The World Health Organization ranks headache as one of the top 10 most disabling medical conditions in the world for men and women. The International Headache Committee (IHC) classifies headaches into primary and secondary headaches (13). Primary headaches include migraine, tension, cluster, and other primary types of headaches. Secondary headaches include trauma-related, vascular, and nonvascular types, as well as headaches caused by infection and substance abuse. The sports medicine physician, as well as physicians who treat patients who are physically active, frequently will encounter individuals whose activity will be hindered by headache symptoms. In the past, headaches in athletes have been classified into subtypes such as sports related or effort migraine, exertional headache, effort headache, trauma triggered migraine, and posttraumatic headache (PTH) (13). It is possible to have some overlapping symptoms when diagnosing various types of headache in the athlete. For example, an athlete with a history of migraines may experience a tension headache, concussion, or posttraumatic headache (PTH) in combination with migraine symptoms. The sports medicine physician who is aware of the subtypes of headache will be better equipped to treat common headache syndromes and also know when to consider imaging or when to refer patients for specialist care.
The purpose of this article is to review some major subtypes of headaches, especially those that may be seen frequently by sports medicine physicians and health care providers who treat physically active patients. Treatment of the subtypes will be covered also, as well as return to activity and play issues that may arise for sports medicine physicians treating high school, National Collegiate Athletic Association (NCAA), and professional sports teams.
Migraine headache is a common chief complaint, especially in primary care and emergency department settings. It is thought that migraine headaches comprise 4.5% of all emergency department visits and account for 10 million physician visits each year. The World Health Organization has placed migraine as the 19th leading cause of disease burden in the world (25). Various theories have been proposed to explain the pathophysiology of migraines. Currently, it is hypothesized that the biological cause of migraine headache is cortical spreading depression (CSD) (26). CSD is a wave of tissue depolarization in response to a migraine trigger that migrates across the cerebral cortex and causes prolonged neuronal dysfunction. CSD causes reduced cerebral blood flow and increases permeability of the blood–brain barrier. Blood-born factors are released, which activate nociceptive afferent fibers from trigeminal ganglion innervating arteries, resulting in pain. Other pathways activated cause the release of vasoactive neuropeptides, which continue to stimulate the trigeminovascular system, causing further inflammation and pain. It is generally accepted that migraine headache may have a genetic basis that is more complex than Mendelian or autosomal recessive and autosomal dominant inheritance (6).
Migraine without Aura
Migraine without aura is the most common subtype of migraine headache. Typical features of migraine without aura, or what used to be termed common migraine, are unilateral, pulsing pain, lasting from 4 to 72 h, and often are accompanied by nausea, photophobia, and phonophobia. This subtype of migraine is often triggered by physical activity. To diagnose migraine without aura, the patient has to have at least five headaches with at least two of the previously listed symptoms. A key diagnostic criterion for the sports medicine physician also should include the patient avoiding physical activity that precipitates migraine symptoms. In the female patient, migraine without aura is associated often with onset of the menstrual cycle. In younger pediatric patients, migraine without aura can often present with bilateral symptoms, which tend to transition to unilateral symptoms in adulthood. The causes of migraine without aura now are believed to be neurobiological. Initially, these headaches were thought to be vascular in nature. However central nervous system involvement has been shown, and with the increased use of triptans, whose specific action on 5HT receptors is proven well, the cause of migraine without aura now is thought to be multifactorial.
Migraine with Aura
Migraine with aura also has been termed classic, hemiplegic, ophthalmic, and complicated migraine in past classification schemes. These headaches usually present as transient painful attacks with a sudden onset over 5 to 20 min, and last at least 60 min. The aura is defined as neurological symptoms that occur before the onset of a migraine headache. There must be focal neurological symptoms that are reversible, including sensory, speech, and visual changes. Premonitory symptoms can begin up to 2 d in advance and can include fatigue, depression, nausea, photophobia, phonophobia, scotomata, paresthesias, motor weakness, and sensory deficits. Further subtypes of migraine with aura have been described, including typical aura with migraine headache, typical aura with nonmigraine headache, and typical aura without headache. Patients who experience migraine with aura may have symptoms that are similar to those patients with a serious or life-threatening condition, including transient ischemic attack and cerebrovascular accident, subarachnoid hemorrhage (SAH), intracranial pressure (ICP), and infection. During the initial evaluation, knowing the patient’s medical history is crucial, that is, if they have had similar symptoms or aura in the past. A previous history of symptoms that mimic serious conditions, where no serious pathology was found, may prevent unnecessary intervention or imaging procedures.
