- Email: [email protected]
A family with hemiplegic migraine and focal seizures
European )ournal
of Paediatric
A family U KRAMER,a
Neurology
1997;
1: 35-38
with hemiplegic T LERMAN-SAGI,d
migraine
D MARGALITH,D
and focal seizures
S HARELJ
‘Institute for Child Development, and Pediatric Neurology Unit, Tel-Aviv Sourasky Medical Medicine, Tel-Aviv, Israel and bChild Development Center, Kaplan Hospital, Rehovot, Israel
Center, Sackler
Faculty of
Familial hemiplegic migraine is a distinctive form of migraine with autosomal dominant inheritance. The patients undergo attacks of migraine complicated by hemiplegia. Seizures have not been reported as comprising a part of this syndrome. We describe three generations of a family with hemiplegic migraine and focal seizures occurring concurrently with the migrainous attacks. There were five affected family members whose clinical features included unilateral headache and transient hemiplegia. Two family members also had focal seizures during the migrainous attacks. One of the patients was treated with carbamazepine with good results. The only associated neurological finding was ataxia which was found in the oldest patient. The presence of focal seizures during an episode of hemiplegic migraine suggests that the two phenomena of migraine and focal seizures may share the same underlying pathophysiology. Keywords:
Epilepsy.
Migraine.
Familial.
Hemiplegia.
Introduction
Patient l-7
Different forms of migraine with associated transient neurological deficit, formerly defined as complicated migraine, comprise 2-5% of total migranotic patients’s2 Familial hemiplegic migraine (FHM), initially described by Clarke in 1910,3 is a distinctive form of migraine with an autosomal dominantmode of inheritance. The gene is localized on the short arm of chromosome 19.4 Many families with FHM have been reported,5-8 with fever, confusion, paranoia or coma having been described during severe attacks of some of the affected individuals.4n5 To the best of our knowledge, this is the first report in the English literature of the occurrence of seizures concomitant with the hemiplegic events.
The grandfather, a 60-year-old Jewish male, was the son of non-consanguineous parents of Greek origin, who first presented at the age of 26 years with an acute right hemiplegia followed by a prolonged headache. Initially, the frequency was one episode per year; however, his condition deteriorated with time, and he currently suffers between one event per day to one per month. A typical attack starts with blurred vision in one eye, lasts for a few minutes, and is followed by an ipsilateral hemiplegia which lasts for about 15 minutes. Most attacks are followed by an occipital headache that lasts from between a few hours to 2 days. The attacks involve both sides of the head, with the majority being on the right side. None of the attacks have ever been accompanied by seizures. There are no associated medical problems. The neurological examination revealed dysmetria on finger-to-nose testing, dysdiadochokinesis and an abnormal tandem gait. The EEG recording was
Case histories (the family pedigree appears in Fig. 1)
Received 20.1.97. Correspondence:
Revised 4.4.97. Accepted 29.4.97. Uri Kramer, Institute for Child Development,
1 OVO-3798/97/010035+4
$18.00
14 Ballour
Street, Tel-Aviv
65211
Israel
0 1997
European
Paediatric
Neurology
Society
Case study: U Kramer et al.
36
All descendents healthy 9 healthy descenda
I
II
Fig. 1.
Pedigree of a family with hemiplegic
normal. He was treated with propranolol and carbamazepine, but compliance was poor and no improvement was detected.
Patient II- 1 One of Patient I-l’s children, a lPyear-old male, had three episodes of acute right hemiplegia with dysarthria which had occurred 5, 4 and 1 year(s) previously and which lasted 5-15min each time. There was no associated headache or aura. The examination he underwent in a hospital emergency room immediately following one of the episodes revealed no abnormalities (the studies included a normal brain CT scan with contrast material, an EEG and an echocardiogram). His current neurological status is within the normal limit and he has not experienced a further similar event.
