and were photosensitive; the headache was
in fact an epileptic aura of occipital seizures. In another family with generalized
tonic-clonic febrile seizures, with migraine (with or without aura) and photosensivity in a part of subjects a linkage to chromosomes 14q and 12q was showed. Some
studies of the genes encoding for ion channels showed their alterations resulted in
changed neuronal excitability; it often represents clinical association of migraine and
epilepsy. Familiar Hemiplegic Migraine is a rare type of autosomal dominant migraine with peculiar aura characterized by unilateral motor weakness. The CACNA1A gene located on the chromosome 19 is known in 17 different mutations. It
encodes the poreforming, voltage dependent Ca(v)2.1calcium channels. These mutations influence CSD and P/Q-type calcium channels mediate glutamate release in
cortical neurons. Mutations in this gene have been linked to several human disorders, including familiar hemiplegic migraine type 1; in animals Cacna1a induced
absence-like seizures. The sodium channel alfa1 subunit gene - SCN1A located on
2q24 is now the most clinically significant epilepsy gene. Its mutations were associated with the familiar epilepsy syndrome-genetic epilepsy with febrile seizure plus
(GEFs+0, Dravet syndrome, and familiar hemiplegic migraine). More than 150
mutations in SCN1A have been described in families with epilepsy. Several other
genetic findings that link migraine with epilepsy have been reported. A genetic defect in ion channels seems to be crucially shared pathophysiological mechanism of
migraine and epilepsy. Voltage-gated ion channels are part of an extensive signaling pathways that affect neuronal excitability through various mechanisms [18].
TREATMENT (TABLES 2, 3)
The hypothesis that disturbed excitability may be a main pathological mechanism underlying the onset of both epilepsy and migraine/headache and that it may be
related to neurotransmitters or ionic dysfunctions has contributed to the interest in
the use of antiepileptic drugs (AEDs). Indeed, some antiepileptic drugs are useful in
both conditions. These drugs reduce neuronal excitability by various mechanisms.
As a class, AEDs also reduce migraine frequency and are well tolerated. However
some AEDs as phenytoin, oxcarbazepine or clonazepam, are not effective. AEDs
that act primarily via use-dependent block of voltage-gated channels or via gabaergic mechanisms appear to influence hyperexcitability mechanisms that are not relevant to migraine. As a glutamate is a key mediator in triggering migraine and mi29
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graine pain, so glutamate receptor antagonists may be useful in migraine prophylaxix and therapy. On the other hand some AEDs including valproate, topiramate,
gabapentin and pregabaline are effective both as antiepileptic as well as antimigraine drugs as preventive agents. In U.S. valproate in 1996 and topiramate in 2004
were approved for migraine prophylaxis. Topiramate block voltage-gated sodium
channels, enhance GABAa receptor mediated currents, inhibite of l-type calcium
channels and carbonic anhydrase; it also inhibit AMPA/kainite inotropic glutamate
receptors. The doses of valproate that are effective in migraine - 500 mg /day are
lower than those approved for epilepsy. Gabapentin, at dose of 1800-2400 mg/day
has been shown to be superior to placebo for migraine. For topiramate, a dose of
50-100 mg/day was effective. Subsequent trials suggested that levetiracetam and
zonisamide also may help prevent the onset of migraine and may be helpful in
prophylaxis [15]. Limited cinical data indicate that lamotrigine reduces frequency,
duration and intensity of migraine aura although it does not reduce the frequency of
migraine attacks [19]. Ionotropic glutamate receptors are involved in both migraine and epilepsy with NMDA receptors which are critical for CSD. Effectiveness
of AEDs in the prophylaxis phase may be explained by the anticipation of the
CSD event that induces secondary trigemino-vascular system activation and lowers
the seizure threshold. However, in both epilepsy and migraine the same proportion
of patients- around 30% are still pharmacoresistant.