There are many options for the pharmaceutical treatment of migraine headache. A headache diary can help the athlete avoid migraine triggers. NSAID, triptans, and combination analgesics are all considered first-line therapies. The over-the-counter (OTC) combination pill of acetaminophen/aspirin/caffeine or Excedrin has been shown to be highly effective and safe for the treatment of migraine headaches and associated symptoms (15). If the patient responds poorly to OTC, triptans can be tried; however triptans carry some risks of adverse cardiovascular events, so these should be used with caution. Newer therapies offer combinations of triptans and NSAID and are shown to be superior to monotherapy (23). Intranasal and intramuscular preparations of triptans are available as well. Ergotamines are still prescribed, although their use is less common now secondary to more frequent adverse effects. Prophylactic therapy is an option for patients who experience frequent migraine headache and those patients who do not respond to abortive therapy. For those physicians who treat NCAA athletes, it is important to note that caffeine is banned in amounts that would cause concentrations in the urine to rise over 15 μg·mL−1, and beta-blockers are banned in some sports such as riflery. For those patients and especially athletes who do not want to take medications, and those who cannot tolerate certain adverse effects of medication, acupuncture may be a helpful therapy (18).
Tension-type headache (TTH) is the most common type of primary headache (13). Worldwide TTH may cause more disability than migraine headache (25). Terms to describe TTH previously included tension headache, stress headache, and psychogenic headache. In the revised The International Headache Classification, 2nd edition (ICHD-2) guidelines, further distinctions were made between subtypes of TTH. Despite being the most prevalent type of headache, diagnosis is often difficult as there tends to be very few classic symptoms. In the subtype of TTH termed infrequent episodic TTH, patients exhibit symptoms less than 1 d per month. With frequent episodic TTH, headaches arise 1 to 14 d per month. Chronic TTH patients have headaches 15 d or more a month. Further dividing TTH into subtypes has been useful to guide treatment; patients with infrequent episodic TTH usually respond well to symptomatic treatments, where chronic TTH therapy usually involves prophylactic treatments. There is not always tenderness of the pericranial muscle groups in TTH. However this is the most common abnormal finding with TTH, especially with tenderness over the frontal, temporal, masseter, sternocleidomastoid, and trapezius muscles. Patients often complain of bilateral, nonthrobbing headache that is dull, “band-like,” “like a tight cap,” or “like a heavy weight on my head or shoulders.”
The exact mechanism of TTH is not understood fully. Given the various subtypes and variation in presentation even in the same patient, it is likely that many factors contribute, including heightened sensitivity to peripheral and central pain pathways. Common triggers for TTH are stress and head and neck movements. Patients with TTH do not seem to react to factors that precipitate migraine headaches.
Treatment of TTH can be divided into acute and preventive strategies. Despite being the most common headache syndrome, treatment of TTH is difficult and lacks consistently proven methods (2). For acute treatment, NSAID and acetaminophen are used for abortive therapy as first-line medications. Combination medications containing analgesics and caffeine also may be used. The use of opioids and barbiturates is not recommended especially for athletes given the risk of sedation, dependence, and possible rebound headache. Medications should be given at maximum doses early in the symptomatic patient with the overall goal to minimize the frequency of treatments and to avoid medication overuse headache (MOH). Treatment for the prevention of TTH includes medications such as tricyclic antidepressants and selective serotonin reuptake inhibitors. Acupuncture and physical therapies may have some benefit but lack consistent evidence. Behavioral therapies including biofeedback, relaxation, and stress management also may have a role in preventive treatment (18,20).
