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Trauma-triggered migraine and acute confusional migraine
JOURNAL OF ADOLESCENT HEALTH 2000;27:119–124
CASE REPORT
Trauma-Triggered Migraine and Acute Confusional Migraine LAWRENCE NEINSTEIN, M.D. AND ETAN MILGROM, M.D. KEY WORDS: Migraine headaches Trauma-triggered migraine Acute confusional migraine Anisocoria and migraine
Migraines following minor head injuries and those associated with acute confusional states have been reported in the literature since 1967 (1,2). However, the clinical picture, particularly when associated with trauma, is still not well recognized among clinicians. This case, occurring at a summer camp, is presented to alert clinicians to this dramatic clinical picture, which can be confused with serious neurologic problems. Despite the frequency of migraine symptoms in the general population and especially in the first 3 decades of life, migraine attacks are not well appreciated as possible significant sequelae to sports participation and injury. This case involves features of both trauma-induced and confusional migraine. Focal neurologic features such as anisocoria can be particularly confusing in such patients. Prior reports of both trauma-triggered migraine (TTM) and acute confusional migraine (ACM) are reviewed. Case: A 14-year-old white male presented to his overnight camp infirmary with a laceration across his lower lip, about 10 minutes after being hit by an elbow during a basketball game. At the time of the examination, the patient complained of the acute
From the USC School of Medicine and USC University Park Health Center (L.N.), Los Angeles, California; and UCLA School of Medicine (E.M.), Los Angeles, California. Address reprint requests to Lawrence Neinstein, M.D., Executive Director, USC University Park Health Center, 849 W 34th Street, Los Angeles, CA 90089-0311. Manuscript accepted August 5, 1999.
onset of bitemporal pain, right greater than left, with some dizziness and nausea. Six months previously a history of a “concussive head injury” occurred after the teen butted heads with an opponent during a soccer game. Workup at that time showed no abnormalities other than the acute onset of confusion and disorientation just after the traumatic event. There was also a history of severe migraines in the patient’s mother. On this examination, the teen was slightly lethargic but in no acute distress and oriented to name, date, and place. His general examination including heart, lungs, and abdomen were normal. He was noted to have anisocoria, right greater than left, with both pupils being responsive to light and leftsided hyperreflexia with a diminished heel-to-toe response on the left. His fundi were normal and his strength was equal bilaterally. Over the next 10 to 15 minutes, the teen became more disoriented and mildly obtunded. An intravenous (IV) drip was started along with oxygen and he was rapidly transported to the nearest emergency room for further evaluation. During the transport, the patient became more difficult to arouse. The evaluation in the emergency room, including a complete blood count, electrolytes, glucose, drug screen, and a head computerized tomography (CT) scan, was completely normal. A pediatric neurologist concluded that the patient had sustained an acute confusional migraine and was discharged home and then to camp the following day. The next evening, while walking, he expe-
© Society for Adolescent Medicine, 2000 Published by Elsevier Science Inc., 655 Avenue of the Americas, New York, NY 10010
1054-139X/00/$–see front matter PII S1054-139X(99)00099-3
120
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JOURNAL OF ADOLESCENT HEALTH Vol. 27, No. 2
Table 1. Characteristics of Trauma-Triggered Migraine (TTM)
Reference
Age Patients (Years)
M:F
Headache
Matthews (18) Haas (20)
4 25
12–20 4:0 2–38 17:8
4/4 25/25
Bennett (23) Sandyk (24) Ashworth (25) Whitty (2) Morris (19) Espir (21) Kalenak (22) Total
3 2 7 1 1 1 1 45
18 –20 14 –15 12–70 25 NR 22 19 2–70
3/3 2/2 6/7 1/1 1/1 1/1 1/1 44/45
3:0 2:0 7:0 male male male male 37:8
Duration of Confusion (Hours)
Past Family History History Agitation Trauma Migraine Migraine Examination
several hours 1 hour–several days ⬍12 h NR 30 m–2 days NR NR NR NR 30 min– several days
(82.2% M) (97%)
CT or MRI
0/4 NR
4/4 25/25
0/4 NR
NR 15/25
3/4 abnl NR
NR NR
NR NR 0/7 NR NR NR NR None
3/3 2/2 7/7 1/1 1/1 1/1 1/1 All
1/3 NR NR NR NR NR NR 1/7
2/3 NR 2/7 Yes NR NR Yes 21/37
1/3 abnl 0/2 abnl 1 abnl 1 abnl abnl abnl abnl 9/14
0/3 abnl 0/2 abnl NR NR NR NR NR none
(14.3%)
(56.7%)
(64% abnl)
abnl ⫽ abnormal; CT ⫽ computerized tomography; M ⫽ male; F ⫽ Female; MRI ⫽ magnetic resonance imaging; NR ⫽ not recorded.
rienced the sudden onset of ataxia leading him to collapse in his counselor’s arms. Examination within 10 minutes of this episode revealed disorientation and confusion, an ataxic gait, and anisocoria. The rest of his examination was normal. The patient was placed in the supine position and high-dose oxygen (8 L) was administered via nasal cannula. After an hour of oxygen administration, the patient returned to his normal baseline orientation and examination. He was given 25 mg of sumatriptan orally after consultation with a pediatric neurologist. The following day the patient received a full neurologic evaluation, including magnetic resonance imaging (MRI) and magnetic resonance angiography, which revealed no abnormalities. The patient returned to camp 2 days later with sumatriptan nasal sprays and ibuprofen tablets to be used as needed. His neurologist recommended that he not engage in contact sports.