Table 1. Clinical differentiation of occipital epilepsy and migraine with aura
(acc. to Panayiotopoulos - 11)
Clinical feature
Duration
Frequency
Colored circular patterns
Black/white linear patterns
Moving in visual field
Expanding from center of visual field
Tonic deviation of eyes
Impairment of consciousness
Convulsions
Postictal headache
Vomiting
30
Occipital epilepsy Migraine with aura
< minute
4-30 min
daily
rarely daily
yes
rarely
exceptional
as a rule
yes
no
rare
yes
yes
no
frequent
rare
frequent
exceptional
(migralepsy)
frequent
as a rule
rare
frequent
Barbara Chmielewska, Krzysztof Turowski
Migraine-triggering epileptic seizures - migralepsy
Table 2. Mechanisms of AEDs and evidence
prophylaxis.
Mechanisms
Power of evidence
Na+ channels
no strong evidence
Phenytoin
Oxcarbazepine
Carbamazepine
(limited)
Lamotrygine
(aura)
of efficacy in migraine
GABAa receptors
no evidence
Phenobarbital
Clonazepam
____________________________________________________________________
GABA transporter
limited evidence
Tiagabine
____________________________________________________________________
GABA metabolism
no evidence
Vigabatrin
____________________________________________________________________
Mixed mechanisms
Valproate
yes
Topiramate
yes
Zonisamide
limited evidence
____________________________________________________________________
New mechanisms
Gabapentin
yes
Levetiracetam
limited evidence
Table 3. Drugs approved for migraine prophylaxis
Choice
1st line
2nd line
3rd line
possibly effective
Agents
beta-blockers
amitriptiline
valproate
topiramate
gabapentin
levtiracetam
zonisamide
lamotrygine
carbamazepine
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REFERENCES
1. Gowers WR. The border-land of epilepsy: faints, vagal attacks, vertigo, migraine, sleep symptoms, and their treatment. Chapter V. Philadelphia, 1907.Eds.
P. Blackiston’s Son & Co. Reprint 1995. Arts & Boeve, Nijmegen, pp 76-102.
2. Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy,
with EEG correlation. Neurology 1993,43,2476-83.
3. International Headache Society. The International Classification of Headache
Disorders. Cephalalgia 2nd ed, 2004, 24 (suppl 1), 9-160.
4. Berg AT, Berkovic SR, et al. Revised terminology and concepts for organization
of seizures and epilepsies: report of the ILAE Commission on Classification and
Terminology, 2005-2009. Epilepsia 2010,51,676-85.
5. Breslau N, Rasmussen BK. The impact of migraine: epidemiology, risk factors
and co-morbidities. Neurology 2001,56 (suppl.1),S4-12.
6. Rogawski M. Migraine, epilepsy and migralepsy: myths and realities. National
Headache Foundation,7th Research Summit, Oct.16,2009.
7. Labate A, Sturniolo M, et al. Migraine attack triggering a generalized seizure: is
this a case of migralepsy or occipitaltal epileptic headache ? Neurol Sci
2012,33,957-959.
8. Kumar B, Silvia WC, et al. Migralepsy - a clinical report. Intl J Chem Pharm
Res, 2012,1,45-48.
9. Sances G, Guaschino E, et al. Migralepsy: a call for revision of the definition.
Epilepsia 2009,50,2487-96.
10. Verotti A, Coppola G, et al. Should “migralepsy” be considered an obsolete
concept? A multicenter retrospective clinical/EEG study and review of the literature. Epilepsy & Behavior 2011,11,52-9.
11. Panayiotopoulos CP. Visual phenomenon and headache in occipitital epilepsy: a
review, a systematic study and differentiation from migraine. Epileptic Disord
1999,1,205-16.
12. Giroud M, Couillaut G, et al. Epilepsy with Rolandic paroxysms and migraine: a
non fortuitous association. Results of a controlled study. Pediatrie 1989,44,65964.