Cluster headaches are part of a group of disorders termed trigeminal autonomic cephalgias (13). They present as severe unilateral pain in the orbital, supraorbital, and temporal regions. The attacks can be as frequent as every other day up to eight times per day. They are accompanied by ipsilateral autonomic signs including rhinorrhea, lacrimation, sweating, miosis, ptosis, and eyelid edema. Cluster headaches are not common, usually affecting men, with a lifetime prevalence of about 0.1% (27). They are thought to be triggered by alcohol, cigarette smoking, and previous head trauma. Cluster headaches may be inherited by autosomal dominant mechanism in about 5% of all cases. The attacks tend to come more frequently in groups called cluster periods, which usually last for several weeks. Some patients may go without an attack for several years. About 10% to 15% of these patients with cluster headache will develop chronic cluster headache, defined as having attacks for 1 year without any remission period or a remission period that lasts less than 1 month (16). First-line treatment of cluster headache includes subcutaneous sumatriptan and oxygen therapy (4,8). Intranasal sumatriptan is also available and has been shown to be effective. There is some evidence that glucocorticoid therapy is beneficial for acute treatment of cluster headache. Prednisone 30 mg·d−1 or dexamethasone 8 mg·d−1 have been used (8). Verapamil is currently the medication of choice for preventive therapy.
Subdural hematoma occurs when there is bleeding into the space between the dura and arachnoid membranes. The most common cause is trauma that causes tearing of the bridging veins that drain into the dural sinuses. Subdural hematoma also can occur from arterial rupture and intracranial hypotension. Other infrequent causes are ruptured aneurysm, coagulopathy, arteriovenous malformation, complications from surgery, and meningioma. The clinical presentation of subdural hematoma (SDH) can vary. SDH can be seen in coma in up to 50% of cases. Classically SDH has been described in up to 38% of cases as having a lucid interval following trauma, with a steady neurologic decline into unconsciousness. Symptoms of SDH include headache, nausea, vomiting, ataxia, cranial nerve palsies, and anisocoria. Subdural hematoma can be divided into acute, subacute, and chronic presentations. Acute SDH symptoms arise within 1 to 2 d after initial trauma, subacute SDH symptoms arise after 3 to 14 d, and chronic SDH symptoms are seen 15 d after a traumatic injury. The IHC notes that headache is common after documented trauma in acute and subacute SDH in 11% to 53% of cases (25). Treatment of SDH is determined largely by the severity of the patient’s symptoms. Clinical status, the Glasgow coma score, the size of the lesion, and neuroimaging findings are used to determine whether surgical intervention is necessary.
SAH occurs when there is bleeding into the subarachnoid space (13). SAH is the most common cause of severe, rapid onset headache and is a neurosurgical emergency. The average mortality rate in a recent review of SAH was 51% (14). Symptoms can be debilitating and have been described classically as “thunder-clap headache.” Trauma is the most common cause of SAH, followed by ruptured aneurysm. There have been reports of SAH in patients who engage in weightlifting, with the proposed causing an increase in ICP and blood pressure from performing the Valsalva maneuver, where arterial pressure can rise to greater than 400/300 mm Hg (12). Symptoms include the sudden onset of severe unilateral headache, nausea, vomiting, mental status changes, and nuchal rigidity. Treatment for SAH depends on the severity of symptoms, whether the patient has SAH caused by trauma or ruptured aneurysm. These patients require ICU monitoring, bed rest, and careful attention to avoid any activity that may increase risk of rebleeding.
Headaches caused by the use of medication or substance, illegal drugs, or withdrawal of the medication or substance will be seen in the general population as well as athletes. MOH previously has been named analgesic rebound headache and drug-induced headache (13). It is possible a headache arises acutely as an adverse effect of a particular medication. Medication also can make a preexisting primary headache worse. Medications that athletes may use frequently known to cause headaches include NSAIDs, analgesics, and oral contraceptives. Other substances that the sports medicine physician must consider are caffeine, nicotine, anabolic steroids, alcohol, marijuana, and cocaine. A detailed history and determining the timeline from ingesting the substance to the time of symptoms is critical in determining if a medication or substance is the cause of headache. If a medication is new, and withdrawing the medication resolves the headache, it may be the cause. If a patient has been taking a medication regularly and the medication is discontinued, they may experience a withdrawal headache. Often the common medications to treat headaches are overused: including NSAIDs, opioids, triptans, ergotamines, and analgesics (7). Often MOH is encountered in patients who have headache syndromes that are difficult to treat such as migraine and TTH.