Discussion Migraine syndromes have been reported that include both acute confusion with and without headache (2–16) and migraine syndromes following minor head trauma (1,13,17–27). This teen presented with symptoms of both of these clinical entities. Minor head trauma leading to migraine attacks were first reported by Hass and Sovner (1) and Whitty (2). Hass and Sovner described 25 patients with temporary posttraumatic neurologic phenomena and made three points: (1) these posttraumatic attacks look like spontaneous classical migraine attacks and probably have similar mechanism; (2) the process probably involves the cerebral vasculature; (3) the manifestations may include hemiparesis, visual disturbances
or confusion, somnolence or irritability, and probably involve a common process (20). In their patients, the head trauma that triggered attacks was mild but generally forceful enough to daze the patient. There was no history of loss of consciousness. Almost all had a short latency period between the head trauma and the onset of neurologic symptoms, which varied from several seconds to about 4 hours but averaged 1 to 10 minutes. The symptoms and signs disappeared after 1 to 12 hours in most cases. Reported cases of trauma-triggered migraine (TTM), the majority of which were in children and adolescents, are listed in Table 1. Most cases were in males, but this may reflect the male bias in contact sports, particularly in the 1970s and 1980s. Almost all reported patients had an associated headache with symptoms lasting 30 minutes to several days with most lasting less than 12 hours. Only 14% had a prior history of migraine unassociated with head trauma, while 56.7% had a family history of migraines. Sixtyfour percent had an abnormal physical examination and the 5 that had CT scans had normal findings. Although the prevalence of migraine has been reported to be as high as 15% to 20% in males and 23% to 29% in females (2), its prevalence in amateur and professional athletes has not been well studied. Ferrera and Reicho noted that in the absence of loss of consciousness and with a lag period between trauma and the onset of symptoms, the symptoms are not likely to be solely related to posttraumatic conditions (13). Individuals with this condition sometimes develop spontaneous migraines later and conversely, patients who have spontaneous migraines can develop migraines related to minor head trauma (13).
5–14 9 –14 9 –11 6 –15
4 5
2 13
6 2 1 2 12
1 3 61
Sheth (12) Ferrera (13) Soriani (15) Nezu (16) Pietrini (8)
Haan (9) O’Neill (11) Total
M:F
female 0:3 32:29 (52.5% M)
1:5 1:1 male 1:1 6:6
1:1 11:2
3:3 3:2
3:3
3:1
Headache
1/1 3/3 46/56 (82%)
2/2 10/12
NR 1/2
none 13/13
4/4 5/5
3/6
4/4
12 6 30 min–24 h
1–12 NR none 6 –12 1–12
10 11⁄2–24
11⁄2–9 1⁄2–24
1–24
4 –24
Duration of Confusion (hours) Agitation
1/1 none 35/56 (62.5%)
NR 2/2 24 none 10/12
1/2 8/13
4/4 5/5
2/6
2/4
Trauma
1/1 1/3 23/61 (37.7%)
3/6 1/2 none none 4/12
none 4/13
2/4 1/5
6/6
none
none 1/3 30/59 (51%)
4/6 none none NR 10/12
none 7.13
4/4 none
2/6
2/4
Past History Migraine
1/1 3/3 47/61 (77%)
3/6 1/2 none 2/2 8/12
1/2 10/13
4/4 4/5
6/6
3/4
Family History Migraine Examination
nl all nl 14/56 abnl (25% abnl)
NR all nl 1/1 abnl 1 abnl 3/12 abnl
all nl 1 abnl
1 abnl 1 abnl
all abnl
all nl
CT or MRI
nl all nl 1/46 abnl (2%)
2/2 nl 10/11 nl 1/11 abnl all nl all nl nl all nl all nl
4/4 nl 2/2 nl
NR
NR
EEG
1/1 abnl 3/3 slow 34/45 (75.5% abnl)
3/5 slow 1/2 slow abnl 1/2 slow 12/12 abnl
2/2 slow 1/4 slow
3/4 slow 1/4 abnl
2/6 slow
3/3 slow
abnl ⫽ abnormal; CT ⫽ computerized tomography; M ⫽ male; F ⫽ female; nl ⫽ normal; MRI ⫽ magnetic resonance imaging; EEG ⫽ electroencephalogram; NR ⫽ not recorded.