Patient II-2 The youngest child of Patient I-l, a 17-year-old female, had suffered five events of headache followed by unilateral hemiplegia and clonic seizures between the ages of 6 and 12 years. The headache always preceded the seizures which were unilateral and clonic, appearing on different body sides in the various attacks. The headache was not localized, but the side of the seizures always corresponded to the side of the hemiplegia; EEGs
migraine
and seizures.
performed during the attacks revealed hemispheric slowing contralateral to the involved body side. Treatment with carbamazepine was finally initiated, and she has not suffered any more hemiplegic events. She experienced another event 3; years after the carbamazepine was tapered off this time involving headache and unilateral hemiplegia but with no seizures - that lasted for 2 h. Treatment with carbamazepine was recently restarted. This patient had never experienced seizures unassociated with hemiplegic migraine. Findings of the last evaluation, including a neurological examination, brain CT, MRI, magnetic resonance angiography (MRA), EEG and blood levels of lactic and pyruvic acids were within normal limits.
Patient II-3 The eldest daughter of Patient I-l, a 26-year-old, had two events of acute hemiplegia at ages 5 and 6 years. No clinical investigations were performed. The findings of the last neurological examination were unremarkable.
Patient W 1 The grandson of Patient I-l (the son of Patient I&3), a 7kyear-old, has had two hemiplegic attacks, the first at age 3 years lasting 1 h and the second at age
Case study: A family
with
hemiplegic
migraine
and focal seizures
6 years lasting 48 h. Both attacks involved the right side of the body and were not associated with headache. An EEG performed during the prolonged hemiplegic event revealed slowing in the hemisphere contralateral to the hemiplegia. The slowing disappeared a few days later. The results of the rest of the evaluation, including CT, MRI and echocardiogram, were normal. However, 2 months after the second hemiplegic attack, he experienced an abrupt and severe retro-orbital pain that was followed by two episodes of unilateral focal seizures with secondary generalization which occurred 4 h apart. The motor behaviour appeared in the body side contralateral to the side of the headache. The first episode was clonic and ceased spontaneously after 15 min and the second episode was tonic and was aborted by administration of intravenous diazepam. The findings of a recent neurological examination were within normal limits.
Discussion The clinical spectrum of migraine with associated transient neurological deficit, formerly referred to as complicated migraine and currently included within the spectra of migraine with aura,9 is well delineated and includes hemiplegia, aphasia, paraesthesia, ophthalmoplegia and hemianopsia.iOJ* Only rarely has headache followed by seizures been included within this spectra.12 The prevalence of epilepsy in patients with migraine ranges between 1 to 17% with a median of 5.9%.r3 In only 16% of the patients with both epilepsy and migraine is there a close temporal association between the two phenomena,r4 and only in the minority of cases does the headache precede the seizures.15 On such occasions, seizures can evolve into status epilepticus. l6 At times, headache followed by seizures is associated with structural brain anomalies.i2J7 In addition, several investigators have described an epileptic event following a typical migrainous aura,1s-2oespecially in cases of benign occipital epilepsy of childhood.21~Z The co-occurrence of seizures during a migrainous attack is attributed to the transient regional ischaemic effect caused by vasospasm.*25 Twomey et a1.16report a case in which a focal infarct was identified in the post mortem examination of a patient with status epilepticus following a migrainous attack. Shuaib and Lee26 reported four patients in whom seizures that followed migraine were suspected to have occurred secondary to cerebral infarction. In addition, studies on regional
37
cerebral blood flow in migraine showed a correlation between oligaemia and onset or progression of aura.= Recent data show that mutations in the gene encoding the a-l subunit of a voltage-gated calcium channel occur in mutant mice with epilepsy2’ and in patients with FHM.= The presence of epileptic seizures following headache in patients with FHM suggests that calcium influx into the neurons in the ischaemic region may be responsible for both the seizures and the hemiplegia during a migrainous attack. An alternative theory postulated that the spreading depression activates an epileptic focus when striking the susceptible cortex in patients with both seizures and migrainous attacks which occasionally coincide.29 This theory is based upon Leao’s observation that the spreading depression of activity in the cortex of rabbits can generate fast components on electrocorticogram.30 Only two patients in the family reported here (II2 and III-l) presented with all three features of migraine, hemiplegia and seizures. The rest displayed either hemiplegia alone, or headache and hemiplegia. The occurrence of hundreds of episodes in one family member while the rest underwent only a few is not surprising and was previously reported by Glista et aZ.* Only the grandfather, who experienced numerous episodes, presented with a neurological deficit, i.e., cerebellar dysfunction. There was no evidence of residual mild hemiparesis in any of the patients. It is quite possible that the progressive ataxia presented by the father is not a sequela but, as suggested by others?’ a phenomenon associated with genetic disorders that map on the same chromosome. Two of the patients were treated with either propranolol and carbamazepine (I-l) or carbamazepine alone (II-2). Since the former was noncompliant, the only true therapeutic experience in this group was that with carbamazepine which prevented the events which later reappeared upon discontinuation of the drug. This finding, however, is not helpful in characterizing- the nature of the events since epileptic, migrainous, and sensory neuropathic phenomena may improve following treatment with carbamazepine. Moreover, successful treatment of FHM with phenobarbital5 and propranolo15~* have also been reported. Other disorders, such as mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and alternating hemiplegia of childhood (AHC) associated with acute hemiplegia are easily ruled out in this family. In this family, the disorder was inherited from the grandfather, and MELAS is transmitted by a mitochondrial genome (i.e. mater-
Case study: U Kramer et al.
