Develop. Med. Child Neurol. 1918, 20, 58G585
Seizure Headaches in Children Kenneth F. Swaiman Yitzchak Frank
Introduction There have been a few reported cases of headaches as sole symptoms of seizure disorders (Halpern and Bental 1958, Chao and Dakis 1964, Jonas 1966, Poch 1974) but there are no criteria to differentiate these c a e s from vascular headaches. This is a report of six children with paroxysmal headaches resulting from seizure disorders. A possible mechanism for the causation of seizure headaches is discussed and criteria for diagnosis are suggested.
The clinical picture of our patients' seizure headaches is that they are usually diffuse or bifrontal, and that they begin abruptly at any time, but only occasionally at night. There are no precipitating factors. The headache may continue for hours, though usually for less than a day. Usually it is accompanied by nausea and vomiting and is followed by a distinct postictal phase of lethargy and sleep. The frequency is variable and often there is a favourable response to anticonvulsants.
Patients The patients have been selected from the population of the Pediatric Neurology Clinic of the University of Minnesota between the years 1966 and 1976. They have had repeated examinations and electroencephalograms (Fig. 1). Their responses to medication are recorded in Table I. ,411 h i x patients had paroxysmal headaches, usually accompanied by nausea and vomiting and followed by postictal lethargy or sleep (Table I ) . Duration of the attacks was relatively short, lasting at most only a few hours. The patients' family histories did not include migraine headaches. All six patients improved with anticonvulsant therapy, but Cases 1 and 2 had recurrence of their headaches when anticonkulsant medications were discontinued.
Discussion The differential diagnosis of headaches in children includes inflammatory, vascular. post-traumatic, psychogenic and muscle contraction headaches (Kriel 1972, Meloff 1973). Both migraine and seizure mechanisms may underlie vascular headaches. In 1966, Jonas described five adults who presented with headache as the sole manifestation of seizures. The headaches were brief, were characterized by abrupt onset and termination, and were followed by postictal lethargy. Electroencephalographic studies revealed paroxysmal abnormalities. The headaches responded to anticonvulsant therapy. Halpern and Bental (1958) reported five children who had paroxysmal or continuous headache as the sole symptom of their convulsive disease. They referred to this state as 'epileptic cephalea'.
C orie\podence fu Kenneth F. Swaiman, M.D., Box 486 Mayo. University of Minnesota Medical School, 420 Delaware Street S.E , Minneapolis. Minnesota 55455.
580
KENNETH F. SWAIMAN
YITZCHAK FRANK
2
Fig. 1. Electroencephalograms of patients 1 to 6 (see Table I).
Chao and Davis (1964) reported 249 patients with 'convulsive equivalent syndrome of childhood', of whom 85 per cent had headaches, 65 per cent had abnormal pains and 45 per cent had other manifestations of epilepsy. Most of them had autonomic symptoms. The headaches responded to anticonvulsant therapy. The features which differentiate seizure headache from migraine headache are the very high incidence of familial history in migraine headache, the location of the headache (often hemicranial in the migraine patients), the presence of aura (much more
common in the migraine group) and the favourable response to anticonvulsants in the seizure headache group (Table 11). The true incidence of seizure headaches is unknown, but probably is greater than recognized because of the confusion with migraine headaches. The electroencephalographic pattern in both adults and children with migraine has been widely investigated (Golla and Winter 1959, Smyth and Winter 1964, Towle 1965, Richey et al. 1966, Whitehouse et al. 1967, Hockaday and Whitty 1969, Hughes 1972). There is disagreement about the frequency
I
M
F
Case Sex
I
None
None
Bifrontal
Bitemporali
Paroxysmal headaches accompanied by nausea and vomiting, followed by sleep
Paroxysmal, very frequent, severe headaches, followed by abdominal pain
11
None
Bifrontal
None
None
Bifrontal
I
Diffuse
of
1
~
1
I
None
headcrche
Bifrontal
Paroxysmal headaches accompanied by nausea and vomiting, starting at night, lasting a few hours Paroxysmal headaches accompanied by vomiting, lasting 1-2 hours, followed by sleep
Paroxysmal headaches accompanied by nausea and vomiting every 2-3 weeks, lasting usually a few hours, followed by sleep
Description of syniptoms
Family history I of headache ,
Location