7.5–17 6 –9 11 7–12 8 – 60 (11/12 ⬍ 23 y) 13 11 10 m– 60 y
10 m–12 y
6
Age (Years) 8 –16
Patients
4
Gascon & Barlow (3) Hass & Sovener (1) Emery (4) Ehyai & Fenichel (5) Amit (10) Shaabat (14)
Reference
Table 2. Characteristics of Acute Confusional Migraines (ACM)
August 2000 TRAUMA-TRIGGERED MIGRAINE 121
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Table 3. Comparison of Signs and Symptoms: Trauma-Triggered Migraine (TTM) Versus Acute Confusional Migraine (ACM)
TTM ACM
Trauma
Past History Migraine
Family History Migraine
Abnl Exam
Abnl CT or MRI
Patients age
Male
Headache History
Adolescent Young adult Children/ Adolescent
⫹⫹⫹
⫹⫹⫹
⫹⫹
none
⫹⫹⫹⫹
⫹
⫹⫹
⫹⫹⫹
none
⫹⫹
⫹⫹⫹
⫹⫹⫹⫹
⫹⫹⫹
⫹⫹
⫹⫹⫹
⫹⫹⫹
⫹
none
Confusion
Agitation
⫹, 0 to 25%. ⫹⫹, 26% to 50%. ⫹⫹⫹, 51% to 75%. ⫹⫹⫹⫹, 76% to 100%. abnl ⫽ abnormal; CT ⫽ computerized tomography; MRI ⫽ magnetic resonance imaging.
In Bennett’s review of TTMs, it was noted that 9 of 11 cases had recurrent attacks with subsequent head trauma (23). One patient described by Matthews illustrates this history (18). This 22 year-old soccer player presented with a history of seven episodes of tunnel vision, tingling of the hand, and then headaches and vomiting following head trauma during soccer games. Aside from TTM, migraine attacks predominantly associated with somnolence and confusion with or without a history of trauma have also been described (2–16). The syndrome of acute confusional migraine (ACM) was first described by Gascon and Barlow in four children aged 8 to 16 years in 1970 (3). Distinctive features of this syndrome include: (1) sudden onset of confusion and agitation in the course of headache attack; (2) possible close relationship with neurologic deficits, suggesting basilar migraine; (3) marked electroencephalogram (EEG) abnormalities in either one or both posterior quadrants; (4) rapid recovery both clinically and on EEG (6). Table 2 reviews the reported cases of acute confusional migraine while Table 3 compares the clinical manifestations of the two syndromes. Similar to TTM, acute confusional migraine occurs mainly in children and adolescents, however, 47.5% occurred in females. The duration of confusion is about 30 minutes to 24 hours, 62% had agitation and 37.7% had a prior history of mild trauma. Acute confusional migraine has also been reported to occur after strenuous exercise (12). There was a personal history of prior migraines in 51% and a family history in 77%. The examination was abnormal in 25% of individuals, but there was only 1 abnormal CT or MRI of 46 performed. However, 75.5% had abnormal EEGs, usually showing slow wave activity or front intermittent rhythmic delta activity. Attacks usually resolve with deep sleep, with partial or total amnesia
of the episode. On awakening the patients appear normal. Both TTM and ACM probably represent variants of migraines and may overlap as in this adolescent’s case. In both TTM and ACM, minor trauma may be the precipitating event. The symptoms may include focal neurologic deficits in association with confusion and agitation. The majority of patients have a family history of migraine. There does appear to be a higher prevalence of abnormal neurologic findings on physical examination in TTM, as found in this teen. In both syndromes, the patient returns to baseline usually within 12 hours. EEGs done during the acute phase may show slow wave activity. The pathophysiology of these 2 syndromes is still speculative. Many theories have been reported including localized cerebral edema from increased vascular permeability and a primary neuronal dysfunction of the upper brain stem (14). Another physical sign associated with migraines that can be particularly confusing in the face of head trauma is anisocoria or oculosympathetic dysfunction. Soriani reported an 11 year-old male with recurrent migraine without headache but with confusion and anisocoria (15). DeMarinis et al. studied 20 headache-free migraine patients and 20 controls and demonstrated hypofunction of the oculosympathetic system (27). Drummond found that there were significant differences between the diameters of the pupils in 38 migraine sufferers during headache-free periods compared to the pupils in 40 control individuals without migraine headaches (28). Purvin demonstrated the features of a postganglionic parasympathetic paresis in 1 woman during a classic migraine (29). Blaik noted that episodic unilateral mydriasis may occur in the context of migraines (30). Although anisocoria is often associated with serious central nervous system pathology such as tumors,
August 2000
aneurysms, or brain herniation, when a patient has isolated, episodic unilateral mydriasis and migraine, further evaluation should be done only if symptoms worsen or change.
Differential Diagnosis The combination of head trauma, focal neurologic symptoms, and/or confusion and headache, nausea, and vomiting can simulate a serious neurologic emergency. Recognition of a migraine attack by a team physician may be difficult if it is a first episode occurring during a contact sport. While a prior history may be helpful, screening sports forms may not contain this information. Consideration should be given to the possibility of toxic or metabolic problems including drug ingestion, hypoglycemia, nonconvulsive seizure disorders, encephalitis, and intracerebral trauma. Trauma-triggered migraines may be mistaken for cerebral concussions and contusions, or for acute epidural and subdural hematomas. Concussion usually implies an immediate brief period of unconsciousness. A contusion usually occurs in the setting of more severe head trauma, typically with immediate unconsciousness. With a contusion, there is usually no latent period between the injury and the onset of focal signs. An acute epidural hematoma may follow relatively mild head trauma. Symptoms may occur after a latent period and without initial unconsciousness and can be confused with a TTM. Electrolytes, glucose, and drug screening may need to be ordered. Without a typical history or prior history of such attacks, particularly in an acute injury, a CT or MRI scan may be necessary. The rapid resolution of symptoms may help to rule out other conditions. An EEG, if done during the acute episode, may show slow wave activity. Nezu et al noted an abnormal single photon emission computerized tomography (SPECT) with regional change in cerebral blood flow, including hypoperfusion in the left posterior cerebral artery, and concluded that SPECT might be helpful for diagnosis of ACM (16).
