What Is Footballer's Migraine? 2023
General
What has come to be called “Footballer’s Migraine” is really a syndrome of symptoms of fortification visual images, numbness and paresthesiae usually one on side of the body in the arm and face, and rare hemiparesis followed by throbbing headache, much like that of an attack of migraine with aura.
These events occur minutes after mild, usually non-concussive head trauma such as may be sustained in soccer, boxing, or mild accidental head trauma. Many of the patients may have spontaneous typical migraine before or after the traumatic event and most of them have a history of migraine in their family. “Footballer” in this sense refers to a soccer player, not an American type football player. Footballer’s Migraine is not mentioned in ICDH-3.
This is an article by Britt Talley Daniel MD, member of the American Academy of Neurology, the American Headache Society, migraine textbook author, and blogger.
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Diagnosis
Most cases concern patients with migraine who develop symptoms of migraine with aura (visual, numbness, language trouble) after mild non-concussive head injury. However, Whitty’s[i] case in 1967 had no headache.
In Matthews’[ii] 1972 article all his patients had visual symptoms and migrainous paresthesiae followed by headache, but his case 3 also had “difficulty with speech.”
Read my article, “Migraine with Aura",” on my website, www.doctormigraine.com.
Haas and Sovner[iii] in 1969 writing about “Migraine attacks triggered by mild head trauma, and their relation to certain post-traumatic disorders of childhood” reported in children leg weakness or hemiparesis, slurred or garbled speech, migrainous paresthesiae, lethargy or sleepiness, and vomiting.
Morris[iv] in a letter to the British Medical Journal in 1972 regarding his own experiences following blows to the face after tackles playing rugby, described:
light-headedness, followed after about 15 minutes by homonomous hemianopia with fortification spectra, and tingling of the hand, side of the face, and tongue. Tiredness and nausea followed about two hours later lasting several hours. Morris did not describe headache.
Haas, et al,[v] in 1975 writing in Archives of Neurology about “Juvenile head trauma syndromes and their relationship to migraine” described 4 clinical types: hemiparesis; somnolence, irritability, and vomiting; blindness; and brain stem signs.
Literature review
There are few references in the early neurologic literature. Graham[vi] writing in 1966 in the Handbook of Clinical Neurology referred to "youngsters with classical migraine who develop a characteristic attack when hit on the head in a football match."
Whitty[vii] writing in 1967 in The Lancet on “Migraine without headache” mentioned a patient who had migraine which had been induced by boxing in his youth. Whitty’s case 6 follows:
A man aged 55, for 12 months had had attacks of fortification spectra followed by numbness and paraesthesiae in the hand, arm, and face. Symptoms were on both right and left sides and lasted ½ to 1 hour. Speech not affected, but he could not write properly when the right hand was involved. No headaches, nausea, or vomiting. Apart from chronic bronchitis with productive winter cough he was otherwise well. Skull X-rays and an electroencephalogram normal. Family history of typical migraine with a visual aura in a first cousin and in a maternal aunt. 30 years previously, when an amateur boxer, he had had attacks of numbness and weakness of the left side lasting ½ to 1 hour and associated with throbbing headaches after fights in which he received punishment to the head. They ceased when he gave up boxing.
Matthews[viii] writing on the subject "Footballer’s Migraine" in the British Medical Journal in 1972 stated that:
Migraine may be a formidable obstacle to the enjoyment of life but is less well known as an occupational hazard and a threat to professional advancement. I have encountered classical migraine, including incapacitating visual field defects, occurring only when playing football and precipitated by head trauma, in five young men--two whole-time professionals, one a part-time professional, and two amateurs. Two, including the part-time professional, had given up the game on this account.
Case 3 from Matthews’ article follows:
A boy of 12 was playing somewhat inexpertly in goal when he was struck on the side of the head by the ball. Within a few minutes he complained of blurred vision and a little later developed numbness of the right hand and difficulty with speech. As this improved, it was followed by severe headache and he was taken to a hospital casualty department by an alarmed games master. The almost equal alarm aroused in the casualty officer was allayed by the boy’s rapid recovery and when I saw him a few days later he was quite well. He had no previous history of migraine and his subsequent progress is unknown.
