Migraine: Beyond the Pain

Chronic migraines are a condition that cause "intense pulsing or throbbing pain in one area of the head" (6), and are often accompanied by other symptoms which include nausea, vomiting, and visual disturbances (6). The pain of a migraine can last from up to a couple of hours to several days, and greatly reduces daily productivity in those who suffer from them (6). The triggers and pain threshold differ among individuals, but all can agree that the experience is unpleasant (6). Often times those who suffer from migraines do not seek treatment, or stop taking medication because they feel as though they can handle the pain (9). However recent studies may indicate that migraines can have even more serious consequences beyond the pain.

A recent study in mice has indicated that migraines may cause permanent damage in the brain (3). There is evidence that migraines act as transient strokes, rendering parts of the brain without oxygen (3). The study focused on cortical spreading depression, which is believed to be the underlying cause of migraines (3). Cortical spreading depression (CSD) causes a slow moving wave of potassium ions to signal a large number of neurons all at once, and is followed by a severe reduction in normal neuronal activity in the region (3). In addition to being implicated in migraines, CSD also occurs in stroke and traumatic brain injury (3). In this study, CSD was triggered in the mice, and microelectrodes were used to measure the amount of oxygen present during the migraine (3). It was found that cortical spreading depression caused swelling in the neurons in addition to a short term drop in oxygen levels (3). It was also found that CSD caused a temporary loss of dendritic spines, which are responsible for forming synapses with other neurons (3). These changes in dendritic spines were a result of the decreased supply of oxygen to the neurons (3). The study showed that the changes were temporary, but, there is a possibility that the damage can accumulate (3). For future study, the researchers plan to examine whether dendrites can regain normal function after they have been damaged by cortical spreading depression (3).

Episodic migraines have also been implicated in cognitive impairment in sufferers (7). It has been shown that deficits in cognitive ability are most noticeable during the actual migraine attack, but have also been shown to continue between attacks (7). These deficits include, but are not limited to, delayed visual memory, reduced overall intelligence, executive function (cognitive control) deficits, and reduced ability to concentrate (2, 4, 5). There have been conflicting results between different studies in determining the effect of migraine on cognitive function. In some studies it has been shown that these impairments are only temporary and return to normal functioning levels after the migraine has ceased (5). One study that tested the cognitive ability of 95 elderly migraineurs showed no change in cognitive ability during an attack (1). These results have all been determined through neuropsychological assessments and the results are inconclusive (7).

Few studies have linked reduced cognitive ability with brain abnormalities, but there is increasing evidence to support the connection (7). In a recent study, the relationship between executive function deficits and frontal lobe abnormalities in migraineurs was examined. Abnormalities in the frontal lobe are associated with executive function deficits (7). The researchers investigated executive function in relation to the frontal cortex gray matter in twenty four adult female migraineurs (7). Subjects were required to perform three executive function tasks, and their behavioral measures were recorded (7). The tasks were performed while the subjects were migraine free for at least seven days (7). The study found that when compared to control subjects, the migraineurs showed reduced frontal gyrus grey matter density, and responded slower to cognitive tasks (7). It was found that migraineurs did not differ from control subjects in common everyday tasks (7). However the study did associate a slower reaction time to cognitive tasks in migraineurs, which in healthy subjects is associated with inattention and fatigue (7). From this study it was concluded that migraineurs with abnormal frontal grey matter density showed a slower response time while performing cognitive tasks, while other executive function abilities were preserved and unaffected (7).

It is difficult to conclude the extent to which migraines cause permanent brain damage, and the results seem to be conflicting. In the study of cortical spreading depression in mice, the effects of CSD seem to be temporary; dendritic spines regain function, and oxygen levels return to normal. However only future research will determine if these short term effects can accumulate to cause permanent damage. Furthermore, there is still some debate as to whether cortical spreading depression is the only underlying cause of migraines (8). It is theorized that underlying problems with the vascular system and serotonin levels in addition to cortical spreading depression are responsible for migraines (8). With these additional systems involved, it is difficult to determine whether migraines are responsible for brain damage themselves, or if it is the malfunction of these other systems that cause damage to the brain.