Paroxysmal headaches accompanied by vomiting, lasting about 6 hours, followed by lethargy
I
~
~
I
7
10
7
13
Age at onset (yrs)
Cyanotic at birth; normal developmental milestones
-
Cyclic, vomiting
Past history
Response to medications ______ No response to methysergide maleate, diazepam, or to a medication containing ergotamine tartrate, alkaloids of belladonna, and phenobarbitals : improvement occurred with phenytoin Bilateral multifocal Mild Headaches eliminated by spikes and excessive co-ordination ' primidones : they difficulties recurred when he did irregular theta activity not take his medications Normal Headaches eliminated by Bursts of highvoltage theta activity primidone beginning in the right frontal area and spreading Normal No response to subFrequent bursts of lingual ergotamine irregular polyspike tartrate: partial and wave activity 1 improvement occurred originating on the with mephobarbital and left phenytoin Bursts of spikes and Normal No response to medication containing spike-wave caffeine, phenacetin, complexes aspirin, and butalbital : originating from the left posterior improvement occurred with phenobarbital quadrant Normal Headaches eliminated Irregular and rhythmic slowing; by primidone: later spikes more frequent l recurrence responded to on the left 1 increased primidone dose
Neurological examination _______ Rhythmic discharges Normal (4Hz) in frontaltemporal areas bilaterally
Interictul electroencephalogratn
TABLE I Characteristics of seizure headaches
KENNETH F. SWAIMAN
YITZCHAK FRANK
TABLE I1 Characteristics of migraine headaches and seizure headaches Characteristics
Frequency Duration Starting time Location Precipitating factors Family history Electroencephalography
1
Migraine headaches
Convulsive headaches
Variable Many hours to days Usually late afternoon; rarely awaken patients from sleep Hemicranium or diffuse Emotional disturbance, school stress, fatigue
Variable Several hours During sleep or any time
85-90
Unusual Spike and wave discharges;bilateral spikes, rhythmic theta bursts Almost uniform postictal state consisting of somnolence and/or sleep Anticonvulsants Cerebral injury, central nervous system infections
%
Post-headache phase
Primarily diffuse slowing; occasionally focal slowing Fatigue or somnolence in many patients
Effective drugs Other history
Ergot, methysergide maleate None
and type of the electroencephalographic changes in migraine (Hughes 1972). It is noteworthy that most of the studies demonstrate a very low incidence of electroencephalographic epileptiform discharges in the inter-migraine period. There are also some specific electroencephalographic changes in migraine patients, including augmented hyperventilation response (Towle 1965) and an H-response to photic stimulation (Golla and Winter 1959, Richey et al. 1966). We feel that obvious epileptogenic activity in the electroencephalogram usually differentiates between convulsive headaches and migraine headaches. The pathophysiology which links abnormal brain discharge and seizure headache is an intriguing subject. The dural arteries, part of the venous sinuses, the proximal parts of the large intracranial vessels and the dural floor of the skull are sensitive to pain (Ray and Wolff 1940). The stimuli which produced pain included distension, stretching, stroking and faradic stimulation of the blood vessels. The pain arising from distension of the middle meningeal arteries is accompanied by nausea. Manipulation of brain paren-
Diffuse None
chyma does not cause pain. The stimulation of the intracranial portion of the internal carotid arteries, as well as proximal parts of the anterior, middle and posterior cerebral arteries, results in pain in the region of the homolateral eye. Therefore, at least partially, innervation of these vessels is by cranial nerve V. Pain induced by traction on the middle fossa venous structures and on the middle cerebral artery can be eliminated by injection of procaine into the trigeminal ganglia, but arteries of the brain have been shown to be supplied with other nerve fibre endings, including those of other cranial nerves and the autonomic nervous system (Dahl and Nelson 1964, Nelson and Rennels 1970). The autonomic nervous system is the most likely pathway through which an abnormal brain discharge can influence the intracranial blood vessels. Multiple fibre systems connect the hypothalamus to higher and lower brain centres; the largest is the medial forebrain bundle. This bundle is formed by fibres arising in the septa1 region and olfactory cortex of the temporal lobe. The fibres subsequently pass through
583
DEVELOPMENTAL MEDICINE AND CHlLD NEUROLOGY.