38 nal inheritance). Neither is AHC applicable since the necessary features of early age of onset, dystonic posturing, abnormal ocular movements and mental retardation are absent. It seems unlikely that other causes for recurrent strokes are involved since there is no evidence for old infarcts in the radiological evaluation performed in three of the patients. In conclusion, the presence of seizures within a classic hemiplegic migraine event, is an additional piece of evidence that migraine and epilepsy are not just comorbidity disorders, but that a migraine attack can present itself with focal seizure. This suggests that both may share an identical pathophysiological mechanism, either of a regional ischaemic event or a spreading depression, that generates an epileptic discharge.
12 Pearce JMS, Foster JB. An investigation of complicated migraine. Neurology 1965; 15: 333-340. 13 Andermann E, Andermann F. Migraine-epilepsy relationship: epidemiological and genetic aspects. In: Andermann FA, Lugaresi E (eds) Migraine and Epilepsy. Boston: Butterworth, 1987: 281-291. 14 Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy, with EEG correlation. Neurology 1993; 43: 2476-2483. 15 Schon F, Blau JN. Post-epileptic headache and g5y,aine. ] Nemo1 Neurosurg Psych 1987; 50: 1148-
16 Twomey 17 18 19
References ,._-_ ._,-. __.~._ _ ._.. _ 1
Lanzi G, Balottin U, Borgatti R. A prospective study of juvenile migraine with aura. Headache 1994; 34:
275-278.
20 21
2 Nevo Y, Kramer 3
4 5 6 7
8 9 10
U, Rieder-Groswasser I, Hare1 S. Clinical categorization of 312 children with chronic headache. Brain Dev 1994; 16: 441444. Clarke JM. On recurrent motor paralysis in migraine with report of a family in which recurrent hemiplegia accompanied the attacks. Br Med J 1910; 1: 1534-1538. Joutel A, Bousser MG, Biousse V et al. A gene for familial hemiplegic migraine maps to chromosome 19. Nature Genet 1993; 5: 4045. O’Hare JA, Feely MJ, Callaghan N. Clinical aspects of familial hemiplegic migraine in two families. Irish Med ] 1981; 74: 291-295. Ophoff RA, Van Eijk R, Sandkuijl LA et al. Genetic heterogenicity of familial hemiplegic migraine. Genomics 1994; 22: 21-26. Marchioni E, Galimberti CA, Soragna D et al. Familial hemiplegic migraine versus migraine with prolonged aura: an uncertain diagnosis in a family report. Neurology 1995; 45: 33-37. Glista GG, Mellinger JF, Rooke ED. Familial hemiplegic migraine. Mayo Clin Proc 1975; 50: 307-311. Olesen J. The classification and diagnosis of headache disorders. Neural Clin 1990; 8: 793-799. Rossi LN, Numenthaler M, Vassella F. Complicated migraine in children. Clinical characteristics and course in 40 personal cases. Neuropediatics 1980; 11:
27-35. 11 Barlow
CF. Headache and migraine in childhood. Clinics in Developmental Medicine No 91. Philadelphia: JB Lippincott Co, 1984: 93-125.