Management When the diagnosis of TTM or ACM is made, the family can usually be reassured that the symptoms will likely resolve within 24 hours. If there is prior history of these occurrences, it is reasonable to discharge the individual home with a caregiver; however, there are no firm guidelines. Treatment may
TRAUMA-TRIGGERED MIGRAINE
123
include antimigraine medications, but this has not been prospectively studied in these individuals. Several patients with TTM and ACM have been highly responsive to low-dose prophylactic therapy (7). This teen was placed on sumatriptan at the recommendation of the consultant, but this is an “off-label” use. In addition, the manufacturer recommends that sumatriptan not be used in management of hemiplegic or basilar migraine. Several studies have examined sumatriptan’s use in children and adolescents, and although found to have some beneficial effects, the effect may be different from or less than that found in adults (32,33,34). No studies examine the recurrence rates of these episodes. Although the majority of individuals do not appear to have recurrences, in some of the reported cases there are repeat episodes of migraine associated with either trauma or confusion. This teen responded dramatically to high-flow oxygen. This has not previously been evaluated or commented on in prior reports. Since oxygen may be the easiest available intervention in some athletic situations, it may be a helpful diagnostic and therapeutic intervention. Oxygen therapy is known to be highly effective in aborting cluster-type headaches and was used in this situation because of its availability in the summer camp setting. The question of future participation in contact sports is unresolved and clearly has great impact on this and any adolescent who is active in sports. Possible long-term sequela of this supposedly “benign” condition, particularly in those with repeated episodes, is not known. The combination of head trauma, focal neurologic symptoms including anisocoria, headaches, and altered mental status should be considered a medical emergency situation. Awareness of the possibility of migraine and reviewing the appropriate history questions may help with the correct diagnosis. However, in light of the potentially serious set of symptoms, and particularly in the context of a head injury, the diagnosis of TTM becomes a diagnosis of exclusion and a thorough workup should be undertaken to rule out any serious underlying etiology.
Conclusion This report describes a teenage male with many of the clinical patterns of the previously described attacks. He was young, had sustained a minor head injury without loss of consciousness, and then developed focal neurologic signs, followed by headache,
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confusion, and increasing somnolence. His symptoms resolved within hours, the neurologic workup was normal, and his examination returned to baseline within 12 hours.
JOURNAL OF ADOLESCENT HEALTH Vol. 27, No. 2
16. Nezu A, Kimura S, Ohtsuki N, et al. Acute confusional migraine and migrainous infarction in childhood. Brain Dev 1997;19:1148 –51. 17. Greenblatt SH. Posttraumatic transient cerebral blindness. JAMA 1973;225:1073– 6. 18. Matthews WB. Footballer’s migraine. Br Med J 1972;2:326 –7.
References 1. Hass DC, Sovner RD. Migraine attacks triggered by mild head trauma and their relation to certain post-traumatic disorders in childhood. J Neurol Neurosurg Psychiatry 1969;32:548 –54. 2. Whitty CWM. Migraine without headache. Lancet 1967;2: 283–5. 3. Gascon G, Barlow C. Juvenile migraine presenting as an acute confusional state. Pediatrics 1970;45:628 –35. 4. Emery III ES. Acute confusional state in children with migraine. Pediatrics 1977;60:110 – 4. 5. Ehyai A, Fenichel GM. The natural history of acute confusional migraine. Arch Neurol 1978;35:368 –9. 6. Moretti G, Manzoni GC, Terzano MG, et al. Clinical and electroencephalographic aspects of confusional migraine in adults. Acta Bio Med Ateneo Parmense 1981;52:59 – 65. 7. Parrino L, Pietrin I, Spaggiari MC, et al. Acute confusional migraine attacks resolved by sleep: Lack of significant abnormalities in post-ictal polysomnograms. Cephalalgia 1986;6:95– 100. 8. Pietrini V, Terzano MG, D’Andrea G, et al. Acute confusional migraine: Clinical and electroencephalographic aspects. Cephalalgia 1987;7:29 –37. 9. Haan J, Ferrari MD, Brouwer OF. Acute confusional migraine. Case report and review of literature. Clin Neurol Neurosurg 1988;90:275– 8. 10. Amit R. Acute confusional state in childhood. Child Nerv Syst 1988;4:255– 8. 11. O’Neill F, D’Cruz OF, Walsh DJ. Acute confusional migraine: Case series and review of literature. Wisconsin Med J 1992;91: 130 –1. 12. Sheth RD, Riggs JE, Bodensteiner JB. Acute confusional migraine: Variant of transient global amnesia. Pediatr Neurol 1995;12:129 –31. 13. Ferrera PC, Reicho PR. Acute confusional migraine and trauma-triggered migraine. Am J Emerg Med 1996;14:276 – 8. 14. Shaabat A. Confusional migraine in childhood. Pediatr Neurol 1996;15:23–5. 15. Soriani S, Scarpa P, Arnaldi C, et al. Migraine aura without headache and ictal fast EEG activity in an 11 year old boy. Eur J Pediatr 1996;155:126 –9.