1978, 20
can be propagated into the hypothalamus, and thence through mesencephalic nuclei into the autonomic nervous system, causing headaches and other autonomic phenomena. It is known that such propagation is possible over axonal pathways (Jasper et al. 1969). Some of these patients will have other autonomic phenomena such as abdominal pain and pallor; almost all have nausea and vomiting.
the preo,itico-hypothalamic zone and into the paramedian regions of the mesencephalic tegmentum (Haymaker et al. 1969). It also receives fibres from the amygdalopiriform complex, the hippocampus (via the fornix) and the septa1 nuclei (Haymaker 1969~).The lateral zone of the hypothalamus receives fibres from the upper brainstem, ’mainly from the periaqueductal gray matter and some of the paramedian mesencephalic tegmental nuclei’ (Haymaker 19696). It is probably through these nuclei that the connection to blood vessels and visceral organs is achieved. A seizure discharge in the temporal lobe, any part of the limbic system or other parti of the cortex (Angevine et nl. 1964)
AUTHORS’ APPOINTMENTS
Kenneth F. Swaiman, M.D., Professor and Director; Yitzchak Frank, M.D., Medical Fellow; Division of Pediatric Neurology, University of Minnesota Medical School, Minneapolis, Minnesota 55455.
SUMMARY
Six children with paroxysmal headaches resulting from seizure disorders are reported. The clinical picture of seizure headaches includes the following features : they are usually diffuse or bifrontal; they begin abruptly at any time and last for minutes or several hours; in the majority of cases they are accompanied by nausea and vomiting and followed by postictal lethargy or sleep; there are no precipitating factors; they respond to anticonvulsants. 7he factors which differentiate between seizure headache and migraine are discussed. Seizure headache can be the sole clinical manifestation of seizure foci in the limbic system and other parts of the cortex. Some of these patients will have other autonomic phenomena such as pallor and abdominal pain; nearly all have nausea and vomiting. RESUME
S I Xcas de cephalies paroxystiques chez I’enfant, provenant de troubles comitiaux sont presentis. L’allure clinique des cephalies critiques presente les caractkres suivants : elles sont habituellement diffuses ou bi-frontales, elles commencent brutalement a n’importe quel moment et durent de quelques minutes a plusieurs heures. Dans la majorit6 des cas, elles sont accompagnies de naustes et de vomissements et suivies d’une lethargie post-critique ou de sommeil; il n’y a pas de facteurs annonciateurs; les medications anticomitiales sont actives. Les facteurs qui differencient cephalees critiques et migraines sont discutis. Les ciphalkes critiques peuvent &trela seule manifestation clinique de foyer comitial dans le \ysttme limbique et les autres parties du cortex. Quelques sujets prtsentent d’autres manifestations vigetatives telles que psleurs et douleurs abdominales. Presque tous ont des nausees et des vomissements. ZUSAMMENFASSUNG
Es wird iiber sechs Kinder mit paroxysmalen Kopfschmerzen infolge eines Krampfleidens berichtet. Das klinische Bild der Krampf-Kopfschmerzen bietet folgende charakteristischen Befunde : Die Schmerzen sind gewohnlich diffus oder bifrontal, sie beginnen abrupt, konnen
584
KENNETH F. SWAIMAN
YITZCHAK FRANK
zu jeder Zeit auftreten und dauern Minuten bis einige Stunden an. In der Mehrzahl der Falle klagen die Patienten iiber Ubelkeit, erbrechen und fallen anschliessend in einen postiktalen Dammerzustand oder Schlaf; es gibt keine ursachlichen Faktoren; die Kopfschmerzen sprechen auf die Behandlung mit Antikonvulsiva an. Auf die unterschiedlichen Befunde bei krampfbedingten Kopfschmerzen und bei Migrane wird ausfiihrlich eingegangen. Krampfebedingte Kopfschmerzen konnen die einzige klinische Manifestation von Krampffoci im limbischen System und anderen Teilen des Cortex sein. Bei einigen Patienten treten auch andere vegetative Symptome wie Blasse und Bauchschmerzen auf. Nahezu alle Kinder Klagen iiber Ubelkeit und Erbrechen. RESUMEN
