- Email: [email protected]
EEG findings during basilar migraine attacks in children
Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
Case report
EEG findings during basilar migraine attacks in children G.P. Ramelli a ,*, M. Sturzenegger b, F. Donati b, K. Karbowski b a
Department of Paediatrics, Universita¨ts-Kinderklinik, Inselspital, CH-3010 Berne, Switzerland b Department of Neurology, University of Berne, Berne, Switzerland Accepted for publication: 22 June 1998
Abstract We present clinical and EEG findings in 4 children with basilar migraine (BM) (three female and one male, age 11 to 13.5 years). All patients had an EEG during the acute attack and a follow-up EEG within 4 to 18 days. In two patients the EEG, done within 4 h of the onset of symptoms (initial stage), showed diffuse polymorphic subdelta-delta activity. In two other children the EEG, performed 16 h after the onset of symptoms, showed delta-theta activity predominant over the occipital regions. Resolution of these abnormalities during follow-up was observed in all patients. We wish to stress the danger of misinterpretation of the slow wave activity in the EEG of patients with BM attacks. Together with the clinical findings and their evolution, EEG results should not be interpreted as a sign of a structural brain-stem lesion, such as infarction or inflammation. 1998 Elsevier Science Ireland Ltd. All rights reserved Keywords: Basilar migraine; EEG findings; Child
1. Introduction Bickerstaff (1961a) was the first to describe migraine patients with symptoms indicating dysfunction of brain areas supplied by the vertebrobasilar arteries during an attack. Basilar migraine (BM) occurs predominantly in young females and, in addition to headache and vomiting, may present with bilateral visual symptoms, dysarthria, vertigo, tinnitus, decreased hearing, double vision, ataxia, bilateral sensory symptoms or weakness, and qualitatively or quantitatively altered consciousness (IHS, 1988; Sturzenegger and Meienberg, 1985). Thus, clinical findings of a patient examined during an attack may suggest a serious neurological disorder. In such a situation, further investigations are often necessary and the correct diagnosis is only made retrospectively (Sturzenegger and Meienberg, 1985). No EEG abnormalities were described in the original description of the syndrome, but the temporal relationship between attacks and EEG recordings was not stated (Bickerstaff, 1961b). The first EEG during a BM attack was reported by Slatter (1968). Later, either single cases with * Corresponding author. Tel.: +41 31 6322111; fax:+41 31 6329448.
EEG recordings were reported or larger series were published that did not document EEG findings in sufficient detail (Hockaday, 1979). We describe 4 children with BM, in whom severe transient electroencephalographic abnormalities were observed during the attack. We discuss the relevance of these findings with respect to differential diagnosis.
2. Patients, methods and findings Between July 1996 and March 1997, 4 children (3 females and 1 male aged 11 to 13.5 years) were admitted to the Department of Paediatrics, University of Berne for acute neurological disturbances compatible with BM. 2.1. Patient 1 This 12-year old girl had had no previous headaches. Family history was unremarkable. She had no history of medication or trauma. Three hours before hospital admission she reported severe occipital headache with acute onset of blurred and later tunnel vision. She was confused and
0013-4694/98/$ - see front matter 1998 Elsevier Science Ireland Ltd. All rights reserved PII S0013-4694 (98 )0 0094-7
EEG 97782
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
375
somnolent. She was then referred to our hospital. We found a totally disoriented girl. On neurological examination there were bilateral extensor plantar responses. There was no abnormality in routine blood and CSF analysis. The EEG 4 h after symptom onset showed diffuse polymorphic, highvoltage subdelta-delta activity of 0.5–2 Hz. A follow-up EEG was performed 4 days after the acute attack and showed a marked improvement. The patient recovered completely and was discharged 5 days later. She had amnesia about the attack. 2.2. Patient 2 During the previous 2 years, this 13.5-year-old boy had suffered from recurrent unilateral headaches with nausea and photosensitivity at about 2-month intervals. His mother had attacks of migraine without aura. There was no history of medication or trauma. Two hours before admission the boy reported severe occipital headache, nausea and he vomited. One hour later he became confused, disoriented and aggressive, his mother noted dysarthric speech and he reported blurred vision. We found a confused and lethargic boy with a Glasgow Coma Score of 10. Tendon reflexes were very brisk. A routine blood test and CSF analysis were normal. The EEG 4 h after symptom onset showed diffuse polymorphic, high-voltage subdelta-delta activity of 0.5–2 Hz (Fig. 1a). The following day (30 h after symptom onset) he was clinically normal but EEG showed persistent posterior delta activity (Fig. 1b). He was discharged 3 days later. A follow-up EEG performed 7 days after the acute attack showed normalization (Fig. 1c). 