19. Morris AM. Footballer’s migraine. Br Med J 1972;2:769 –70. 20. Hass DC, Pineda GS, Lourie H. Juvenile head trauma syndromes and their relationship to migraine. Arch Neurol 1975; 32:727–30. 21. Espir MLE, Hodge ILD, Matthews PHN. Footballer’s migraine. Br Med J 1972;2:352. 22. Kalenak A, Petro DJ, Brennan W. Migraine secondary to head trauma in wrestling. Am J Sports Med 1978;6:112–3. 23. Bennett DR, Fuenning IS, Sullivan G, et al. Migraine precipitated by head trauma in athletes. Am J Sports Med 1980;8: 202–5. 24. Sandyk R. Footballer’s migraine—a report of 2 cases. S Afr Med J 1983;63:434. 25. Ashworth B. Migraine, head trauma and sport. Scottish Med J 1985;30:240 –2. 26. Haas DC, Lourie H. Trauma-triggered migraine: An explanation for common neurological attack after mild head injury. J Neurosurg 1988;68:181– 8. 27. DeMarinis M, Assenza S, Carletto F. Oculosympathetic alterations in migraine patients. Cephalagia 1998;18:77– 84. 28. Drummond PD. Cervical sympathetic deficit in unilateral migraine headache. Headache 1991;31:669 –72. 29. Purvin VA, Adie’s tonic pupil secondary to migraine. J Neuroophthal 1995;15:43– 4. 30. Blaik Z, Hiremagular S. Episodic unilateral mydriasis and headaches. Tenn Med 1998;91:107– 8. 31. Jacobson DM. Benign episodic unilateral mydriasis. Clinical characteristics. Ophthalmology 1995;102:1623–7. 32. Hamalainen ML, Hoppu K, Santavuori P. Sumatriptan for migraine attacks in children. A randomized placebo-controlled study: Do children with migraine respond to oral sumatriptan differently from adults. Neurology 1997; 48: 1100 –3. 33. Korsgaard AG. The tolerability, safety and efficacy of oral sumatriptan 50 mg and 100 mg for the acute treatment of migraine in adolescents. Presented at the 3rd International Congress on Headache in Childhood and Adolescence, May 4 – 6, 1995, Budapest. 34. Linder SL. Subcutaneous sumatriptan in the clinical setting: The first 50 consecutive patients with acute migraine in a pediatric neurology office. Headache 1996;36:419 –22.
CASE REPORT
Trauma-Triggered Migraine and Acute Confusional Migraine LAWRENCE NEINSTEIN, M.D. AND ETAN MILGROM, M.D. KEY WORDS: Migraine headaches Trauma-triggered migraine Acute confusional migraine Anisocoria and migraine
Migraines following minor head injuries and those associated with acute confusional states have been reported in the literature since 1967 (1,2). However, the clinical picture, particularly when associated with trauma, is still not well recognized among clinicians. This case, occurring at a summer camp, is presented to alert clinicians to this dramatic clinical picture, which can be confused with serious neurologic problems. Despite the frequency of migraine symptoms in the general population and especially in the first 3 decades of life, migraine attacks are not well appreciated as possible significant sequelae to sports participation and injury. This case involves features of both trauma-induced and confusional migraine. Focal neurologic features such as anisocoria can be particularly confusing in such patients. Prior reports of both trauma-triggered migraine (TTM) and acute confusional migraine (ACM) are reviewed. Case: A 14-year-old white male presented to his overnight camp infirmary with a laceration across his lower lip, about 10 minutes after being hit by an elbow during a basketball game. At the time of the examination, the patient complained of the acute
From the USC School of Medicine and USC University Park Health Center (L.N.), Los Angeles, California; and UCLA School of Medicine (E.M.), Los Angeles, California. Address reprint requests to Lawrence Neinstein, M.D., Executive Director, USC University Park Health Center, 849 W 34th Street, Los Angeles, CA 90089-0311. Manuscript accepted August 5, 1999.