Se aportan seis casos de niiios con cefaleas paroxisticas a consecuencia de enfermedades con crisis agudas. El cuadro clinico de 10s ataques de cefalea incluye 10s datos siguientes: son por lo general difusas o bifrontales; empiezan abruptamente en cualquier momento y duran desde minutos a varias horas; en la mayoria de 10s casos se acompaiian de nauseas y v6mitos y se siguen de letargia postictal y sueiio; no existen factores desencadenantes y responde a 10s anticonvulsilantes. Se discuten 10s factores diferenciales entre la crisis de cefalea y la migraiia. Los ataques de cefalea pueden ser la h i c a manifestacibn de crisis focales en el sistema limbic0 y otros puntos del c6rtex. Algunos de estos pacientes pueden tener otros fen6menos vegetativos tales como palidez y dolor abdominal; casi todos tienen nauseas y v6mitos. REFERENCES Angevine,, J. B., Locke, S., Yakovlev, P. L. (1964) ‘Limbic nuclei of thalamus and connections of limbic cortex: V. Thalamocortical projection of the magnocellular medial dorsal nucleus in man.’ Archives of Neurology, 10, 165-180. Chao, O., Davis, S. D. (1964) ‘Convulsive equivalent syndrome of childhood.’ Journal of Pediatrics, 64, 499-508. Dahl, E., Nelson, E. (1964) ‘Electron microscopic observations on human intracranial arteries. 11. Innervation.’ Archives of Neurology, 10, 158-164. Golla, F. L., Winter, A. L. (1959) ‘Analysis of cerebral response to flicker in patients complaining of episodic headache.’ Electroencephalography and Clinical Neurophysiology, 11, 539-549. Halpern, L., Bental, E. (1958) ‘Epileptic cephalea.’ Neurology, 8, 615-620. Haymaker, W. (1969~)‘Hypothalamus, pituitary gland, midbrain and related regions.’ In Haymaker, W. (Ed.) Bing’s Local Diagnosis in Neurological Diseases, 15th Edn. St. Louis: C . V. Mosby. p. 465. (1969b) ‘Hypothalamus, pituitary gland, midbrain and related regions.’ Zn: Haymaker, W. (Ed.) Bing’s Local Diagnosis in Neurological Diseases, 15th edn. St. Louis: C. V. Mosby. p. 467. - Anderson, E., Nauta, W. J. H. (Eds.) (1969) The Hypothalamus. Springfield, 111.: C. C. Thomas. p. 164. Hockaday, J. M., Whitty, C. W. M. (1969) ‘Factors determining the electroencephalogram in migraine. A study of 560 patients according to clinical type of migraine.’ Brain, 92,769-788. Hughes, J. R. (1 972) ‘EEG in headaches.’ Headache, 11,162-170. Jasper, H. H., Ward, A. A., Pope, A. (1969) ‘Mechanisms of propagation: Extracellular studies.’ In Jasper, H. H., Ward, A., Pope, A. (Eds.) Basic Mechanisms of the Epilepsies. Boston: Little, Brown. p. 421. Jonas, A. D. (1966) ‘Headaches as seizure equivalents.’ Headache, 6,78-87. Kriel. R. L. (1972) ‘Headache.’ In Swaiman. K. F.., Wright, - . F. S. (Eds.) . . The Practice of Pediatric Neurolom. _. St.’Louis:‘C. V: Mosby. p. 154. Meloff, K. L. (1973) ‘Headache in pediatric practice.’ Headache, 13, 125-129. Nelson, E., Rennels, M. (1970) ‘Innervation of intracranial arteries.’ Brain, 93, 475490. Poch, G. F. (1974) ‘Epileptic headaches.’ Archives de Neurobiologie, 37 (suppl.), 1977. Rav. B. S.. Wolff. H. G. (1940) ‘ExDerimentalstudies on headache: Pain sensitive structures of the head and their significance in headache.’ Archives of Surgery, 41, 813-856. Richey, E. T., Kooi, K. A., Waggoner, R. W. (1966) ‘Visually evoked responses in migraine.’ Electroencephalography and Clinical Neurophysiology, 21,23-27. Smyth, V. 0. G., Winter, A. L. (1964) ‘The EEG in migraine.’ Electroencephalography and Clinical Neurophysiology, 16, 194-202. Towle, P. A. (1965) ‘The electroencephalographic hyperventilation response in migraine.’ Elecfroencephalography and Clinical Neurophysiology, 19, 390-393. Whitehouse, D., Pappas, J. A., Escala, P. A., Livingstone, S. (1967) ‘Electroencephalographic changes in children with migraine.’ New England Journal of Medicine, 276, 23-27.