22
23 24 25
JA, Abbott RJ, Franks AJ et al. Status epilepticus complicating migraine. Acta Neural Stand 1988; 77: 335-338. Barlow CF. Headache and migraine in childhood. Clinics in Developmental Medicine No 91. Philadelphia: JB Lippincott Co, 1984: 126-154. Ehrenberg BL. Unusual clinical manifestations of and the borderland of epilepsy remigraine explored. Semin Ncurol 1991; 11: 118-127. Baser LS. The relation of migraine and epilepsy. Brain 1969; 92: 285-300. Gill R, Lefevre JP, Burelout Y. Migraine, seizures and epileptic focal EEG. Abnormalities in a young adult: a nine year follow-up. Headache 1984; 24: 23-25. De Romanis F, Buzzi MG, Cerbo R. Migraine and epilepsy with infantile onset and electroencephalographic findings of occipital spike-wave complexes. Headache 1991; 31: 378-383. Terzano MG, Manzoni GC, Parrino L. Benign epilepsy with occipital paroxysms and migraine: the question of intercalated attacks. In: Andermann FA, Lugaresi E (eds) Migraine and Epilepsy. Boston: Butterworth, 1987: 83-96. Olesen J. Cerebral and extracranial circulatory disturbances in migraine: pathophysiological implications. Cerebrovasc Brain Metab Rev 1991; 3: l-28. Barolin GS. Migraine and epilepsies - a relationship? Epilepsia 1966; 7: 53-66. Ninck B. Migraine and epilepsy. Eur Nemo1 1970; 3:
168-178. 26 Shuaib A, Lee MA. Seizures in migraine: an underlying
cerebral
infarction?
500-502. 27 Fletcher CF, Lutz CM, O’Sullivan 28
29 30 31
warning of Headache 1987; 27:
TN et al. Absence epilepsy in tottering mutant mice is associated with calcium channel defects. Cell 1996; 87: 607-616. Ophoff RA, Terwindt GM, Vergouwe MN et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the calcium channel gene CACNLlA4. Cell 1996; 87: 543-552. Bazil CW. Migraine and epilepsy. Neural Clin 1994; 12: 115-128. Leao AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944; 7: 391-396. Haan J, Terwindt GM, Bos PL et al. Familial hemiplegic migraine in the Netherlands. Clin Neural Neurosurg 1994; 96: 244-249.
of Paediatric
A family U KRAMER,a
Neurology
1997;
1: 35-38
with hemiplegic T LERMAN-SAGI,d
migraine
D MARGALITH,D
and focal seizures
S HARELJ
‘Institute for Child Development, and Pediatric Neurology Unit, Tel-Aviv Sourasky Medical Medicine, Tel-Aviv, Israel and bChild Development Center, Kaplan Hospital, Rehovot, Israel
Center, Sackler
Faculty of
Familial hemiplegic migraine is a distinctive form of migraine with autosomal dominant inheritance. The patients undergo attacks of migraine complicated by hemiplegia. Seizures have not been reported as comprising a part of this syndrome. We describe three generations of a family with hemiplegic migraine and focal seizures occurring concurrently with the migrainous attacks. There were five affected family members whose clinical features included unilateral headache and transient hemiplegia. Two family members also had focal seizures during the migrainous attacks. One of the patients was treated with carbamazepine with good results. The only associated neurological finding was ataxia which was found in the oldest patient. The presence of focal seizures during an episode of hemiplegic migraine suggests that the two phenomena of migraine and focal seizures may share the same underlying pathophysiology. Keywords:
Epilepsy.
Migraine.
Familial.
Hemiplegia.
Introduction
Patient l-7
Different forms of migraine with associated transient neurological deficit, formerly defined as complicated migraine, comprise 2-5% of total migranotic patients’s2 Familial hemiplegic migraine (FHM), initially described by Clarke in 1910,3 is a distinctive form of migraine with an autosomal dominantmode of inheritance. The gene is localized on the short arm of chromosome 19.4 Many families with FHM have been reported,5-8 with fever, confusion, paranoia or coma having been described during severe attacks of some of the affected individuals.4n5 To the best of our knowledge, this is the first report in the English literature of the occurrence of seizures concomitant with the hemiplegic events.
