It is clear that comorbid factors are significant in the development and maintenance of headaches (Lipton and Silberstein, 1994). Originally coined by Feinstein (1970), the term comorbidity is used to refer to the greater than coincidental association of two conditions in the same individual. When the relationship between two disorders may be the result of pure chance, this is not considered to be comorbidity. It can be hypothesized that psychiatric factors and headaches may interact in three general ways: 1) etiologic, which would be extremely rare; 2) psychophysiologic or biobehavioral--in this case there is a real physiologic disorder that can be influenced by psychological factors (which is true of virtually any medical disorder); and 3) environmental or genetic risk factors that produce a brain state giving rise to both conditions (i.e., there may be some common biology underlying both conditions) (Puca, 2000; Sheftell and Atlas, in press). This last mechanism seems to be the most likely one underlying comorbidity of chronic headache and other medical disorders. Many have oversimplified the relationship between pain and psychiatric comorbidity, for example, viewing chronic pain as the cause of comorbid depression or pain itself as a form of somatic depression. However, the relationship is probably more complex and based upon common biologic mechanisms.
In this article, we will briefly look at psychiatric issues in migraine and chronic daily headache. Sufferers have daily or near daily headaches (>15 per month for more than four hours a day) not caused by other disorders. The most frequent subtype of this is transformed migraine, which is considered to be a complication of migraine. Patients with migraine and chronic daily headache seem to present multiple comorbid states (Puca, 2000; Sheftell and Atlas, 2002), which might suggest that these patients have a circular vulnerability between psychological conditions and chronic somatic pathologies. This vulnerability derives from both genetic and environmental factors and probably involves some neurotransmitter dysfunction pattern that produces the clinical variability.
Migraine is a common, chronic neurological disorder that affects 12% or more of the adult population in Western countries (Scher et al., 1999). It is a heterogeneous condition that results in a spectrum of disability within and among different subjects (Stewart et al., 1994). The disability of migraine can be severe and a considerable burden to the sufferer and to society. Despite significant disability, migraine is an under-recognized, under-diagnosed and under-treated condition (Stewart et al., 1994). Migraine results from altered neurochemical, electric and vascular changes in the nervous system (Goadsby, 2001; Lipton and Stewart, 1997), and although headache is the most common feature, migraine comprises more than just headache. The clinical manifestations of migraine are variable, across a broad spectrum of presentations (Moskowitz, 1990). See Figure 1 for migraine diagnostic criteria.
Transformed migraine is the most frequently seen headache syndrome at major tertiary care centers. This disorder has been variously called chronic, evolutive or mixed migraine. Patients with transformed migraine often have a past history of episodic migraine, reporting a process of transformation characterized by headaches that become more frequent over months to years with the associated symptoms becoming less severe (Sandrini et al., 1993). Patients then develop a pattern of chronic daily headache that phenomenologically may resemble that of chronic tension-type headache (few migraine symptoms), with some attacks of full-blown migraine superimposed. The second edition of the International Headache Society (IHS) classification provides criteria for chronic migraine, much stricter than the criteria for transformed migraine, which, in turn, are not included in the IHS classification (Headache Classification Subcommittee of the International Headache Society, 2004). Because most headache centers in the United States use the terms synonymously, in this article we refer to transformed migraine as defined in Figure 2.
Migraine is an episodic disorder (<15 days per month) characterized by attacks of headache and associated symptoms. Association between migraine and a variety of psychiatric and somatic conditions has been reported in the literature since it was described as a discrete syndrome. The association between migraine, depression and anxiety has been consistently reported.
Breslau et al. (1991) found in a population study that, compared with controls, migraine sufferers are four to five times more likely to have affective disorders including dysthymia, major depression and bipolar disorder (Breslau and Davis, 1993). The same group also found that patients with migraine were three times more likely to develop depression, and patients with depression were also three times more likely to develop migraine than controls.
The same profile was found between migraine and panic disorder (PD), but patients with severe non-migraine headache did not show the same correlation: Non-migraine headache was predictive of psychiatric disorder, but the reverse was not true (Breslau et al., 2000; Merikangas, 1996; Moldin et al., 1993).
Stewart et al. (1989), in a population study examining headache occurrence and prevalence of PD, reported that male participants with PD were seven times more likely than those without the condition to report a migraine headache in the previous week. Furthermore, 9.5% of females and 5.5% of males with PD reported 25% of the total migraine headaches recorded in the one-week recall period.
Breslau et al. (2003) found a bidirectional association between depression and migraine. The researchers interviewed participants ages 25 to 55 with migraine (n=496), other headaches of comparable severity (n=151) and controls with no history of severe headaches (n=539). Participants were interviewed first in 1997, then reinterviewed in 1999. At baseline, major depression predicted the first-onset migraine during the two-year follow-up period (odds ratio=3.4); migraine at baseline predicted the first-onset major depression during the follow-up period (odds ratio=5.8). Prospective associations from major depression to severe headaches and vice versa were not significant.
In a population study, Patel et al. (in press) assessed the prevalence of major depression in individuals with migraine, probable migraine (a subtype of migraine missing just one migraine feature) and controls. The overall prevalence of major depression was 28.1% for migraine, 19.5% for probable migraine, 23.9% for migraine and probable migraine polled together, and 10.3% for the control group. The prevalence of major depression was elevated in all migraine groups compared to controls on both crude and adjusted (by age, sex, education) prevalence ratios.
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