Psychiatric Comorbidity in Chronic Daily Headache: Pathophysiology, Etiology, and Diagnosis Vincenzo Guidetti, MD and Federica Galli, PhD
Address Department of Child and Adolescent Neurology and Psychiatry, Interuniversity Center for the Study of Headache and Neurotransmitter Disorders Section of Rome, University of Rome “La Sapienza,” Via dei Sabelli 108, 00185 Rome, Italy. E-mail:
[email protected] Current Pain and Headache Reports 2002, 6:492–497 Current Science Inc. ISSN 1531–3433 Copyright © 2002 by Current Science Inc.
Chronic daily headache is a challenge for clinical practitioners and researchers. Etiology, pathophysiology, diagnosis, treatment, and prognosis of chronic daily headache present many questions that need answers. A chance occurrence of psychiatric disorders (mostly anxiety and mood disorders) in patients with chronic daily headache should not be excluded. This results in the need to understand the involved mechanisms, which requires us to draw new insights into the etiology, diagnosis, treatment, and prognosis of chronic daily headache. Psychiatric comorbidity seems to be cross-related to each of these dimensions, although the meanings need to be drawn. Each domain is discussed, considering the status of knowledge and stressing the future lines of research.
Introduction Chronic daily headache (CDH) represents a frequent and problematic challenge in adult and pediatric clinical practice. Many aspects of the etiology, diagnosis, and treatment of CDH need to be explained. The diagnosis of CDH is a function of a quantitative parameter (an almost daily frequency of the crises); however, we do not have clear qualitative parameters (a certain symptomologic characterization of the crises). The etiology and pathophysiology of CDH have no clear explanation; several hypotheses have been advanced [1–4, 5•,6•,7,8••]. The implication of analgesic overuse has been considered in chronic headache [9–16], although we do not have common diagnostic criteria for classifying rebound headache. In adults, the percentages of analgesic overuse range from 72% [17] to 87% [14] to 91% [18]. The prevalence of medication abuse in a general CDH population is
25% [19]. The International Headache Society (IHS) classification [20] does not provide criteria to classify CDH, which is considered to be a previous term for chronic tension-type headache. Proposals for new classification systems have been advanced for adults [21–23,24•, 25–27] and children [28–30,31••,32••,33]. The treatment of CDH has several issues that need to be explained. The choice of the treatment should be tailored to the characteristics of each patient. Analgesic overuse requires specific interventions [34,35•,36•], including drug withdrawal and the initiation of other (prophylactic or nonpharmacologic) treatments. The presence of comorbid diseases or disorders should be considered in treatment planning. The assessment of comorbid psychiatric disorders in patients with headache should be realized and adequately treated, and the negative prognostic meaning in adults [37] and children or adolescents should be considered [38,39]. The presence of psychiatric comorbidity seems to be more prevalent in patients with migraine who chronically use substances [40].
Psychiatric Comorbidity: Conceptual Framing The term comorbidity is a general medical word that dates back to Feinstein in 1970 [41]. Initially, it related to the occurrence of two distinct diseases in the same patient. The current conceptualization of the term implies an association between an index disease or disorder and one or more coexisting physical or psychologic pathologies. That Feinstein’s definition [41] was adopted does not imply a hierarchy between the index disorders and the additional disorders, nor does it relate to the concept of a disease or disorder as the starting point of our analysis or in terms of a time sequence. The transposition of the conceptualization to the psychiatric field is more recent, but unclear [42]. The content and implications of the concept of comorbidity have been altered throughout time. Comorbidity refers to disorders (behavioral and psychologic problems that deviate from normality) or diseases (well defined as clinical entities), not to the existence of related occurring symptoms (syndrome). However, recognizing comorbidities may be an initial step in identifying new syndromes. In addition, clarifying the direction, meaning, and weight of
Psychiatric Comorbidity in Chronic Daily Headache • Guidetti and Galli