2.3. Patient 3 This 11-year-old girl had no history of headache and she had been in good health until the day of admission. Her mother suffered from migraine without aura. Two hours before admission, while playing tennis, she reported severe frontal headache and nausea, some minutes later she showed a ataxic gait and she reported dizziness and blurred vision, and her speech became dysarthric. Still later she reported blindness and showed a confusional state. On admission she showed impaired consciousness with disorientation, was poorly responsive to stimuli and her Glasgow Coma Score was 12. Routine urine and blood tests including complete blood count, sedimentation rate, electrolyte, liver and kidney function, plasma glucose and CSF were normal. CT scan of the brain showed no abnormalities. The EEG was recorded 16 h after onset of the attack and showed delta-theta activity over the posterior regions. There were no epileptiform discharges and reactivity was poor. A follow-up EEG performed 10 days later was normal. 2.4. Patient 4 This 12.5-year-old girl had suffered migraine without
Fig. 1. EEG recordings in a 13.5-year old boy with BM. (a) EEG recording 4 h after symptom onset: diffuse high amplitude subdelta-delta activity. (b) EEG recording 30 h after onset of symptoms: nearly continuous delta activity over the posterior regions. (c) EEG recording 7 days after onset of symptoms: normalization of EEG recording, showing predominant alpha activity over the posterior regions.
376
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
Table 1 History and clinical findings of our patients Patient
Sex Age at first BM attack (years) Family history of migraine Patient history of migraine Headache Visual symptoms Gait ataxia Dysarthria Confusion Amnesia GCS Lumbar puncture CT scan
1
2
3
4
F 12 Negative Negative + + − − + +
a
a
F 11 Positive (mother) Negative + + + + + + 12 + +
F 12.5 Positive (father) Positive + + + + + +
+
M 13.5 Positive (mother) Positive + + − + + + 10 +
a
a
+ +
M, male; F, female; GCS, Glasgow Coma Scale; CT, computed tomography; +, present; −, absent. a
Not done.
aura with nausea and photosensitivity for several years with an attack rate of one per month. Her father suffered from migraine without aura. Two hours before hospital admission she reported severe occipital headache. She was sent home from school. One hour later at home she became restless, started screaming, showed an ataxic gait, and her speech became dysarthric and barely understandable. She behaved like a blind person. On admission she was totally disoriented and lethargic. There were no abnormalities on motor examination, but the tendon reflexes were very brisk, with bilateral extensor plantar responses. Routine blood and urine test, CSF results and CT scan were normal. The first EEG was recorded 16 h after onset of the attack and showed delta-theta activity over the posterior regions. Reactivity was poor. A follow-up EEG performed 10 days after the acute attack was normal. The main clinical characteristics of the 4 patients are summarized in Table 1. In all 4 patients this was the first BM attack, but two patients had previously had other types of migraine attacks. Family history for migraine was positive in 3 patients, with the mother being affected in two. Severe paroxysmal headache was present in all patients and was occipitally located in 3. The most distressing symptoms
were visual disturbances including blurred vision, tunnel vision and amblyopia, and altered consciousness with confusion or amnesia. Three patients had dysarthria and one patient had gait ataxia. The symptoms disappeared in all cases within 24 to 48 h. A computed tomographic (CT) scan of the brain performed in two patients was normal. CSF analysis was normal in all 4 patients. Drug intoxication was excluded by history and by blood and urine analysis for barbiturates, carbamates, phenothiazine and benzodiazepines. No patient had a history of trauma. EEG results are summarized in Table 2. All patients had an EEG during the acute attack with definitively pathologic findings. Two patients had the EEG 4 h after the first symptoms (initial stage) and both showed diffuse polymorphic, high-voltage subdelta-delta activity (Fig. 1a). On the second day (30 h), patient 2 was clinically normal, but the EEG showed persistent posterior delta activity (Fig. 1b). In the two other patients, the first EEG was recorded 16 h (decreasing symptoms) after the onset of the attacks and showed delta-theta activity over the posterior regions. There were no epileptiform discharges and reactivity was poor. A follow-up EEG was performed in all 4 children 4 to 18 days after the acute attack, and showed a marked improvement (Fig. 1c).