Matthews pointed out that a diagnosis of migraine was certain in his patients and that the circumstance of focal and concerning neurologic symptoms of visual change and paresthesiae along with severe headache occurring after a blow to the head caused great concern in the mind of attendant officials and medical personnel who naturally feared some much worse neurologic condition such as aneurismal rupture or subdural hematoma had occurred.
Matthews continued:
Migraine-induced in this way is not common among footballers and is not mentioned in standard texts on sporting injuries…The ball weighs from 14 to 16 ounces (400 to 450g) at the beginning of the game, and although the modern waterproof ball does not increase in weight by the 20% common with the leather ball on a wet pitch, the impact, even when traveling at the quite ordinary speed of 30 miles an hour, is not inconsiderable.
The footballer is trained to meet the ball, from whatever direction it comes and whatever its intended destination, in a restricted area in the midline in the frontal region. The neck muscles are contracted and the force of the contact may be increased by a sharp movement of the head.
Haas and Sovner[ix] pointed out that early reports about patients “beginning their ‘career’ in migraine after suffering head trauma”[x];[xi],[xii],[xiii] do not include patients having individual migraine attacks minutes or hours after a blow to the head. They reported 5 cases of migraine attacks triggered by mild head trauma with a variety of neurological manifestations as part of the attacks. Three of the cases occurred without headache. Case 4 from their paper follows:
R.G., a 19 year-old man, has had four migraine attacks. The first was at age 12. On Saturday afternoon he had been briefly stunned by a blow to the head while playing football. On Sunday morning he awoke with a mild headache. One hour later he got paraesthesiae in his left hand, forearm and arm. All symptoms faded shortly.
The second attack was in June 1967 at age 17. He recalls being hit on the head and believes that the trauma was related to the attack, but the temporal relationship between the two has slipped his mind.
The third attack was in March 1968 at age 18. At about 1.15 a.m. he was hit forcefully on the lip in a fistfight and was momentarily stunned. At about 3 a.m., while sitting in a car, he noted numbness in the tips of his left fingers. This sensation quickly ascended to involve the entire left upper limb and the left side of his lips, tongue, and nose. At the same time, he developed a severe right supraorbital headache with nausea. The numbness faded in an hour and he slept off the headache.
The fourth attack was on 20 April 1969 at age 19. At 11 a.m. he carelessly struck his head against the arm of a couch and was momentarily stunned. At 12 noon a right supraorbital headache began and soon was severe. Later nausea and vomiting occurred. At 1 p.m. numbness began in his left finger tips and soon spread to involve his entire left upper limb and the left side of his lips, tongue, and nose.
His left hand became clumsy and he had trouble in writing (he is left-handed). He lost left-sided vision. The numbness and hemianopia faded away in several hours, but the headache lasted some 12 hours. Neurological examination just after the end of the headache showed slight clumsiness of fine movements of the left hand and slight rotary-horizontal nystagmus on lateral gaze. The next day the examination by one of us (D.C.H.) was normal.
In 1975 Haas, et al,[xiv] wrote on “Juvenile Head Trauma Syndromes and Their Relationship to Migraine” in the Archives of Neurology. They reported 25 patients who had 50 attacks of “temporary neurological phenomena triggered by head trauma.” The age of their patients ranged from 2 to 38 and the head blows that started the attacks were strong enough to “daze the patient momentarily.” Two blows produced brief loss of consciousness. In almost all attacks, a history of a latent period between the head trauma and the onset of neurological symptoms occurred.
One of Haas, et al, cases with hemiparesis, follows:
One June 1, 1972, a 14 year-old boy was struck forcefully on the right side of his head by a large rubber ball. Moments later, he noticed difficulty seeing in the right visual field. Severe left posterior cerebral headache began in 30 minutes; one hour later, he experienced fluctuating numbness in the right side of the face, right arm and leg, vomiting and difficulty in speaking.