onset of bitemporal pain, right greater than left, with some dizziness and nausea. Six months previously a history of a “concussive head injury” occurred after the teen butted heads with an opponent during a soccer game. Workup at that time showed no abnormalities other than the acute onset of confusion and disorientation just after the traumatic event. There was also a history of severe migraines in the patient’s mother. On this examination, the teen was slightly lethargic but in no acute distress and oriented to name, date, and place. His general examination including heart, lungs, and abdomen were normal. He was noted to have anisocoria, right greater than left, with both pupils being responsive to light and leftsided hyperreflexia with a diminished heel-to-toe response on the left. His fundi were normal and his strength was equal bilaterally. Over the next 10 to 15 minutes, the teen became more disoriented and mildly obtunded. An intravenous (IV) drip was started along with oxygen and he was rapidly transported to the nearest emergency room for further evaluation. During the transport, the patient became more difficult to arouse. The evaluation in the emergency room, including a complete blood count, electrolytes, glucose, drug screen, and a head computerized tomography (CT) scan, was completely normal. A pediatric neurologist concluded that the patient had sustained an acute confusional migraine and was discharged home and then to camp the following day. The next evening, while walking, he expe-
© Society for Adolescent Medicine, 2000 Published by Elsevier Science Inc., 655 Avenue of the Americas, New York, NY 10010
1054-139X/00/$–see front matter PII S1054-139X(99)00099-3
120
NEINSTEIN AND MILGROM
JOURNAL OF ADOLESCENT HEALTH Vol. 27, No. 2
Table 1. Characteristics of Trauma-Triggered Migraine (TTM)
Reference
Age Patients (Years)
M:F
Headache
Matthews (18) Haas (20)
4 25
12–20 4:0 2–38 17:8
4/4 25/25
Bennett (23) Sandyk (24) Ashworth (25) Whitty (2) Morris (19) Espir (21) Kalenak (22) Total
3 2 7 1 1 1 1 45
18 –20 14 –15 12–70 25 NR 22 19 2–70
3/3 2/2 6/7 1/1 1/1 1/1 1/1 44/45
3:0 2:0 7:0 male male male male 37:8
Duration of Confusion (Hours)
Past Family History History Agitation Trauma Migraine Migraine Examination
several hours 1 hour–several days ⬍12 h NR 30 m–2 days NR NR NR NR 30 min– several days
(82.2% M) (97%)
CT or MRI
0/4 NR
4/4 25/25
0/4 NR
NR 15/25
3/4 abnl NR
NR NR
NR NR 0/7 NR NR NR NR None
3/3 2/2 7/7 1/1 1/1 1/1 1/1 All
1/3 NR NR NR NR NR NR 1/7
2/3 NR 2/7 Yes NR NR Yes 21/37
1/3 abnl 0/2 abnl 1 abnl 1 abnl abnl abnl abnl 9/14
0/3 abnl 0/2 abnl NR NR NR NR NR none
(14.3%)
(56.7%)
(64% abnl)
abnl ⫽ abnormal; CT ⫽ computerized tomography; M ⫽ male; F ⫽ Female; MRI ⫽ magnetic resonance imaging; NR ⫽ not recorded.
rienced the sudden onset of ataxia leading him to collapse in his counselor’s arms. Examination within 10 minutes of this episode revealed disorientation and confusion, an ataxic gait, and anisocoria. The rest of his examination was normal. The patient was placed in the supine position and high-dose oxygen (8 L) was administered via nasal cannula. After an hour of oxygen administration, the patient returned to his normal baseline orientation and examination. He was given 25 mg of sumatriptan orally after consultation with a pediatric neurologist. The following day the patient received a full neurologic evaluation, including magnetic resonance imaging (MRI) and magnetic resonance angiography, which revealed no abnormalities. The patient returned to camp 2 days later with sumatriptan nasal sprays and ibuprofen tablets to be used as needed. His neurologist recommended that he not engage in contact sports.
Discussion Migraine syndromes have been reported that include both acute confusion with and without headache (2–16) and migraine syndromes following minor head trauma (1,13,17–27). This teen presented with symptoms of both of these clinical entities. Minor head trauma leading to migraine attacks were first reported by Hass and Sovner (1) and Whitty (2). Hass and Sovner described 25 patients with temporary posttraumatic neurologic phenomena and made three points: (1) these posttraumatic attacks look like spontaneous classical migraine attacks and probably have similar mechanism; (2) the process probably involves the cerebral vasculature; (3) the manifestations may include hemiparesis, visual disturbances
or confusion, somnolence or irritability, and probably involve a common process (20). In their patients, the head trauma that triggered attacks was mild but generally forceful enough to daze the patient. There was no history of loss of consciousness. Almost all had a short latency period between the head trauma and the onset of neurologic symptoms, which varied from several seconds to about 4 hours but averaged 1 to 10 minutes. The symptoms and signs disappeared after 1 to 12 hours in most cases. Reported cases of trauma-triggered migraine (TTM), the majority of which were in children and adolescents, are listed in Table 1. Most cases were in males, but this may reflect the male bias in contact sports, particularly in the 1970s and 1980s. Almost all reported patients had an associated headache with symptoms lasting 30 minutes to several days with most lasting less than 12 hours. Only 14% had a prior history of migraine unassociated with head trauma, while 56.7% had a family history of migraines. Sixtyfour percent had an abnormal physical examination and the 5 that had CT scans had normal findings. Although the prevalence of migraine has been reported to be as high as 15% to 20% in males and 23% to 29% in females (2), its prevalence in amateur and professional athletes has not been well studied. Ferrera and Reicho noted that in the absence of loss of consciousness and with a lag period between trauma and the onset of symptoms, the symptoms are not likely to be solely related to posttraumatic conditions (13). Individuals with this condition sometimes develop spontaneous migraines later and conversely, patients who have spontaneous migraines can develop migraines related to minor head trauma (13).