-
585
Seizure Headaches in Children Kenneth F. Swaiman Yitzchak Frank
Introduction There have been a few reported cases of headaches as sole symptoms of seizure disorders (Halpern and Bental 1958, Chao and Dakis 1964, Jonas 1966, Poch 1974) but there are no criteria to differentiate these c a e s from vascular headaches. This is a report of six children with paroxysmal headaches resulting from seizure disorders. A possible mechanism for the causation of seizure headaches is discussed and criteria for diagnosis are suggested.
The clinical picture of our patients' seizure headaches is that they are usually diffuse or bifrontal, and that they begin abruptly at any time, but only occasionally at night. There are no precipitating factors. The headache may continue for hours, though usually for less than a day. Usually it is accompanied by nausea and vomiting and is followed by a distinct postictal phase of lethargy and sleep. The frequency is variable and often there is a favourable response to anticonvulsants.
Patients The patients have been selected from the population of the Pediatric Neurology Clinic of the University of Minnesota between the years 1966 and 1976. They have had repeated examinations and electroencephalograms (Fig. 1). Their responses to medication are recorded in Table I. ,411 h i x patients had paroxysmal headaches, usually accompanied by nausea and vomiting and followed by postictal lethargy or sleep (Table I ) . Duration of the attacks was relatively short, lasting at most only a few hours. The patients' family histories did not include migraine headaches. All six patients improved with anticonvulsant therapy, but Cases 1 and 2 had recurrence of their headaches when anticonkulsant medications were discontinued.
Discussion The differential diagnosis of headaches in children includes inflammatory, vascular. post-traumatic, psychogenic and muscle contraction headaches (Kriel 1972, Meloff 1973). Both migraine and seizure mechanisms may underlie vascular headaches. In 1966, Jonas described five adults who presented with headache as the sole manifestation of seizures. The headaches were brief, were characterized by abrupt onset and termination, and were followed by postictal lethargy. Electroencephalographic studies revealed paroxysmal abnormalities. The headaches responded to anticonvulsant therapy. Halpern and Bental (1958) reported five children who had paroxysmal or continuous headache as the sole symptom of their convulsive disease. They referred to this state as 'epileptic cephalea'.
C orie\podence fu Kenneth F. Swaiman, M.D., Box 486 Mayo. University of Minnesota Medical School, 420 Delaware Street S.E , Minneapolis. Minnesota 55455.
580
KENNETH F. SWAIMAN
YITZCHAK FRANK
2
Fig. 1. Electroencephalograms of patients 1 to 6 (see Table I).
Chao and Davis (1964) reported 249 patients with 'convulsive equivalent syndrome of childhood', of whom 85 per cent had headaches, 65 per cent had abnormal pains and 45 per cent had other manifestations of epilepsy. Most of them had autonomic symptoms. The headaches responded to anticonvulsant therapy. The features which differentiate seizure headache from migraine headache are the very high incidence of familial history in migraine headache, the location of the headache (often hemicranial in the migraine patients), the presence of aura (much more
common in the migraine group) and the favourable response to anticonvulsants in the seizure headache group (Table 11). The true incidence of seizure headaches is unknown, but probably is greater than recognized because of the confusion with migraine headaches. The electroencephalographic pattern in both adults and children with migraine has been widely investigated (Golla and Winter 1959, Smyth and Winter 1964, Towle 1965, Richey et al. 1966, Whitehouse et al. 1967, Hockaday and Whitty 1969, Hughes 1972). There is disagreement about the frequency
I
M
F
Case Sex
I
None
None
Bifrontal
Bitemporali
Paroxysmal headaches accompanied by nausea and vomiting, followed by sleep
Paroxysmal, very frequent, severe headaches, followed by abdominal pain
11
None
Bifrontal
None
None
Bifrontal
I
Diffuse
of
1
~
1
I
None
headcrche
Bifrontal
Paroxysmal headaches accompanied by nausea and vomiting, starting at night, lasting a few hours Paroxysmal headaches accompanied by vomiting, lasting 1-2 hours, followed by sleep
Paroxysmal headaches accompanied by nausea and vomiting every 2-3 weeks, lasting usually a few hours, followed by sleep
Description of syniptoms
Family history I of headache ,
Location
Paroxysmal headaches accompanied by vomiting, lasting about 6 hours, followed by lethargy