Headaches are caused frequently by intracranial, extracranial, and systemic infections (13). Common upper respiratory infections, influenza, and sinusitis can all present with a myriad of symptoms including headache. More concerning is the headache associated with fever and constitutional symptoms, seen in bacterial and viral meningitis and encephalitis. Commonly associated symptoms seen in cases of meningitis such as stiff neck, photophobia, rash, or recent travel to countries known to be endemic for encephalitis should alert the sports medicine physician to consider a more rapid work-up. This includes assessing the need for imaging, blood cultures, empirical treatment with antibiotics, and possibly lumbar puncture.
Chiari Malformation Type 1
Chiari Type I (CM-1) is defined as low-lying cerebellar tonsils that are shaped abnormally and have herniated below the level of the foramen magnum (13). Usually clinically significant Chiari malformations have herniated >5 mm below the foramen magnum. CM-1 is uncommon, with prevalence estimated at 0.1% to 0.5% (24). Often CM-1 does not become symptomatic until adulthood. However the most common presenting symptom is occipital headache, and this can be exacerbated by coughing, performing the Valsalva maneuver, or position. Other symptoms can include dizziness, hoarseness, dysarthria, hiccups, hearing loss, bradycardia, and syncope. It is likely that severe symptoms from larger types of Chiari malformation, including brain stem compression, increased ICP, syringomyelia, and cerebellar dysfunction, would not be tolerated by high-level athletes. PTH can be more intense and prolonged in athletes with Chiari malformation. However given frequent Valsalva-like maneuvers seen in strength training and other activities, the sports medicine physician may consider this diagnosis in the patient with prolonged occipital and neck headache (11). Some symptoms of CM-1 will resolve spontaneously over time, although surgical repair is often necessary, and there is some controversy over whether or not these should be repaired early in life or one should wait until they become more symptomatic (19).
Primary Exertional Headache
Exertional headache is described as a headache brought on specifically by physical activity. They usually start with exercise and become more severe with prolonged exercise. Exertional headache also has been termed “weight-lifter’s headache.” These types of headaches only occur during or after physical exercise. They are bilateral, throbbing, and pulsating in nature and usually last from 5 min to 48 h. Pathophysiology of exertional headache is not well understood. The International Headache Society (IHS) classifies exertional headache as a primary headache, but they also can be caused by a preexisting condition (13). Exertional headache has been associated also with intracranial abnormalities including aneurysm, primary and metastatic tumors, vascular abnormalities, CM-1 malformation, arterial dissection, and intracranial hemorrhage (21). Other theories explaining the cause of exertional headache involve possible increase of intrathoracic pressure being transmitted to the base of the brain; during exercise, elevated blood pressures may cause pain-sensitive venous sinuses to dilate causing pain. There also may be some mechanisms similar to migraine headache, as physical activity is often a trigger for migraine headaches as well. One study examined incompetence of the internal jugular vein as a cause for exertional headache and found retrograde jugular flow using venous duplex ultrasound more frequently in patients with exertional headache compared to control (9). Treatment has consisted largely of indomethacin, at doses between 25 and 150 mg·d−1. Firm evidence for treatment is lacking, and use of indomethacin is largely anecdotal. Propranolol and naproxen have been reported also to show some benefit for patients (17).