Table 2 EEG findings Patient no.
1 2 3 4
During attack
EEG follow-up
Latency (h)
Frequency (Hz)
Localization
Days after attack
Findings
4 4 16 16
0.5–2/Subdelta-delta activity 0.5–2/Subdelta-delta activity 3–6/Delta-theta 3–6/Delta-theta
Diffuse Diffuse Posterior Posterior
4 7 10 18
Improved Normal Normal Normal
Latency is the interval from first symptoms to recording.
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
3. Discussion Only a few patients with an EEG recorded during an acute basilar migraine (BM) attack have been described, and the reported findings were quite variable (Jacome, 1987). This is most probably due to the fact that recordings were made at different stages of the attack, which is known to take a protracted course. The clinical presentation and the subsequent course in our 4 children fulfil the IHS criteria for diagnosis of BM (IHS, 1988). All had significant EEG abnormalities during the acute stage of the attack, which had resolved on follow-up examinations within 1 to 2 weeks. Two patients with an EEG recorded within 4 h of symptom onset (initial stage) showed diffuse polymorphic high-voltage subdelta-delta activity, which was poorly reactive. The second patient showed persistent posterior delta activity 30 h later, despite complete clinical recovery. The other two patients had an EEG in the late stage of an attack (16 h after symptom onset) and demonstrated bilateral slow theta-delta activity with the maximum over the posterior regions. The data reported in the literature suggest two patterns of EEG abnormalities occurring in children with BM. Most studies document a high-voltage slow wave activity seen predominantly over the posterior regions during an attack (Table 3). Only Parain and Samon-Dollfus (1984) found beta activity, but the relation of this finding to the exact stage of the attack was not stated. The occipital slowing has been attributed to ischemia in the territory of the posterior cerebral arteries (Lapkin et al., 1977). The second type of abnormality described in several reports concerns the interictal EEG of children pretending to suffer from BM and shows occipital spikes and
377
spike-wave activity (Camfield et al., 1978). Similar findings have been reported in children with benign occipital epilepsy (Gastaut, 1983). These two syndromes may occur in the same patient (Newton and Aicardi, 1983) and may have a common underlying pathophysiology. We could not demonstrate epileptiform discharges in our patients during the attacks or interictally. Thus, there are two distinct syndromes, BM and occipital seizures, which can present with a very similar clinical picture, but which should not be confounded, since EEG findings, clinical course extending to the long term, and therapy, are different (Panayiotopoulos, 1980, 1991). Our results demonstrate that EEG findings change in the course of a BM attack: in the acute initial stage there is diffuse slowing, whereas later on, when symptoms fade or have already resolved, there is slowing confined to the posterior regions. Processes in the posterior fossa are known to cause marked EEG abnormalities. Involvement of brain-stem structures due to ischemia, hemorrhage, inflammation or space-occupying lesions may produce EEG changes similar to those found during a BM attack. However, these changes are progressive and not transient. The clinical features are usually different, and brain imaging quickly allows differentiation. Diagnostically the EEG findings during a BM attack can help to exclude an epileptic disorder such as occipital seizure, partial complex status epilepticus or psychogenic unconsciousness. The latter would show normal tracings. BM in children, though not frequent, often presents as a dramatic event. Knowledge of the severe but transient nature of the EEG abnormalities occurring during an attack and
Table 3 Transient EEG abnormalities in children with BM attacks: review of the literature Authors
Patients, age
Timea
EEG findings
Gascon and Barlow, 1970
1 boy, 8 years
Shortly after
Lapkin and Golden, 1978
1 boy, 12 years
18 h after admission
Eviatar, 1981 Parain and Samon-Dollfus, 1984
3 girls, 3 boys 6 boys, 3 girls, 9 to 14 years
Ictal Arrival in a pediatric ward
De Romanis et al., 1993
4 girls, 2 boys, 3 to 8 years
For up to 72 h in 4 patients, 24 h in 2 patients
Jacome, 1987
1 girl, 13 years
Ictal
Beaumanoir and Jekiel, 1987
4 girls, 3 boys, 7 to 16 years
Ictal
Bouquet and Cernibori, 1981 Cernibori and Bouquet, 1984
2 girls, 2 boys, 13 to 15 years 8 children, 2 to 14 years
Ictal Ictal
Diffuse delta slowing bilateral theta waves Background disorganization and rhythmic bilateral occipital delta activity Posterior slowing Excess of beta activity in 8 (in 6 diffuse, in 2 cases predominantly frontal). One patient: posterior abnormal slow wave activity Diffuse high-voltage slow (delta) waves associated with spikes and sharp waves Posteriorly predominant sharp and slow wave complexes High-amplitude monomorphic slow posterior activity Slow posterior activity Diffuse slow wave activity of higher amplitude posteriorly. In 5 with unilateral dominance
a
Detailed timing of EEG records in relation to symptom onset is only rarely stated.
