A survey of neurologists found that patients seek consultation for headaches more than any other complaint and represent up to one-third of total patients in their care (World Health Organization [WHO], 2004). Migraines constitute a common primary headache disorder that are marked by severe pain on one or both sides of the head, nausea or upset stomach, and hypersensitivity to sound or light (International Headache Society, 2004). The pain is often described as pulsating and of moderate to severe intensity. A majority of patients experience pain localized to one side of the head, though this pain may eventually spread to the other side. A subset of migraine sufferers experience neurological symptoms that may include sensory, perceptual, motor, and/or cognitive disturbances; these symptoms are known as the migraine aura (Hooker & Raskin, 1986). These symptoms tend to resolve within 1 hour but lead to the onset of a migraine. Migraine attacks can last from 4 to 72 hours and most commonly affect adults between the ages of 35 and 45 years. It is estimated that approximately 6–8% of men and 15–18% of women experience some form of migraine each year. Further, migraines have been identified as one of the top 20 causes of disability among adults of all ages; as a result, estimates of their financial cost to society are high (WHO, 2004).
As a primary headache disorder, migraines are believed to have a genetic basis, though exact etiology remains largely unknown (Gardner, 2006). A vascular theory of migraine was widely accepted for many years, wherein it was thought that the pain associated with migraine headaches was the result of dilated cranial vessels (Wolff, 1948). This model has been criticized due to recent research suggesting that cranial vessel dilation is not necessary for migraine pain to occur (e.g., Schoonman et al., 2008).
A more recent theory of migraine pathophysiology points to a neurogenic origin and classifies migraine as a CNS disorder (Agnoli & De Marinis, 1985; Cutrer & Charles, 2008). Headache pain is believed to be generated centrally and to involve the serotonergic system (Goadsby, 2000; Hamel, 2007; Hargreaves & Shepheard, 1999; Silberstein, 2004). A range of evidence implicating serotonin in the experience and prevention of acute attacks supports this theory (e.g., Ferrari, Roon, Lipton, & Goadsby, 2001; Silberstein, 2005).
Today clinicians widely agree that migraine is a neurovascular disorder, though recent evidence from human imaging studies suggests that vasodilation may not play an important role in headache pathophysiology (Schoonman et al., 2008). Future research utilizing technological advancements will likely elucidate the neuropathological mechanisms of migraine.
Neuropsychological testing may play a role in determining the impact of migraines on an individual's cognitive functioning, but evidence of cognitive declines in migraine sufferers is presently inconclusive (O’Bryant, Marcus, Rains, & Penzien, 2006). In reality, research on neuropsychological profiles associated with migraine is limited despite the prevalence and severity of migraine headaches. Even those studies examining relationships between cognitive performance and migraines have led to conflicting findings. Although some studies suggest that there are no significant differences in cognitive functioning between migraine sufferers and healthy controls (e.g., Bell, Primeau, Sweet, & Lofland, 1999), other studies indicate that migraine patients show deficits across a number of neuropsychological domains (e.g., Hooker & Raskin, 1986).
In a study by Bell et al. (1999), cognitive performance of patients with chronic migraines, patients with nonheadache chronic pain, and patients with mild traumatic brain injury (TBI) were compared. Across domains of cognitive efficiency, memory, and visuoperceptual ability, no differences between chronic pain and migraine patients were found, though the mild TBI patients performed significantly worse. Notably, this study did not include a control group of healthy subjects. However, a large community study suggests that these findings hold across the life span among people with and without migraine; though age is predictive of cognitive functioning, migraine diagnosis is not (Jelicic, van Boxtel, Houx, & Jolles, 2000).
That being said, a body of literature suggests that the cognitive abilities of migraine sufferers versus healthy controls do indeed differ, especially across memory and attention domains. There is some evidence suggesting that cognitive functioning is impaired among migraine sufferers only when they are experiencing an acute attack (Meyer, Thornby, Crawford, & Rauch, 2000). Other investigations suggest more lasting impairment in cognitive functioning.
For example, Hooker and Raskin (1986) compared migraine patients with and without aura to healthy controls, finding that both migraine groups obtained significantly lower scores than the control group on a tactual learning task and delayed story recall. Furthermore, migraine without aura patients significantly outperformed migraine with aura patients on the grooved pegboard and aphasia screening tasks. These results led Hooker and Raskin to conclude that migraine sufferers experience greater impairment on a neuropsychological battery than those without migraines. In addition, they argue that migraine with aura may lead to greater functional impairment than migraine without aura, though other evidence suggests that impairments are greater for those with migraine without aura across verbal memory domains (Le Pira et al., 2000). Another line of research suggests that the length of headache history and frequency of attacks may predict level of impairment (Calandre, Bembibre, Arnedo, & Becerra, 2002). Clearly, additional research is necessary to elucidate the relationships between migraine and neuropsychological functioning.
Associations between migraine and psychological functioning are more straightforward. For example, the experience of migraines increases a person's likelihood of experiencing depression (and vice versa; see Breslau, Lipton, Stewart, Schultz, & Welch, 2003). Relationships between migraine and anxiety have also been uncovered; migraine sufferers are more likely to develop panic disorder than individuals without migraine, and associations between migraine and other anxiety disorders are currently being researched (Silberstein, 2001; Smitherman, Penzien, & Maizels, 2008). Due to the well-established effects of anxiety and depression on cognitive functioning, it is important to consider possible psychiatric comorbidities when evaluating the emotional and cognitive functioning of migraine patients.
Diagnosis of migraines is largely based on clinical presentation and symptom report. As suggested earlier, migraines are divided into two major subtypes: migraine with aura and migraine without aura (International Headache Society, 2004). To meet criteria for migraine without aura, a patient must have experienced five or more headache attacks lasting anywhere from 4 to 72 hours. The headaches must be characterized by two or more of the following symptoms: moderate to severe pain, pulsating quality, unilateralization, and exacerbation by routine physical activity. Furthermore, at least one of the following symptoms should accompany the attack: nausea or vomiting, sensitivity to light, and/or sensitivity to sound.
Migraine with aura was previously identified as “classic” migraine. To meet criteria for migraine with aura, the patient must have experienced neurological symptoms that last for less than 60 minutes; these neurological symptoms must occur either before, during, or after a headache with symptoms similar to those of migraine without aura.
Although this offers some distinction between migraine types from a descriptor standpoint, diagnosis must more specifically attempt to determine the underlying etiology as they may result from a variety of structural anomalies including tumors, infections, and vascular malformations. Cerebrovascular presentation must also be considered as should metabolic issues, hypoxia, hypoglycemia, as well as various other presentations. Differential diagnosis must consider other primary headache disorders such as cluster headaches, hypnic headaches, short-lasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing headaches, and tension-type headaches (Siloberstein & Young, 1995).
Treatment for migraines typically involves some form of pharmacological intervention. Serotonin agonists have been shown to be successful in the treatment of acute headache attacks and several preventive forms of pharmacotherapy are effective, including GABA inhibitors, beta-adrenergic blocking agents, and tricyclic antidepressants (Goadsby, 2000). Analgesics and anti-inflammatory medications have also been shown to successfully treat acute attacks (Lipton et al., 1998).
Biofeedback and relaxation training are also sometimes used to provide relief from migraine pain. Research suggests that such techniques are effective, with comparable effectiveness to prophylactic medication (Andrasik, 2004).
Migraine and epilepsy are both common disorders as well as common comorbidities WelchKMALewisD. Migraine and epilepsy. Neurol Clin. (1997); vol. 15
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