13. Silberstein SD, Lipton RB, et al. Migraine. In: Epilepsy. Comprehensive textbook. 2nd ed. J.Engel, Jr, TA. Pedley, eds. Lippincott Williams & Wilkins. Philadelphia USA 2008, pp 2733-2743.
14. Niedermeyer E. Migraine-triggered epilepsy.Clin EEG 1993,24,37-43.
15. Verotti A, Striano P, et al. Migralepsy and related conditions: advances in pathophysiology and classification. Seizure 2011,20,271-5.
32
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Migraine-triggering epileptic seizures - migralepsy
16. Mateo I, Froncea N, et al. Migraine-associated seizures with recurrent and reversible magnetic resonance imaging abnormalities. Headache 2004,44,265-70.
17. Parisi P, Piccioli M, et al. Hypothesis on neurophysiological mechanisms linking
epilepsy and headache. Med Hypotheses.2008,70,1150-4.
18. Rogawski M. Common pathophysiologic mechanisms in migraine and epilepsy.
Arch Neurol 2008,65,709-14.
19. D’Amico D. Pharmacological prophylaxix of chronic migraine: a review of double-blind placebo-controlled trials. Neurol Sci 2010,31 (suppl 1):S23-8.
ABSTRACT
Epilepsy and migraine are chronic neurological disorders with episodic paroxysmal manifestation of altered brain function and a return to baseline between attacks that frequently occur together in children or adults. Migraine-like headaches
are frequently seen in the postictal period of a seizure or a seizure occurs during or
following a migraine attack. Relationships between migraine and epilepsy have
long be postulated. Epidemiological and clinical studies has demonstrated that both
entities are highly comorbid and one condition may be mistaken for the other. The
most recent International Classification of Headache Disorders, Second Edition
(2004) introduced the term migralepsy or migraine-triggered seizures for the clinical entity that fulfills the two criteria: migraine with aura and an one type of an epileptic attack occurring during or within one hour of an aura. There have been only
about 60 cases of possible migralepsy published. This paper describes clinical, diagnostic and therapeutic aspects of migralepsy.
Key words: migralepsy, symptoms, patomechanism, diagnosis, treatment.
STRESZCZENIE
Padaczkę i migrenę, należące do najczęstszych przewlekłych schorzeń
neurologicznych, łączy okresowe występowanie napadowych zaburzeń czynności
ośrodkowego układu nerwowego, z powrotem do prawidłowego funkcjonowania
pomiędzy napadami. Schorzenia te nierzadko współwystępują u jednego chorego.
Bóle głowy typu migrenowego są częstym zaburzeniem po napadzie padaczkowym,
podobnie jak napady padaczkowe ujawniają się w czasie lub tuż po aurze
przypominającej migrenową. Zależności łączące te schorzenia postrzegano od
dawna. Badania epidemiologiczne i kliniczne dowiodły nie tylko współzależności,
ale także częstych trudności diagnostycznych w różnicowaniu
napadów
migrenowych i padaczkowych. Najnowsza Międzynarodowa Klasyfikacja Bólów
Głowy II, z r.2004 wyróżniła nową jednostkę chorobową, tj. napady padaczkowe
wyzwalane przez migrenę (migralepsję), w dziale powikłań migreny. Do
rozpoznania migralepsji, niezbędne jest równoczesne spełnienie dwu warunków:
występowanie migreny z aurą, w czasie której lub w okresie do godziny po aurze
występują napady padaczkowe o cechach morfologicznych zgodnych z klasyfikacją
napadów sutalonych przez Międzynarodową Ligę Przeciwpadaczkową (1989 r.).
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Migralepsja jest rzadkim schorzeniem, opisano około 60 przypadków. Niniejsza
praca przedstawia kliniczne, patogenetyczne, diagnostyczne i terapeutyczne aspekty
schorzenia.
Słowa kluczowe: migralepsja, objawy, patomechanizm, diagnostyka, leczenie
Artykuł zawiera 32926 znaków ze spacjami
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