378
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
their interpretation in the context of the clinical setting may well prevent further dramatization.
Acknowledgements The authors would like to thank Jame McDougall for her assistance in preparing the manuscript. References Beaumanoir, A. and Jekiel, M. Electrographic observations during attacks of classical migraine. In: F. Andermatt and E. Lugaresi, (Eds.), Migraine and Epilepsy. Butterworths, Boston, 1987, pp. 163–180. Bickerstaff, E.R. Basilar artery migraine. Lancet, 1961a, 1: 15–17. Bickerstaff, E.R. Impairment of consciousness in migraine. Lancet, 1961b, 2: 1057–1059. Bouquet, F. and Cernibori, A. Prolonged consciousness disorders in attacks of basilar artery migraine. Rev. Neurobiol., 1981, 27: 671–676. Cernibori, A. and Bouquet, F. Loss of consciousness during basilar artery migraine attack in childhood: EEG and clinical studies. Electroenceph. clin. Neurophysiol., 1984, 58: 72. Camfield, P.R., Matrakos, K. and Andermann, F. Basilar migraine, seizures, and severe epileptiform EEG abnormalities: a relative benign syndrome in adolescents. Neurology, 1978, 28: 584–588. De Romanis, F., Buzzi, G., Assenza, S., Brusa, L. and Cerbo, R. Basilar migraine with electroencephalographic findings of occipital spike-wave complexes: a long-term study in seven children. Cephalalgia, 1993, 13: 192–196.
Eviatar, L. Vestibular testing in basilar artery migraine. Ann. Neurol., 1981, 9: 126–130. Gascon, G. and Barlow, C.G. Juvenile migraine, presenting as an acute confusional state. Pediatrics, 1970, 45: 628–635. Gastaut, H. A new type of epilepsy: benign partial epilepsy of childhood with occipital spike-waves. Clin. Electroencephalogr., 1983, 22: 13–22. Headache Classification Committee of the International Headache Society Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia, 1988, 8 (Suppl. 7): 13–17. Hockaday, J.M. Basilar migraine in childhood. Dev. Med. Child. Neurol., 1979, 21: 455–463. Jacome, D.E. EEG Features in basilar artery migraine. Headache, 1987, 27: 80–83. Lapkin, L.M., French, J.H., Golden, G.S. and Rowan, A.J. The electroencephalogram in childhood basilar artery migraine. Neurology, 1977, 27: 580–583. Lapkin, L.M. and Golden, G.S. Basilar artery migraine. Am. J. Dis. Child., 1978, 132: 278–281. Newton, R. and Aicardi, J. Clinical findings in children with occipital spike-wave complexes suppressed by eye-opening. Neurology, 1983, 33: 1526–1529. Panayiotopoulos, C.P. Basilar migraine? Seizures, and severe epileptic EEG abnormalities. Neurology, 1980, 30: 1122–1125. Panayiotopoulos, C.P. Basilar migraine. Neurology, 1991, 41: 1707. Parain, D. and Samon-Dollfus, D. Electroencephalograms in basilar artery migraine. Electroenceph. clin. Neurophysiol., 1984, 58: 392–399. Slatter, K.H. Some clinical and EEG findings in patients with migraine. Brain, 1968, 91: 85–98. Sturzenegger, M. and Meienberg, O. Basilar artery migraine: a follow-up study of 82 cases. Headache, 1985, 25: 408–415.