I
~
~
I
7
10
7
13
Age at onset (yrs)
Cyanotic at birth; normal developmental milestones
-
Cyclic, vomiting
Past history
Response to medications ______ No response to methysergide maleate, diazepam, or to a medication containing ergotamine tartrate, alkaloids of belladonna, and phenobarbitals : improvement occurred with phenytoin Bilateral multifocal Mild Headaches eliminated by spikes and excessive co-ordination ' primidones : they difficulties recurred when he did irregular theta activity not take his medications Normal Headaches eliminated by Bursts of highvoltage theta activity primidone beginning in the right frontal area and spreading Normal No response to subFrequent bursts of lingual ergotamine irregular polyspike tartrate: partial and wave activity 1 improvement occurred originating on the with mephobarbital and left phenytoin Bursts of spikes and Normal No response to medication containing spike-wave caffeine, phenacetin, complexes aspirin, and butalbital : originating from the left posterior improvement occurred with phenobarbital quadrant Normal Headaches eliminated Irregular and rhythmic slowing; by primidone: later spikes more frequent l recurrence responded to on the left 1 increased primidone dose
Neurological examination _______ Rhythmic discharges Normal (4Hz) in frontaltemporal areas bilaterally
Interictul electroencephalogratn
TABLE I Characteristics of seizure headaches
KENNETH F. SWAIMAN
YITZCHAK FRANK
TABLE I1 Characteristics of migraine headaches and seizure headaches Characteristics
Frequency Duration Starting time Location Precipitating factors Family history Electroencephalography
1
Migraine headaches
Convulsive headaches
Variable Many hours to days Usually late afternoon; rarely awaken patients from sleep Hemicranium or diffuse Emotional disturbance, school stress, fatigue
Variable Several hours During sleep or any time
85-90
Unusual Spike and wave discharges;bilateral spikes, rhythmic theta bursts Almost uniform postictal state consisting of somnolence and/or sleep Anticonvulsants Cerebral injury, central nervous system infections
%
Post-headache phase
Primarily diffuse slowing; occasionally focal slowing Fatigue or somnolence in many patients
Effective drugs Other history
Ergot, methysergide maleate None
and type of the electroencephalographic changes in migraine (Hughes 1972). It is noteworthy that most of the studies demonstrate a very low incidence of electroencephalographic epileptiform discharges in the inter-migraine period. There are also some specific electroencephalographic changes in migraine patients, including augmented hyperventilation response (Towle 1965) and an H-response to photic stimulation (Golla and Winter 1959, Richey et al. 1966). We feel that obvious epileptogenic activity in the electroencephalogram usually differentiates between convulsive headaches and migraine headaches. The pathophysiology which links abnormal brain discharge and seizure headache is an intriguing subject. The dural arteries, part of the venous sinuses, the proximal parts of the large intracranial vessels and the dural floor of the skull are sensitive to pain (Ray and Wolff 1940). The stimuli which produced pain included distension, stretching, stroking and faradic stimulation of the blood vessels. The pain arising from distension of the middle meningeal arteries is accompanied by nausea. Manipulation of brain paren-
Diffuse None
chyma does not cause pain. The stimulation of the intracranial portion of the internal carotid arteries, as well as proximal parts of the anterior, middle and posterior cerebral arteries, results in pain in the region of the homolateral eye. Therefore, at least partially, innervation of these vessels is by cranial nerve V. Pain induced by traction on the middle fossa venous structures and on the middle cerebral artery can be eliminated by injection of procaine into the trigeminal ganglia, but arteries of the brain have been shown to be supplied with other nerve fibre endings, including those of other cranial nerves and the autonomic nervous system (Dahl and Nelson 1964, Nelson and Rennels 1970). The autonomic nervous system is the most likely pathway through which an abnormal brain discharge can influence the intracranial blood vessels. Multiple fibre systems connect the hypothalamus to higher and lower brain centres; the largest is the medial forebrain bundle. This bundle is formed by fibres arising in the septa1 region and olfactory cortex of the temporal lobe. The fibres subsequently pass through
583
DEVELOPMENTAL MEDICINE AND CHlLD NEUROLOGY.