The grandfather, a 60-year-old Jewish male, was the son of non-consanguineous parents of Greek origin, who first presented at the age of 26 years with an acute right hemiplegia followed by a prolonged headache. Initially, the frequency was one episode per year; however, his condition deteriorated with time, and he currently suffers between one event per day to one per month. A typical attack starts with blurred vision in one eye, lasts for a few minutes, and is followed by an ipsilateral hemiplegia which lasts for about 15 minutes. Most attacks are followed by an occipital headache that lasts from between a few hours to 2 days. The attacks involve both sides of the head, with the majority being on the right side. None of the attacks have ever been accompanied by seizures. There are no associated medical problems. The neurological examination revealed dysmetria on finger-to-nose testing, dysdiadochokinesis and an abnormal tandem gait. The EEG recording was
Case histories (the family pedigree appears in Fig. 1)
Received 20.1.97. Correspondence:
Revised 4.4.97. Accepted 29.4.97. Uri Kramer, Institute for Child Development,
1 OVO-3798/97/010035+4
$18.00
14 Ballour
Street, Tel-Aviv
65211
Israel
0 1997
European
Paediatric
Neurology
Society
Case study: U Kramer et al.
36
All descendents healthy 9 healthy descenda
I
II
Fig. 1.
Pedigree of a family with hemiplegic
normal. He was treated with propranolol and carbamazepine, but compliance was poor and no improvement was detected.
Patient II- 1 One of Patient I-l’s children, a lPyear-old male, had three episodes of acute right hemiplegia with dysarthria which had occurred 5, 4 and 1 year(s) previously and which lasted 5-15min each time. There was no associated headache or aura. The examination he underwent in a hospital emergency room immediately following one of the episodes revealed no abnormalities (the studies included a normal brain CT scan with contrast material, an EEG and an echocardiogram). His current neurological status is within the normal limit and he has not experienced a further similar event.
Patient II-2 The youngest child of Patient I-l, a 17-year-old female, had suffered five events of headache followed by unilateral hemiplegia and clonic seizures between the ages of 6 and 12 years. The headache always preceded the seizures which were unilateral and clonic, appearing on different body sides in the various attacks. The headache was not localized, but the side of the seizures always corresponded to the side of the hemiplegia; EEGs
migraine
and seizures.
performed during the attacks revealed hemispheric slowing contralateral to the involved body side. Treatment with carbamazepine was finally initiated, and she has not suffered any more hemiplegic events. She experienced another event 3; years after the carbamazepine was tapered off this time involving headache and unilateral hemiplegia but with no seizures - that lasted for 2 h. Treatment with carbamazepine was recently restarted. This patient had never experienced seizures unassociated with hemiplegic migraine. Findings of the last evaluation, including a neurological examination, brain CT, MRI, magnetic resonance angiography (MRA), EEG and blood levels of lactic and pyruvic acids were within normal limits.
Patient II-3 The eldest daughter of Patient I-l, a 26-year-old, had two events of acute hemiplegia at ages 5 and 6 years. No clinical investigations were performed. The findings of the last neurological examination were unremarkable.
Patient W 1 The grandson of Patient I-l (the son of Patient I&3), a 7kyear-old, has had two hemiplegic attacks, the first at age 3 years lasting 1 h and the second at age
Case study: A family
with
hemiplegic
migraine
and focal seizures
6 years lasting 48 h. Both attacks involved the right side of the body and were not associated with headache. An EEG performed during the prolonged hemiplegic event revealed slowing in the hemisphere contralateral to the hemiplegia. The slowing disappeared a few days later. The results of the rest of the evaluation, including CT, MRI and echocardiogram, were normal. However, 2 months after the second hemiplegic attack, he experienced an abrupt and severe retro-orbital pain that was followed by two episodes of unilateral focal seizures with secondary generalization which occurred 4 h apart. The motor behaviour appeared in the body side contralateral to the side of the headache. The first episode was clonic and ceased spontaneously after 15 min and the second episode was tonic and was aborted by administration of intravenous diazepam. The findings of a recent neurological examination were within normal limits.