Several hours after the trauma, examination in the hospital revealed mild dysphasia, right homonymous hemianopsia, and mild right hemiparesis. A few hours later, the visual field defect and the hemiparesis disappeared, and the next day the dysphasia and headache faded away. Four similar previous episodes had followed mild head trauma, the first at age 11.
Ashworth[xv] writing in 1985 in the Scottish Medical Journal on “Migraine, head trauma and sport” described 7 patients who developed an attack of migraine by heading a football or a blow on the face in a rugby tackle. Ashworth stated:
The attack is sometimes alarming and clearly cannot be explained on a basis of trauma alone. Some people only have attacks in this particular circumstance but the majority have spontaneous episodes at other times.
McCrory, et al,[xvi] wrote on “Prevalence of headache in Australian footballers” in 2004 in British Journal of Sports Medicine in which they surveyed the prevalence and risk factors for headache in a population of elite professional Australian footballers. A total of 160 headache questionnaires utilizing ICDH-II criteria were studied and headaches were found in 80% of players with 49% reporting headaches during match play and 60% during training.
In the footballers, 22% of headaches conformed to ICDH-II definition of migraine, but when the less strict definition of “footballer’s migraine” was used 34% of headaches met these criteria. The authors concluded that headaches are common in Australian footballers and the syndrome may not be properly identified using only a strict ICDH-II definition of migraine.
Pathophysiology
Most of the articles on this subject date about thirty years ago when the prominent and sole cause of migrainous neurologic events was thought to relate to arterial spasm (the aura) and arterial vasodilatation (the headache). Haas and Sovner[xvii] stated in 1969:
We believe that our patients are inordinately sensitive to traumatic cerebral arterial spasm and perhaps to its sequelae as well, in part due to their genetic predisposition for migraine.
All the reviewed authors considered the attacks of neurological sequelae to be “Migraine” and the word migraine is included in several of the titles of the articles and mentioned in the bulk of the texts. Two of six of the patients of Haas and Sovner in 1969[xviii] with trauma-triggered attacks also had spontaneous migraines similar to their traumatic induced ones.
Haas and Sovner began their discussion of the article with the following statement: “We firmly believe that the post-traumatic attacks in our cases 1 through 5 were typically migrainous except for their having been triggered by a blow to the head.” Matthews in 1972[xix] said, “In these patients the diagnosis of migraine is indisputable…” Morris’[xx] account is interesting because he had both spontaneous and traumatic induced attacks and he called them “typical migraine.” Haas, et al,[xxi] stated in 1975:
Further support for the existence of a migrainous mechanism in the trauma-triggered attacks comes from their clinical similarity to accepted descriptions of classical migraine attacks, especially to those that occur in juveniles.
Solomon in 1998[xxii] stated that:
Although trauma may be one of many triggers of migraine, trauma is sometimes the sole or predominant precipitating factor; e.g., footballer's migraine… Trauma may trigger the first attack of migraine in a susceptible individual. Biochemical and epidemiologic studies suggest that trauma may be the main etiologic factor of migraine in some cases.
Haas, et al., in 1969[xxiii] discussed their patients as:
having had immediate cerebral arterial spasm, severe enough to produce marked focal ischemia with its resultant hypoxia and disturbance of cerebral function…Platelet aggregation occurs when blood flow decreases and the platelets then release 5-hydroxy-tryptamine (serotonin). 5- hydroxyl-tryptamine, itself a dilator of the micro-circulation, induces the release of vasoactive polypeptides, (kinins) from plasma.
Cortical Spreading Depression. The current view of the pathophysiologic changes in these patients with Footballer’s Migraine is that trauma induces Leao’s Cortical Spreading Depression, a reaction of neuronal and glial depolarization which passes like a wave over the cerebral cortex and then resets.
The red line represents Cortical Spreading Depression moving from the occipital lobe, forward to the central areas of the brain, and then resetting.