1978, 20
can be propagated into the hypothalamus, and thence through mesencephalic nuclei into the autonomic nervous system, causing headaches and other autonomic phenomena. It is known that such propagation is possible over axonal pathways (Jasper et al. 1969). Some of these patients will have other autonomic phenomena such as abdominal pain and pallor; almost all have nausea and vomiting.
the preo,itico-hypothalamic zone and into the paramedian regions of the mesencephalic tegmentum (Haymaker et al. 1969). It also receives fibres from the amygdalopiriform complex, the hippocampus (via the fornix) and the septa1 nuclei (Haymaker 1969~).The lateral zone of the hypothalamus receives fibres from the upper brainstem, ’mainly from the periaqueductal gray matter and some of the paramedian mesencephalic tegmental nuclei’ (Haymaker 19696). It is probably through these nuclei that the connection to blood vessels and visceral organs is achieved. A seizure discharge in the temporal lobe, any part of the limbic system or other parti of the cortex (Angevine et nl. 1964)
AUTHORS’ APPOINTMENTS
Kenneth F. Swaiman, M.D., Professor and Director; Yitzchak Frank, M.D., Medical Fellow; Division of Pediatric Neurology, University of Minnesota Medical School, Minneapolis, Minnesota 55455.
SUMMARY
Six children with paroxysmal headaches resulting from seizure disorders are reported. The clinical picture of seizure headaches includes the following features : they are usually diffuse or bifrontal; they begin abruptly at any time and last for minutes or several hours; in the majority of cases they are accompanied by nausea and vomiting and followed by postictal lethargy or sleep; there are no precipitating factors; they respond to anticonvulsants. 7he factors which differentiate between seizure headache and migraine are discussed. Seizure headache can be the sole clinical manifestation of seizure foci in the limbic system and other parts of the cortex. Some of these patients will have other autonomic phenomena such as pallor and abdominal pain; nearly all have nausea and vomiting. RESUME
S I Xcas de cephalies paroxystiques chez I’enfant, provenant de troubles comitiaux sont presentis. L’allure clinique des cephalies critiques presente les caractkres suivants : elles sont habituellement diffuses ou bi-frontales, elles commencent brutalement a n’importe quel moment et durent de quelques minutes a plusieurs heures. Dans la majorit6 des cas, elles sont accompagnies de naustes et de vomissements et suivies d’une lethargie post-critique ou de sommeil; il n’y a pas de facteurs annonciateurs; les medications anticomitiales sont actives. Les facteurs qui differencient cephalees critiques et migraines sont discutis. Les ciphalkes critiques peuvent &trela seule manifestation clinique de foyer comitial dans le \ysttme limbique et les autres parties du cortex. Quelques sujets prtsentent d’autres manifestations vigetatives telles que psleurs et douleurs abdominales. Presque tous ont des nausees et des vomissements. ZUSAMMENFASSUNG
Es wird iiber sechs Kinder mit paroxysmalen Kopfschmerzen infolge eines Krampfleidens berichtet. Das klinische Bild der Krampf-Kopfschmerzen bietet folgende charakteristischen Befunde : Die Schmerzen sind gewohnlich diffus oder bifrontal, sie beginnen abrupt, konnen
584
KENNETH F. SWAIMAN
YITZCHAK FRANK
zu jeder Zeit auftreten und dauern Minuten bis einige Stunden an. In der Mehrzahl der Falle klagen die Patienten iiber Ubelkeit, erbrechen und fallen anschliessend in einen postiktalen Dammerzustand oder Schlaf; es gibt keine ursachlichen Faktoren; die Kopfschmerzen sprechen auf die Behandlung mit Antikonvulsiva an. Auf die unterschiedlichen Befunde bei krampfbedingten Kopfschmerzen und bei Migrane wird ausfiihrlich eingegangen. Krampfebedingte Kopfschmerzen konnen die einzige klinische Manifestation von Krampffoci im limbischen System und anderen Teilen des Cortex sein. Bei einigen Patienten treten auch andere vegetative Symptome wie Blasse und Bauchschmerzen auf. Nahezu alle Kinder Klagen iiber Ubelkeit und Erbrechen. RESUMEN