Discussion The clinical spectrum of migraine with associated transient neurological deficit, formerly referred to as complicated migraine and currently included within the spectra of migraine with aura,9 is well delineated and includes hemiplegia, aphasia, paraesthesia, ophthalmoplegia and hemianopsia.iOJ* Only rarely has headache followed by seizures been included within this spectra.12 The prevalence of epilepsy in patients with migraine ranges between 1 to 17% with a median of 5.9%.r3 In only 16% of the patients with both epilepsy and migraine is there a close temporal association between the two phenomena,r4 and only in the minority of cases does the headache precede the seizures.15 On such occasions, seizures can evolve into status epilepticus. l6 At times, headache followed by seizures is associated with structural brain anomalies.i2J7 In addition, several investigators have described an epileptic event following a typical migrainous aura,1s-2oespecially in cases of benign occipital epilepsy of childhood.21~Z The co-occurrence of seizures during a migrainous attack is attributed to the transient regional ischaemic effect caused by vasospasm.*25 Twomey et a1.16report a case in which a focal infarct was identified in the post mortem examination of a patient with status epilepticus following a migrainous attack. Shuaib and Lee26 reported four patients in whom seizures that followed migraine were suspected to have occurred secondary to cerebral infarction. In addition, studies on regional
37
cerebral blood flow in migraine showed a correlation between oligaemia and onset or progression of aura.= Recent data show that mutations in the gene encoding the a-l subunit of a voltage-gated calcium channel occur in mutant mice with epilepsy2’ and in patients with FHM.= The presence of epileptic seizures following headache in patients with FHM suggests that calcium influx into the neurons in the ischaemic region may be responsible for both the seizures and the hemiplegia during a migrainous attack. An alternative theory postulated that the spreading depression activates an epileptic focus when striking the susceptible cortex in patients with both seizures and migrainous attacks which occasionally coincide.29 This theory is based upon Leao’s observation that the spreading depression of activity in the cortex of rabbits can generate fast components on electrocorticogram.30 Only two patients in the family reported here (II2 and III-l) presented with all three features of migraine, hemiplegia and seizures. The rest displayed either hemiplegia alone, or headache and hemiplegia. The occurrence of hundreds of episodes in one family member while the rest underwent only a few is not surprising and was previously reported by Glista et aZ.* Only the grandfather, who experienced numerous episodes, presented with a neurological deficit, i.e., cerebellar dysfunction. There was no evidence of residual mild hemiparesis in any of the patients. It is quite possible that the progressive ataxia presented by the father is not a sequela but, as suggested by others?’ a phenomenon associated with genetic disorders that map on the same chromosome. Two of the patients were treated with either propranolol and carbamazepine (I-l) or carbamazepine alone (II-2). Since the former was noncompliant, the only true therapeutic experience in this group was that with carbamazepine which prevented the events which later reappeared upon discontinuation of the drug. This finding, however, is not helpful in characterizing- the nature of the events since epileptic, migrainous, and sensory neuropathic phenomena may improve following treatment with carbamazepine. Moreover, successful treatment of FHM with phenobarbital5 and propranolo15~* have also been reported. Other disorders, such as mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and alternating hemiplegia of childhood (AHC) associated with acute hemiplegia are easily ruled out in this family. In this family, the disorder was inherited from the grandfather, and MELAS is transmitted by a mitochondrial genome (i.e. mater-
Case study: U Kramer et al.
38 nal inheritance). Neither is AHC applicable since the necessary features of early age of onset, dystonic posturing, abnormal ocular movements and mental retardation are absent. It seems unlikely that other causes for recurrent strokes are involved since there is no evidence for old infarcts in the radiological evaluation performed in three of the patients. In conclusion, the presence of seizures within a classic hemiplegic migraine event, is an additional piece of evidence that migraine and epilepsy are not just comorbidity disorders, but that a migraine attack can present itself with focal seizure. This suggests that both may share an identical pathophysiological mechanism, either of a regional ischaemic event or a spreading depression, that generates an epileptic discharge.
12 Pearce JMS, Foster JB. An investigation of complicated migraine. Neurology 1965; 15: 333-340. 13 Andermann E, Andermann F. Migraine-epilepsy relationship: epidemiological and genetic aspects. In: Andermann FA, Lugaresi E (eds) Migraine and Epilepsy. Boston: Butterworth, 1987: 281-291. 14 Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy, with EEG correlation. Neurology 1993; 43: 2476-2483. 15 Schon F, Blau JN. Post-epileptic headache and g5y,aine. ] Nemo1 Neurosurg Psych 1987; 50: 1148-
16 Twomey 17 18 19
References ,._-_ ._,-. __.~._ _ ._.. _ 1
Lanzi G, Balottin U, Borgatti R. A prospective study of juvenile migraine with aura. Headache 1994; 34:
275-278.