PTH is defined as a secondary headache that develops within 7 d after sustaining head and neck trauma (13). PTH is further divided into acute and chronic subtypes. There can be other varying symptoms that develop after trauma that accompany a headache including dizziness, insomnia, nausea, vomiting, difficulty concentrating, amnesia, and personality changes. It appears female gender and older patients are more affected. It can be challenging for the sports medicine physician to evaluate these symptoms for athletes in sports, especially those sports with high rates of head injury. Frequently PTH symptoms will mimic other types of headaches. Most commonly, after head trauma, up to 80% of patients will have headache symptoms; most often, symptoms similar to TTH are seen (1). Migraine headache and cluster headache symptoms have been reported also. There have been theories suggesting that the pathophysiology of traumatic brain injury (TBI) and migraine have similar features. Even more difficult perhaps is evaluating headache symptoms that arise weeks after the initial trauma. If the particular athlete has a history of headaches previously, a careful work-up is pertinent to decide if the headache symptoms are new, an exacerbation of previous symptoms, or a combination of old and new symptoms. There is also some thought that PTH is a different syndrome than symptoms of headache following a concussion. Treatment of PTH is tailored to the individual patient’s symptoms. Bed rest has been shown to be helpful, along with medicines used for other specific headache syndromes (5). Given continued attention to head injuries and concussion in athletes, and the controversy surrounding how to treat these symptoms following traumatic head injuries, distinguishing between types of headaches can help guide the physician through an appropriate work-up.
Initial evaluation of the athlete with a headache begins with a detailed history and physical examination. The athlete who has experienced head trauma during practice or game situation should have a prompt sideline evaluation. Serial neurological checks should be performed, along with sideline concussion assessment tools if available. The Sport Concussion Assessment Tool 3 and Balance Error Scoring System are relatively rapid and easy to administer during practice and game situations. In particular, the athlete with severe headache, waxing and waning neurological status, prolonged loss of consciousness, evidence of neck trauma, or evidence of skull or facial fractures should be removed from practice or competition. These athletes should be taken for immediate evaluation by a physician. Fluctuations in neurological and mental status or statements such as “this is the worst headache of my life” should be evaluated for SDH and SAH, respectively. For those athletes whose level of care is not determined urgent, attention should be paid to the nature of the incident causing the injury. It is important to remember that concussion and head trauma may be sustained through other mechanisms, including rotational forces at the head and neck, and any traumatic force that may be transmitted caudally.
Pertinent physical examination maneuvers should include full vital signs, orthostatic blood pressure readings, oculomotor and fundoscopic examinations, neurologic examination, and musculoskeletal examination of the head and cervical spine. For nonemergent cases, close follow-up should be arranged until symptoms have resolved and the athlete has started to progress through a stepwise return to full physical activity. Athletes who are diagnosed with a concussion are not given medications that may mask changes in neurological status or NSAID due to risk of exacerbating an intracranial hemorrhage. Acetaminophen may be used for headache and other pain if necessary. Analgesic use should be limited to avoid MOH. In subsequent follow-up visits, medications to treat PTH should still be chosen on a per case basis, based on the physician’s clinical judgment.
Please keep in mind that many headaches can be the result of secondary causes. Once life-threatening causes are ruled out, it is important to consider alternatives such as cervical spine disease, dental issues, ophthalmic disease, infections, sinusitis, hypertension, diet, menstrual cycle, stress, and the environment to list a few. An expanded history and serial physical examinations can help rule out secondary causes. The aforementioned headache diary can be useful while the work-up is ongoing.
Treatment of various types of headaches can be challenging. In the setting of competitive athletics, choosing the most beneficial treatment initially, while avoiding adverse effects, may result in the athlete returning to play sooner and avoid time-consuming costly work-ups. It is pertinent to choose a treatment method that does not impair the athlete’s ability to compete, realizing that most athletes would be held from competition for severe headache symptoms. Please be cognizant to medications that are banned by governing bodies. The table compares common signs and symptoms of headache subtypes and their common treatments.
Whether or not imaging is necessary is also controversial. Aside from emergent and serious cases, a history and physical examination without red flags should eliminate the need for imaging acutely. Those athletes that experience trauma resulting in prolonged symptoms also may be referred later for computed tomography or magnetic resonance imaging. Neuropsychological testing may be considered also to assess cognitive impairment.
The primary care physician who treats patients with an active lifestyle will often encounter the chief complaint of headache. Careful attention to their medical history, present history, and physical examination may avoid unnecessary and expensive medications and imaging. For patients whose condition requires medication, attention to adverse effects may avoid time away from physical activity. For team physicians, it is crucial to avoid medications that are banned by that sport’s governing body. Patients with prolonged symptoms of headache or patients with conditions that seem to be refractory to treatment may benefit from referral to a headache specialist.
The authors declare no conflict of interest and do not have any financial disclosures.
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