Case report
EEG findings during basilar migraine attacks in children G.P. Ramelli a ,*, M. Sturzenegger b, F. Donati b, K. Karbowski b a
Department of Paediatrics, Universita¨ts-Kinderklinik, Inselspital, CH-3010 Berne, Switzerland b Department of Neurology, University of Berne, Berne, Switzerland Accepted for publication: 22 June 1998
Abstract We present clinical and EEG findings in 4 children with basilar migraine (BM) (three female and one male, age 11 to 13.5 years). All patients had an EEG during the acute attack and a follow-up EEG within 4 to 18 days. In two patients the EEG, done within 4 h of the onset of symptoms (initial stage), showed diffuse polymorphic subdelta-delta activity. In two other children the EEG, performed 16 h after the onset of symptoms, showed delta-theta activity predominant over the occipital regions. Resolution of these abnormalities during follow-up was observed in all patients. We wish to stress the danger of misinterpretation of the slow wave activity in the EEG of patients with BM attacks. Together with the clinical findings and their evolution, EEG results should not be interpreted as a sign of a structural brain-stem lesion, such as infarction or inflammation. 1998 Elsevier Science Ireland Ltd. All rights reserved Keywords: Basilar migraine; EEG findings; Child
1. Introduction Bickerstaff (1961a) was the first to describe migraine patients with symptoms indicating dysfunction of brain areas supplied by the vertebrobasilar arteries during an attack. Basilar migraine (BM) occurs predominantly in young females and, in addition to headache and vomiting, may present with bilateral visual symptoms, dysarthria, vertigo, tinnitus, decreased hearing, double vision, ataxia, bilateral sensory symptoms or weakness, and qualitatively or quantitatively altered consciousness (IHS, 1988; Sturzenegger and Meienberg, 1985). Thus, clinical findings of a patient examined during an attack may suggest a serious neurological disorder. In such a situation, further investigations are often necessary and the correct diagnosis is only made retrospectively (Sturzenegger and Meienberg, 1985). No EEG abnormalities were described in the original description of the syndrome, but the temporal relationship between attacks and EEG recordings was not stated (Bickerstaff, 1961b). The first EEG during a BM attack was reported by Slatter (1968). Later, either single cases with * Corresponding author. Tel.: +41 31 6322111; fax:+41 31 6329448.
EEG recordings were reported or larger series were published that did not document EEG findings in sufficient detail (Hockaday, 1979). We describe 4 children with BM, in whom severe transient electroencephalographic abnormalities were observed during the attack. We discuss the relevance of these findings with respect to differential diagnosis.
2. Patients, methods and findings Between July 1996 and March 1997, 4 children (3 females and 1 male aged 11 to 13.5 years) were admitted to the Department of Paediatrics, University of Berne for acute neurological disturbances compatible with BM. 2.1. Patient 1 This 12-year old girl had had no previous headaches. Family history was unremarkable. She had no history of medication or trauma. Three hours before hospital admission she reported severe occipital headache with acute onset of blurred and later tunnel vision. She was confused and
0013-4694/98/$ - see front matter 1998 Elsevier Science Ireland Ltd. All rights reserved PII S0013-4694 (98 )0 0094-7
EEG 97782
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
375
somnolent. She was then referred to our hospital. We found a totally disoriented girl. On neurological examination there were bilateral extensor plantar responses. There was no abnormality in routine blood and CSF analysis. The EEG 4 h after symptom onset showed diffuse polymorphic, highvoltage subdelta-delta activity of 0.5–2 Hz. A follow-up EEG was performed 4 days after the acute attack and showed a marked improvement. The patient recovered completely and was discharged 5 days later. She had amnesia about the attack. 2.2. Patient 2 During the previous 2 years, this 13.5-year-old boy had suffered from recurrent unilateral headaches with nausea and photosensitivity at about 2-month intervals. His mother had attacks of migraine without aura. There was no history of medication or trauma. Two hours before admission the boy reported severe occipital headache, nausea and he vomited. One hour later he became confused, disoriented and aggressive, his mother noted dysarthric speech and he reported blurred vision. We found a confused and lethargic boy with a Glasgow Coma Score of 10. Tendon reflexes were very brisk. A routine blood test and CSF analysis were normal. The EEG 4 h after symptom onset showed diffuse polymorphic, high-voltage subdelta-delta activity of 0.5–2 Hz (Fig. 1a). The following day (30 h after symptom onset) he was clinically normal but EEG showed persistent posterior delta activity (Fig. 1b). He was discharged 3 days later. A follow-up EEG performed 7 days after the acute attack showed normalization (Fig. 1c). 