Se aportan seis casos de niiios con cefaleas paroxisticas a consecuencia de enfermedades con crisis agudas. El cuadro clinico de 10s ataques de cefalea incluye 10s datos siguientes: son por lo general difusas o bifrontales; empiezan abruptamente en cualquier momento y duran desde minutos a varias horas; en la mayoria de 10s casos se acompaiian de nauseas y v6mitos y se siguen de letargia postictal y sueiio; no existen factores desencadenantes y responde a 10s anticonvulsilantes. Se discuten 10s factores diferenciales entre la crisis de cefalea y la migraiia. Los ataques de cefalea pueden ser la h i c a manifestacibn de crisis focales en el sistema limbic0 y otros puntos del c6rtex. Algunos de estos pacientes pueden tener otros fen6menos vegetativos tales como palidez y dolor abdominal; casi todos tienen nauseas y v6mitos. REFERENCES Angevine,, J. B., Locke, S., Yakovlev, P. L. (1964) ‘Limbic nuclei of thalamus and connections of limbic cortex: V. Thalamocortical projection of the magnocellular medial dorsal nucleus in man.’ Archives of Neurology, 10, 165-180. Chao, O., Davis, S. D. (1964) ‘Convulsive equivalent syndrome of childhood.’ Journal of Pediatrics, 64, 499-508. Dahl, E., Nelson, E. (1964) ‘Electron microscopic observations on human intracranial arteries. 11. Innervation.’ Archives of Neurology, 10, 158-164. Golla, F. L., Winter, A. L. (1959) ‘Analysis of cerebral response to flicker in patients complaining of episodic headache.’ Electroencephalography and Clinical Neurophysiology, 11, 539-549. Halpern, L., Bental, E. (1958) ‘Epileptic cephalea.’ Neurology, 8, 615-620. Haymaker, W. (1969~)‘Hypothalamus, pituitary gland, midbrain and related regions.’ In Haymaker, W. (Ed.) Bing’s Local Diagnosis in Neurological Diseases, 15th Edn. St. Louis: C . V. Mosby. p. 465. (1969b) ‘Hypothalamus, pituitary gland, midbrain and related regions.’ Zn: Haymaker, W. (Ed.) Bing’s Local Diagnosis in Neurological Diseases, 15th edn. St. Louis: C. V. Mosby. p. 467. - Anderson, E., Nauta, W. J. H. (Eds.) (1969) The Hypothalamus. Springfield, 111.: C. C. Thomas. p. 164. Hockaday, J. M., Whitty, C. W. M. (1969) ‘Factors determining the electroencephalogram in migraine. A study of 560 patients according to clinical type of migraine.’ Brain, 92,769-788. Hughes, J. R. (1 972) ‘EEG in headaches.’ Headache, 11,162-170. Jasper, H. H., Ward, A. A., Pope, A. (1969) ‘Mechanisms of propagation: Extracellular studies.’ In Jasper, H. H., Ward, A., Pope, A. (Eds.) Basic Mechanisms of the Epilepsies. Boston: Little, Brown. p. 421. Jonas, A. D. (1966) ‘Headaches as seizure equivalents.’ Headache, 6,78-87. Kriel. R. L. (1972) ‘Headache.’ In Swaiman. K. F.., Wright, - . F. S. (Eds.) . . The Practice of Pediatric Neurolom. _. St.’Louis:‘C. V: Mosby. p. 154. Meloff, K. L. (1973) ‘Headache in pediatric practice.’ Headache, 13, 125-129. Nelson, E., Rennels, M. (1970) ‘Innervation of intracranial arteries.’ Brain, 93, 475490. Poch, G. F. (1974) ‘Epileptic headaches.’ Archives de Neurobiologie, 37 (suppl.), 1977. Rav. B. S.. Wolff. H. G. (1940) ‘ExDerimentalstudies on headache: Pain sensitive structures of the head and their significance in headache.’ Archives of Surgery, 41, 813-856. Richey, E. T., Kooi, K. A., Waggoner, R. W. (1966) ‘Visually evoked responses in migraine.’ Electroencephalography and Clinical Neurophysiology, 21,23-27. Smyth, V. 0. G., Winter, A. L. (1964) ‘The EEG in migraine.’ Electroencephalography and Clinical Neurophysiology, 16, 194-202. Towle, P. A. (1965) ‘The electroencephalographic hyperventilation response in migraine.’ Elecfroencephalography and Clinical Neurophysiology, 19, 390-393. Whitehouse, D., Pappas, J. A., Escala, P. A., Livingstone, S. (1967) ‘Electroencephalographic changes in children with migraine.’ New England Journal of Medicine, 276, 23-27.
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