The results of the studies related to cognitve function in migraine sufferers are also conflicting. Some studies link reduced cognitive function to migraines, while others do not. The study that examined frontal lobe density in relation to migraines found that frontal lobe density is decreased in migraine sufferers but migraineurs are still able to perform cognitive tasks just as well as non migraine sufferers. Although brain abnormalities were observed in the subjects in the study, it did not have a clear result as to why executive functions were unaffected and reaction time in performing cognitive tasks decreased. The study was performed when subjects were migraine free, and the slow reaction time was still observed. This indicates that migraines could have a damaging effect on the brain over time, but the fact that this did not produce significant deviations in behavior from non migraineurs suggest that these changes in brain structure are of small consequence, or the effect has yet to be seen.

The concept of the I-function and the subjectivity of pain are enlightening within the context of migraines. The I-function allows one to intend to perform an action, and to perform that action. In the case of the study on cognitive function and frontal lobe abnormalities, the I function is directly involved. Subjects experience a slower reaction time in these cognitive tasks, which suggests that the I function is affected over time by chronic migraines. The cables between the I-function and the rest of the neurons are still connected, but the signal is much slower. Cortical spreading depression is responsible for the disruption of neuronal signaling, as it leads to the temporary loss of dendritic spines, and reduction in synapse formation between neurons. All of these studies indicate that preventative measures are most efficient in countering the effects of migraine, whether these effects are for the short or long term. One such preventative measure is biofeedback, which assists sufferers in learning how to control involuntary activity in the brain such as pain. It teaches an individual how to use his or her I-function to control the pain of the migraine. This method of treatment has been successful for many, which suggests that migraineurs can control that the extent to which pain, and subsequently brain damage, occurs.

 

References
1. A.J. Pearson, E.P. Chronicle, E.A. Maylor and L.A. Bruce, "Cognitive function is not impaired in people with a long history of migraine: a blinded study", Cephalalgia 26 (January (1)) (2006), pp. 74-80.
2. F. Le Pira, G. Zappala, S. Giuffrida, M.L. Lo Bartolo, E. Reggio, R. Morana and F. Lanaia, "Memory disturbances in migraine with and without aura: a strategy problem?", Cephalalgia 20 (June (5)) (2000), pp. 475-478.
3. "Is It Just a Headache? Study Links Migraine to Brain Damage in Mice". 16 Nov. 2007. National Institute of Neurological Disorders and Stroke. Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4 <http://www.ninds.nih.gov/news_and_events/news_articles/news_story_migraine_hypoxia.htm>
4. K.E. Waldie, M. Hausmann, B.J. Milne and R. Poulton, "Migraine and cognitive function: a life-course study", Neurology 59 (2002), pp. 904-908.
5. K. Farmer, R. Cady, J. Bleiberg, D. Reeves, G. Putnam, S. O'Quinn and A. Batenhorst, "Sumatriptan nasal spray and cognitive function during migraine: results of an open-label study", Headache 41 (April (4)) (2001), pp. 377-384.

6. "NINDS Migraine Information Page". 03 Feb. 2009. National Institute of Neurological Disorders and Stroke.

7. N. Schmitz. E.B. Arkink, et al., "Frontal lobe structure and executive function in migraine patients", Neuroscience Letters 440 (August (1)) (2008), pp. 92-96.
8. "Pathophysiology". Mar. 2001. Merck & Co., Inc. Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4 <www.merckmedicus.com/pp/us/hcp/diseasemodules/migraine/pathophysiology_sub.jsp>
9."Prevention - What Do Migraineurs Want from Meds and Doctors?". 5 Sep. 2006. Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4 <http://headaches.about.com/od/migraine101/a/MigraineursWant.htm