2.3. Patient 3 This 11-year-old girl had no history of headache and she had been in good health until the day of admission. Her mother suffered from migraine without aura. Two hours before admission, while playing tennis, she reported severe frontal headache and nausea, some minutes later she showed a ataxic gait and she reported dizziness and blurred vision, and her speech became dysarthric. Still later she reported blindness and showed a confusional state. On admission she showed impaired consciousness with disorientation, was poorly responsive to stimuli and her Glasgow Coma Score was 12. Routine urine and blood tests including complete blood count, sedimentation rate, electrolyte, liver and kidney function, plasma glucose and CSF were normal. CT scan of the brain showed no abnormalities. The EEG was recorded 16 h after onset of the attack and showed delta-theta activity over the posterior regions. There were no epileptiform discharges and reactivity was poor. A follow-up EEG performed 10 days later was normal. 2.4. Patient 4 This 12.5-year-old girl had suffered migraine without
Fig. 1. EEG recordings in a 13.5-year old boy with BM. (a) EEG recording 4 h after symptom onset: diffuse high amplitude subdelta-delta activity. (b) EEG recording 30 h after onset of symptoms: nearly continuous delta activity over the posterior regions. (c) EEG recording 7 days after onset of symptoms: normalization of EEG recording, showing predominant alpha activity over the posterior regions.
376
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
Table 1 History and clinical findings of our patients Patient
Sex Age at first BM attack (years) Family history of migraine Patient history of migraine Headache Visual symptoms Gait ataxia Dysarthria Confusion Amnesia GCS Lumbar puncture CT scan
1
2
3
4
F 12 Negative Negative + + − − + +
a
a
F 11 Positive (mother) Negative + + + + + + 12 + +
F 12.5 Positive (father) Positive + + + + + +
+
M 13.5 Positive (mother) Positive + + − + + + 10 +
a
a
+ +
M, male; F, female; GCS, Glasgow Coma Scale; CT, computed tomography; +, present; −, absent. a
Not done.
aura with nausea and photosensitivity for several years with an attack rate of one per month. Her father suffered from migraine without aura. Two hours before hospital admission she reported severe occipital headache. She was sent home from school. One hour later at home she became restless, started screaming, showed an ataxic gait, and her speech became dysarthric and barely understandable. She behaved like a blind person. On admission she was totally disoriented and lethargic. There were no abnormalities on motor examination, but the tendon reflexes were very brisk, with bilateral extensor plantar responses. Routine blood and urine test, CSF results and CT scan were normal. The first EEG was recorded 16 h after onset of the attack and showed delta-theta activity over the posterior regions. Reactivity was poor. A follow-up EEG performed 10 days after the acute attack was normal. The main clinical characteristics of the 4 patients are summarized in Table 1. In all 4 patients this was the first BM attack, but two patients had previously had other types of migraine attacks. Family history for migraine was positive in 3 patients, with the mother being affected in two. Severe paroxysmal headache was present in all patients and was occipitally located in 3. The most distressing symptoms
were visual disturbances including blurred vision, tunnel vision and amblyopia, and altered consciousness with confusion or amnesia. Three patients had dysarthria and one patient had gait ataxia. The symptoms disappeared in all cases within 24 to 48 h. A computed tomographic (CT) scan of the brain performed in two patients was normal. CSF analysis was normal in all 4 patients. Drug intoxication was excluded by history and by blood and urine analysis for barbiturates, carbamates, phenothiazine and benzodiazepines. No patient had a history of trauma. EEG results are summarized in Table 2. All patients had an EEG during the acute attack with definitively pathologic findings. Two patients had the EEG 4 h after the first symptoms (initial stage) and both showed diffuse polymorphic, high-voltage subdelta-delta activity (Fig. 1a). On the second day (30 h), patient 2 was clinically normal, but the EEG showed persistent posterior delta activity (Fig. 1b). In the two other patients, the first EEG was recorded 16 h (decreasing symptoms) after the onset of the attacks and showed delta-theta activity over the posterior regions. There were no epileptiform discharges and reactivity was poor. A follow-up EEG was performed in all 4 children 4 to 18 days after the acute attack, and showed a marked improvement (Fig. 1c).