5–14 9 –14 9 –11 6 –15
4 5
2 13
6 2 1 2 12
1 3 61
Sheth (12) Ferrera (13) Soriani (15) Nezu (16) Pietrini (8)
Haan (9) O’Neill (11) Total
M:F
female 0:3 32:29 (52.5% M)
1:5 1:1 male 1:1 6:6
1:1 11:2
3:3 3:2
3:3
3:1
Headache
1/1 3/3 46/56 (82%)
2/2 10/12
NR 1/2
none 13/13
4/4 5/5
3/6
4/4
12 6 30 min–24 h
1–12 NR none 6 –12 1–12
10 11⁄2–24
11⁄2–9 1⁄2–24
1–24
4 –24
Duration of Confusion (hours) Agitation
1/1 none 35/56 (62.5%)
NR 2/2 24 none 10/12
1/2 8/13
4/4 5/5
2/6
2/4
Trauma
1/1 1/3 23/61 (37.7%)
3/6 1/2 none none 4/12
none 4/13
2/4 1/5
6/6
none
none 1/3 30/59 (51%)
4/6 none none NR 10/12
none 7.13
4/4 none
2/6
2/4
Past History Migraine
1/1 3/3 47/61 (77%)
3/6 1/2 none 2/2 8/12
1/2 10/13
4/4 4/5
6/6
3/4
Family History Migraine Examination
nl all nl 14/56 abnl (25% abnl)
NR all nl 1/1 abnl 1 abnl 3/12 abnl
all nl 1 abnl
1 abnl 1 abnl
all abnl
all nl
CT or MRI
nl all nl 1/46 abnl (2%)
2/2 nl 10/11 nl 1/11 abnl all nl all nl nl all nl all nl
4/4 nl 2/2 nl
NR
NR
EEG
1/1 abnl 3/3 slow 34/45 (75.5% abnl)
3/5 slow 1/2 slow abnl 1/2 slow 12/12 abnl
2/2 slow 1/4 slow
3/4 slow 1/4 abnl
2/6 slow
3/3 slow
abnl ⫽ abnormal; CT ⫽ computerized tomography; M ⫽ male; F ⫽ female; nl ⫽ normal; MRI ⫽ magnetic resonance imaging; EEG ⫽ electroencephalogram; NR ⫽ not recorded.
7.5–17 6 –9 11 7–12 8 – 60 (11/12 ⬍ 23 y) 13 11 10 m– 60 y
10 m–12 y
6
Age (Years) 8 –16
Patients
4
Gascon & Barlow (3) Hass & Sovener (1) Emery (4) Ehyai & Fenichel (5) Amit (10) Shaabat (14)
Reference
Table 2. Characteristics of Acute Confusional Migraines (ACM)
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Table 3. Comparison of Signs and Symptoms: Trauma-Triggered Migraine (TTM) Versus Acute Confusional Migraine (ACM)
TTM ACM
Trauma
Past History Migraine
Family History Migraine
Abnl Exam
Abnl CT or MRI
Patients age
Male
Headache History
Adolescent Young adult Children/ Adolescent
⫹⫹⫹
⫹⫹⫹
⫹⫹
none
⫹⫹⫹⫹
⫹
⫹⫹
⫹⫹⫹
none
⫹⫹
⫹⫹⫹
⫹⫹⫹⫹
⫹⫹⫹
⫹⫹
⫹⫹⫹
⫹⫹⫹
⫹
none
Confusion
Agitation
⫹, 0 to 25%. ⫹⫹, 26% to 50%. ⫹⫹⫹, 51% to 75%. ⫹⫹⫹⫹, 76% to 100%. abnl ⫽ abnormal; CT ⫽ computerized tomography; MRI ⫽ magnetic resonance imaging.
In Bennett’s review of TTMs, it was noted that 9 of 11 cases had recurrent attacks with subsequent head trauma (23). One patient described by Matthews illustrates this history (18). This 22 year-old soccer player presented with a history of seven episodes of tunnel vision, tingling of the hand, and then headaches and vomiting following head trauma during soccer games. Aside from TTM, migraine attacks predominantly associated with somnolence and confusion with or without a history of trauma have also been described (2–16). The syndrome of acute confusional migraine (ACM) was first described by Gascon and Barlow in four children aged 8 to 16 years in 1970 (3). Distinctive features of this syndrome include: (1) sudden onset of confusion and agitation in the course of headache attack; (2) possible close relationship with neurologic deficits, suggesting basilar migraine; (3) marked electroencephalogram (EEG) abnormalities in either one or both posterior quadrants; (4) rapid recovery both clinically and on EEG (6). Table 2 reviews the reported cases of acute confusional migraine while Table 3 compares the clinical manifestations of the two syndromes. Similar to TTM, acute confusional migraine occurs mainly in children and adolescents, however, 47.5% occurred in females. The duration of confusion is about 30 minutes to 24 hours, 62% had agitation and 37.7% had a prior history of mild trauma. Acute confusional migraine has also been reported to occur after strenuous exercise (12). There was a personal history of prior migraines in 51% and a family history in 77%. The examination was abnormal in 25% of individuals, but there was only 1 abnormal CT or MRI of 46 performed. However, 75.5% had abnormal EEGs, usually showing slow wave activity or front intermittent rhythmic delta activity. Attacks usually resolve with deep sleep, with partial or total amnesia
of the episode. On awakening the patients appear normal. Both TTM and ACM probably represent variants of migraines and may overlap as in this adolescent’s case. In both TTM and ACM, minor trauma may be the precipitating event. The symptoms may include focal neurologic deficits in association with confusion and agitation. The majority of patients have a family history of migraine. There does appear to be a higher prevalence of abnormal neurologic findings on physical examination in TTM, as found in this teen. In both syndromes, the patient returns to baseline usually within 12 hours. EEGs done during the acute phase may show slow wave activity. The pathophysiology of these 2 syndromes is still speculative. Many theories have been reported including localized cerebral edema from increased vascular permeability and a primary neuronal dysfunction of the upper brain stem (14). Another physical sign associated with migraines that can be particularly confusing in the face of head trauma is anisocoria or oculosympathetic dysfunction. Soriani reported an 11 year-old male with recurrent migraine without headache but with confusion and anisocoria (15). DeMarinis et al. studied 20 headache-free migraine patients and 20 controls and demonstrated hypofunction of the oculosympathetic system (27). Drummond found that there were significant differences between the diameters of the pupils in 38 migraine sufferers during headache-free periods compared to the pupils in 40 control individuals without migraine headaches (28). Purvin demonstrated the features of a postganglionic parasympathetic paresis in 1 woman during a classic migraine (29). Blaik noted that episodic unilateral mydriasis may occur in the context of migraines (30). Although anisocoria is often associated with serious central nervous system pathology such as tumors,
August 2000
aneurysms, or brain herniation, when a patient has isolated, episodic unilateral mydriasis and migraine, further evaluation should be done only if symptoms worsen or change.