Treatment
McCrory, et al,[xxiv] writing in 2005 in the British Journal of Sports Medicine on ”Open label study of intranasal sumatriptan (Imigran) for footballer's headache” found that intranasal sumatriptan provided "valuable, effective, and convenient treatment of headache in professional sport." They performed an open label drug trial in elite Australian footballers using intranasal sumatriptan (20 mg) as treatment for acute headache and found that at two hours 86% of attacks of migraine with aura and all of the attacks of migraine without aura responded. They also found that recurrence rates were low.
Probably all of the acute onset triptans and usual migraine preventive drugs could be tried for footballer’s migraine yet there is little published data on the subject.
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Britt Talley Daniel MD
Literature
[i] Whitty CWM. Migraine Without Headache. The Lancet. 1967;2:283-285.
[ii] Matthews WB. Footballer’s Migraine. British Medical Journal. 1972;ii:326-327.
[iii] Haas DC, Sovner RD. Migraine attacks triggered by mild head trauma, and their relation to certain post-traumatic disorders of childhood. J. Neurol. Neurosurg. Psychiat. 1969;32:548-554.
[iv] Morris AM. Footballer’s migraine. British Medical Journal. 1972;ii:769-770.
[v] Haas DC, Pineda GS, Lourie H. Juvenile head trauma syndromes and their relationship to migraine. Arch Neurol. 1975;32:727-730.
[vi] Graham JR. Handbook of Clinical Neurology. 1966. vol. 5:50.
[vii] Whitty CWM. Migraine Without Headache. The Lancet. 1967;2:283-285.
[viii] Matthews WB. Footballer’s Migraine. British Medical Journal. 1972;ii:326-327.
[ix] Haas DC, Sovner RD. Migraine attacks triggered by mild head trauma, and their relation to certain post-traumatic disorders of childhood. J. Neurol. Neurosurg. Psychiat. 1969;32:548-554.
[x] Michael MI, Williams JM. Migraine in children. J. Pediat. 1952;41:18-24.
[xi] Muller E. Gibt es eine sogenannte traumatische Migraine? Mschr. Unfallheilk. 1955;58;143-148.
[xii] Burke EC, Peters GA. Migraine in childhood. Amer. J. Dis. Child. 1956;92:330-336.
[xiii] Barolin GS. Migrane und andere paroxysmale Hirndurch-blutungsstorungen nach Kopftraumen. Wien med. Wschn. 1966;116:462-468.
[xiv] Haas DC, Pineda GS, Lourie H. Juvenile head trauma syndromes and their relationship to migraine. Arch Neurol. 1975;32:727-730.
[xv] Ashworth B. Migraine, head trauma and sport. Scott Med J. 1985;30(4):240-242.
[xvi] McCrory PM, Heywood J, Coffey C. Prevalence of headache in Australian footballers. Br J Sports Med. 2005;39:e10.
[xvii] Haas DC, Sovner RD. Migraine attacks triggered by mild head trauma, and their relation to certain post-tramatic disorders of childhood. J. Neurol. Neurosurg. Psychiat. 1969;32:548-554.
[xviii] Ibid.
[xix] Matthews WB, Footballer’s Migraine. British Medical Journal. 1972;ii:326-327.
[xx]Morris AM. Footballer’s migraine. British Medical Journal. 1972;ii:769-770.
[xxi] Haas DC, Pineda GS, Lourie H. Juvenile head trauma syndromes and their relationship to migraine. Arch Neurol. 1975;32:727-730.
[xxii] Solomon S. John Graham Senior Clinicians Award Lecture. Posttraumatic migraine. Headache. 1998; 38 (10): 772-778.
[xxiii] Haas DC, Sovner RD. Migraine attacks triggered by mild head trauma, and their relation to certain post-tramatic disorders of childhood. J. Neurol. Neurosurg. Psychiat. 1969;32:548-554.
[xxiv] McCrory P, Heywood J, Ugoni A. Open label study of intranasal sumatriptan (Imigran) for footballer's headache. Br J Sports Med. 2005;39(8):552-554.