Table 2 EEG findings Patient no.
1 2 3 4
During attack
EEG follow-up
Latency (h)
Frequency (Hz)
Localization
Days after attack
Findings
4 4 16 16
0.5–2/Subdelta-delta activity 0.5–2/Subdelta-delta activity 3–6/Delta-theta 3–6/Delta-theta
Diffuse Diffuse Posterior Posterior
4 7 10 18
Improved Normal Normal Normal
Latency is the interval from first symptoms to recording.
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
3. Discussion Only a few patients with an EEG recorded during an acute basilar migraine (BM) attack have been described, and the reported findings were quite variable (Jacome, 1987). This is most probably due to the fact that recordings were made at different stages of the attack, which is known to take a protracted course. The clinical presentation and the subsequent course in our 4 children fulfil the IHS criteria for diagnosis of BM (IHS, 1988). All had significant EEG abnormalities during the acute stage of the attack, which had resolved on follow-up examinations within 1 to 2 weeks. Two patients with an EEG recorded within 4 h of symptom onset (initial stage) showed diffuse polymorphic high-voltage subdelta-delta activity, which was poorly reactive. The second patient showed persistent posterior delta activity 30 h later, despite complete clinical recovery. The other two patients had an EEG in the late stage of an attack (16 h after symptom onset) and demonstrated bilateral slow theta-delta activity with the maximum over the posterior regions. The data reported in the literature suggest two patterns of EEG abnormalities occurring in children with BM. Most studies document a high-voltage slow wave activity seen predominantly over the posterior regions during an attack (Table 3). Only Parain and Samon-Dollfus (1984) found beta activity, but the relation of this finding to the exact stage of the attack was not stated. The occipital slowing has been attributed to ischemia in the territory of the posterior cerebral arteries (Lapkin et al., 1977). The second type of abnormality described in several reports concerns the interictal EEG of children pretending to suffer from BM and shows occipital spikes and
377
spike-wave activity (Camfield et al., 1978). Similar findings have been reported in children with benign occipital epilepsy (Gastaut, 1983). These two syndromes may occur in the same patient (Newton and Aicardi, 1983) and may have a common underlying pathophysiology. We could not demonstrate epileptiform discharges in our patients during the attacks or interictally. Thus, there are two distinct syndromes, BM and occipital seizures, which can present with a very similar clinical picture, but which should not be confounded, since EEG findings, clinical course extending to the long term, and therapy, are different (Panayiotopoulos, 1980, 1991). Our results demonstrate that EEG findings change in the course of a BM attack: in the acute initial stage there is diffuse slowing, whereas later on, when symptoms fade or have already resolved, there is slowing confined to the posterior regions. Processes in the posterior fossa are known to cause marked EEG abnormalities. Involvement of brain-stem structures due to ischemia, hemorrhage, inflammation or space-occupying lesions may produce EEG changes similar to those found during a BM attack. However, these changes are progressive and not transient. The clinical features are usually different, and brain imaging quickly allows differentiation. Diagnostically the EEG findings during a BM attack can help to exclude an epileptic disorder such as occipital seizure, partial complex status epilepticus or psychogenic unconsciousness. The latter would show normal tracings. BM in children, though not frequent, often presents as a dramatic event. Knowledge of the severe but transient nature of the EEG abnormalities occurring during an attack and
Table 3 Transient EEG abnormalities in children with BM attacks: review of the literature Authors
Patients, age
Timea
EEG findings
Gascon and Barlow, 1970
1 boy, 8 years
Shortly after
Lapkin and Golden, 1978
1 boy, 12 years
18 h after admission
Eviatar, 1981 Parain and Samon-Dollfus, 1984
3 girls, 3 boys 6 boys, 3 girls, 9 to 14 years
Ictal Arrival in a pediatric ward
De Romanis et al., 1993
4 girls, 2 boys, 3 to 8 years
For up to 72 h in 4 patients, 24 h in 2 patients
Jacome, 1987
1 girl, 13 years
Ictal
Beaumanoir and Jekiel, 1987
4 girls, 3 boys, 7 to 16 years
Ictal
Bouquet and Cernibori, 1981 Cernibori and Bouquet, 1984
2 girls, 2 boys, 13 to 15 years 8 children, 2 to 14 years
Ictal Ictal
Diffuse delta slowing bilateral theta waves Background disorganization and rhythmic bilateral occipital delta activity Posterior slowing Excess of beta activity in 8 (in 6 diffuse, in 2 cases predominantly frontal). One patient: posterior abnormal slow wave activity Diffuse high-voltage slow (delta) waves associated with spikes and sharp waves Posteriorly predominant sharp and slow wave complexes High-amplitude monomorphic slow posterior activity Slow posterior activity Diffuse slow wave activity of higher amplitude posteriorly. In 5 with unilateral dominance
a
Detailed timing of EEG records in relation to symptom onset is only rarely stated.