20 21
2 Nevo Y, Kramer 3
4 5 6 7
8 9 10
U, Rieder-Groswasser I, Hare1 S. Clinical categorization of 312 children with chronic headache. Brain Dev 1994; 16: 441444. Clarke JM. On recurrent motor paralysis in migraine with report of a family in which recurrent hemiplegia accompanied the attacks. Br Med J 1910; 1: 1534-1538. Joutel A, Bousser MG, Biousse V et al. A gene for familial hemiplegic migraine maps to chromosome 19. Nature Genet 1993; 5: 4045. O’Hare JA, Feely MJ, Callaghan N. Clinical aspects of familial hemiplegic migraine in two families. Irish Med ] 1981; 74: 291-295. Ophoff RA, Van Eijk R, Sandkuijl LA et al. Genetic heterogenicity of familial hemiplegic migraine. Genomics 1994; 22: 21-26. Marchioni E, Galimberti CA, Soragna D et al. Familial hemiplegic migraine versus migraine with prolonged aura: an uncertain diagnosis in a family report. Neurology 1995; 45: 33-37. Glista GG, Mellinger JF, Rooke ED. Familial hemiplegic migraine. Mayo Clin Proc 1975; 50: 307-311. Olesen J. The classification and diagnosis of headache disorders. Neural Clin 1990; 8: 793-799. Rossi LN, Numenthaler M, Vassella F. Complicated migraine in children. Clinical characteristics and course in 40 personal cases. Neuropediatics 1980; 11:
27-35. 11 Barlow
CF. Headache and migraine in childhood. Clinics in Developmental Medicine No 91. Philadelphia: JB Lippincott Co, 1984: 93-125.
22
23 24 25
JA, Abbott RJ, Franks AJ et al. Status epilepticus complicating migraine. Acta Neural Stand 1988; 77: 335-338. Barlow CF. Headache and migraine in childhood. Clinics in Developmental Medicine No 91. Philadelphia: JB Lippincott Co, 1984: 126-154. Ehrenberg BL. Unusual clinical manifestations of and the borderland of epilepsy remigraine explored. Semin Ncurol 1991; 11: 118-127. Baser LS. The relation of migraine and epilepsy. Brain 1969; 92: 285-300. Gill R, Lefevre JP, Burelout Y. Migraine, seizures and epileptic focal EEG. Abnormalities in a young adult: a nine year follow-up. Headache 1984; 24: 23-25. De Romanis F, Buzzi MG, Cerbo R. Migraine and epilepsy with infantile onset and electroencephalographic findings of occipital spike-wave complexes. Headache 1991; 31: 378-383. Terzano MG, Manzoni GC, Parrino L. Benign epilepsy with occipital paroxysms and migraine: the question of intercalated attacks. In: Andermann FA, Lugaresi E (eds) Migraine and Epilepsy. Boston: Butterworth, 1987: 83-96. Olesen J. Cerebral and extracranial circulatory disturbances in migraine: pathophysiological implications. Cerebrovasc Brain Metab Rev 1991; 3: l-28. Barolin GS. Migraine and epilepsies - a relationship? Epilepsia 1966; 7: 53-66. Ninck B. Migraine and epilepsy. Eur Nemo1 1970; 3:
168-178. 26 Shuaib A, Lee MA. Seizures in migraine: an underlying
cerebral
infarction?
500-502. 27 Fletcher CF, Lutz CM, O’Sullivan 28
29 30 31
warning of Headache 1987; 27:
TN et al. Absence epilepsy in tottering mutant mice is associated with calcium channel defects. Cell 1996; 87: 607-616. Ophoff RA, Terwindt GM, Vergouwe MN et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the calcium channel gene CACNLlA4. Cell 1996; 87: 543-552. Bazil CW. Migraine and epilepsy. Neural Clin 1994; 12: 115-128. Leao AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944; 7: 391-396. Haan J, Terwindt GM, Bos PL et al. Familial hemiplegic migraine in the Netherlands. Clin Neural Neurosurg 1994; 96: 244-249.