Differential Diagnosis The combination of head trauma, focal neurologic symptoms, and/or confusion and headache, nausea, and vomiting can simulate a serious neurologic emergency. Recognition of a migraine attack by a team physician may be difficult if it is a first episode occurring during a contact sport. While a prior history may be helpful, screening sports forms may not contain this information. Consideration should be given to the possibility of toxic or metabolic problems including drug ingestion, hypoglycemia, nonconvulsive seizure disorders, encephalitis, and intracerebral trauma. Trauma-triggered migraines may be mistaken for cerebral concussions and contusions, or for acute epidural and subdural hematomas. Concussion usually implies an immediate brief period of unconsciousness. A contusion usually occurs in the setting of more severe head trauma, typically with immediate unconsciousness. With a contusion, there is usually no latent period between the injury and the onset of focal signs. An acute epidural hematoma may follow relatively mild head trauma. Symptoms may occur after a latent period and without initial unconsciousness and can be confused with a TTM. Electrolytes, glucose, and drug screening may need to be ordered. Without a typical history or prior history of such attacks, particularly in an acute injury, a CT or MRI scan may be necessary. The rapid resolution of symptoms may help to rule out other conditions. An EEG, if done during the acute episode, may show slow wave activity. Nezu et al noted an abnormal single photon emission computerized tomography (SPECT) with regional change in cerebral blood flow, including hypoperfusion in the left posterior cerebral artery, and concluded that SPECT might be helpful for diagnosis of ACM (16).
Management When the diagnosis of TTM or ACM is made, the family can usually be reassured that the symptoms will likely resolve within 24 hours. If there is prior history of these occurrences, it is reasonable to discharge the individual home with a caregiver; however, there are no firm guidelines. Treatment may
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123
include antimigraine medications, but this has not been prospectively studied in these individuals. Several patients with TTM and ACM have been highly responsive to low-dose prophylactic therapy (7). This teen was placed on sumatriptan at the recommendation of the consultant, but this is an “off-label” use. In addition, the manufacturer recommends that sumatriptan not be used in management of hemiplegic or basilar migraine. Several studies have examined sumatriptan’s use in children and adolescents, and although found to have some beneficial effects, the effect may be different from or less than that found in adults (32,33,34). No studies examine the recurrence rates of these episodes. Although the majority of individuals do not appear to have recurrences, in some of the reported cases there are repeat episodes of migraine associated with either trauma or confusion. This teen responded dramatically to high-flow oxygen. This has not previously been evaluated or commented on in prior reports. Since oxygen may be the easiest available intervention in some athletic situations, it may be a helpful diagnostic and therapeutic intervention. Oxygen therapy is known to be highly effective in aborting cluster-type headaches and was used in this situation because of its availability in the summer camp setting. The question of future participation in contact sports is unresolved and clearly has great impact on this and any adolescent who is active in sports. Possible long-term sequela of this supposedly “benign” condition, particularly in those with repeated episodes, is not known. The combination of head trauma, focal neurologic symptoms including anisocoria, headaches, and altered mental status should be considered a medical emergency situation. Awareness of the possibility of migraine and reviewing the appropriate history questions may help with the correct diagnosis. However, in light of the potentially serious set of symptoms, and particularly in the context of a head injury, the diagnosis of TTM becomes a diagnosis of exclusion and a thorough workup should be undertaken to rule out any serious underlying etiology.
Conclusion This report describes a teenage male with many of the clinical patterns of the previously described attacks. He was young, had sustained a minor head injury without loss of consciousness, and then developed focal neurologic signs, followed by headache,
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confusion, and increasing somnolence. His symptoms resolved within hours, the neurologic workup was normal, and his examination returned to baseline within 12 hours.
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16. Nezu A, Kimura S, Ohtsuki N, et al. Acute confusional migraine and migrainous infarction in childhood. Brain Dev 1997;19:1148 –51. 17. Greenblatt SH. Posttraumatic transient cerebral blindness. JAMA 1973;225:1073– 6. 18. Matthews WB. Footballer’s migraine. Br Med J 1972;2:326 –7.
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