378
G.P. Ramelli et al. / Electroencephalography and clinical Neurophysiology 107 (1998) 374–378
their interpretation in the context of the clinical setting may well prevent further dramatization.
Acknowledgements The authors would like to thank Jame McDougall for her assistance in preparing the manuscript. References Beaumanoir, A. and Jekiel, M. Electrographic observations during attacks of classical migraine. In: F. Andermatt and E. Lugaresi, (Eds.), Migraine and Epilepsy. Butterworths, Boston, 1987, pp. 163–180. Bickerstaff, E.R. Basilar artery migraine. Lancet, 1961a, 1: 15–17. Bickerstaff, E.R. Impairment of consciousness in migraine. Lancet, 1961b, 2: 1057–1059. Bouquet, F. and Cernibori, A. Prolonged consciousness disorders in attacks of basilar artery migraine. Rev. Neurobiol., 1981, 27: 671–676. Cernibori, A. and Bouquet, F. Loss of consciousness during basilar artery migraine attack in childhood: EEG and clinical studies. Electroenceph. clin. Neurophysiol., 1984, 58: 72. Camfield, P.R., Matrakos, K. and Andermann, F. Basilar migraine, seizures, and severe epileptiform EEG abnormalities: a relative benign syndrome in adolescents. Neurology, 1978, 28: 584–588. De Romanis, F., Buzzi, G., Assenza, S., Brusa, L. and Cerbo, R. Basilar migraine with electroencephalographic findings of occipital spike-wave complexes: a long-term study in seven children. Cephalalgia, 1993, 13: 192–196.
Eviatar, L. Vestibular testing in basilar artery migraine. Ann. Neurol., 1981, 9: 126–130. Gascon, G. and Barlow, C.G. Juvenile migraine, presenting as an acute confusional state. Pediatrics, 1970, 45: 628–635. Gastaut, H. A new type of epilepsy: benign partial epilepsy of childhood with occipital spike-waves. Clin. Electroencephalogr., 1983, 22: 13–22. Headache Classification Committee of the International Headache Society Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia, 1988, 8 (Suppl. 7): 13–17. Hockaday, J.M. Basilar migraine in childhood. Dev. Med. Child. Neurol., 1979, 21: 455–463. Jacome, D.E. EEG Features in basilar artery migraine. Headache, 1987, 27: 80–83. Lapkin, L.M., French, J.H., Golden, G.S. and Rowan, A.J. The electroencephalogram in childhood basilar artery migraine. Neurology, 1977, 27: 580–583. Lapkin, L.M. and Golden, G.S. Basilar artery migraine. Am. J. Dis. Child., 1978, 132: 278–281. Newton, R. and Aicardi, J. Clinical findings in children with occipital spike-wave complexes suppressed by eye-opening. Neurology, 1983, 33: 1526–1529. Panayiotopoulos, C.P. Basilar migraine? Seizures, and severe epileptic EEG abnormalities. Neurology, 1980, 30: 1122–1125. Panayiotopoulos, C.P. Basilar migraine. Neurology, 1991, 41: 1707. Parain, D. and Samon-Dollfus, D. Electroencephalograms in basilar artery migraine. Electroenceph. clin. Neurophysiol., 1984, 58: 392–399. Slatter, K.H. Some clinical and EEG findings in patients with migraine. Brain, 1968, 91: 85–98. Sturzenegger, M. and Meienberg, O. Basilar artery migraine: a follow-up study of 82 cases. Headache, 1985, 25: 408–415.