comorbidities has pathophysiologic, nosologic, course, and treatment implications. However, the study of comorbidity may present a series of difficulties related to the little understanding that we have of the etiology and pathophysiology of diseases at the center of our attention. The question is amplified in psychiatry and is more troublesome if the co-occurrence of psychiatric and nonpsychiatric variables are analyzed. We deal mainly with disorders rather than diseases in the field of psychiatry [42]. The research and clinical approaches to comorbidity need to consider several issues. It is important to consider the time factor. The inferences to draw on the existence of specific and not causal relations between two or more disorders depend on the current or lifetime (concurrent or successive) [42] co-existence of disorders. Current comorbidity refers to the presence of two or more disorders at the same time. Lifetime comorbidity is the occurrence of disorders over a period of time that needs to be specified (it may be 6 months, 1 year, or throughout the patient’s lifetime). The concept of successive comorbidity has been suggested to be two disorders that do not overlap over time [42]. If lifetime comorbidity is considered, the temporal margin should be specified carefully to avoid biased conclusions. Andrews [43] suggested to reserve the term comorbidity for the conditions in which the temporal sequence is not specified. He also suggests applying the concept of co-occurrence if two or more disorders occur at the same time. Dealing with comorbidities allows us to describe clinical situations without assuming or embracing causal explanations, even if a better specification of the temporal interval gives us a valid aid in the comprehension and systematization of the subject. A second issue to clarify relates to the concept of homotypic (continuity of disease phenomenology without strong changes over time) or heterotypic (a continuous process assuming different forms over time) comorbidity. Considering comorbidity from different diagnostic groupings (eg, migraine and anxiety or depression) or within a unique diagnostic grouping (eg, dysthymia and major depression) causes additional questions to develop on the co-occurrence pattern, etiology, course, and therapy. Can heterotypic comorbidity represent a marker of severity or worst outcome? Can it represent a means of subtyping disorders? What is the etiology of heterotypic comorbidity? Can it be called a syndrome? What are the causes? Are there correlated causes or shared common factors? The third issue to consider relates to the research of comorbidity in general population-based or clinical studies. Both have pros and cons. Population-based studies avoid the Berkson’s bias, which is the tendency of self-selected patients to consult specialists. A major severity of illnesses, a patient’s characteristics, and the same comorbidity may represent biased selection filters, altering the likely findings. Only population-based studies may provide prevalence and incidence rates and unbiased estimates of risk factors for comorbidity. However, clinical studies may strengthen the
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findings of population-based studies, permitting a better monitoring of comorbidity patterns and courses over time, and presenting data on the better implementation of therapy interventions. Only clinical studies allow for the observation of rare disorders in comorbid presentation. The focus on potential risk factors and the outcome and developmental trend of comorbid patterns may be highlighted by performing clinical studies. The fourth important issue relates to the likely causes of comorbidity. The likelihood that comorbidity solely results from methodologic problems (consequence of Berkson’s bias, information-collection bias, or lack of systematic diagnostic systems) can be ruled out [42]. The concept of epiphenomenal comorbidity has been suggested [42] as a reason for the comorbid association of three conditions: only one may be the product of the other two.
Headache and Psychiatric Comorbidity The studies of psychiatric comorbidity primarily focus on migraine and less frequently on tension-type headache [44]. However, the IHS classification [20] lists psychosocial stress, anxiety, and depression as potential causes for tension-type headache; no suggestions are given for migraine. A characteristic set of psychologic features has been observed among migraine sufferers throughout the 20th century [45–48], according to Wolff’s [49] definition of migraine personality. Since the beginning of the 1990s, prospective population-based studies that observed young adults have systematized the presence of psychologic disorders in headache suffers in terms of “psychiatric comorbidity” [50–55]. Merikangas et al. [52,53] suggested that many of the psychologic features frequently related to migraine are related more to psychopathologic symptoms than to personality characteristics; a syndromic relationship with a peculiar time sequence (anxiety, migraine, and depression) has been suggested [50]. This remark was supported by a populationbased study by Breslau et al. [51,54]; a bi-directional influence between migraine and depression has been suggested [56], with one increasing the onset of the other. These studies have not shown evidence of CDH cases because there are no data available on CDH and psychiatric comorbidity in the nonclinical population. More recently, Breslau et al. [56] advanced the hypothesis that migraine and severe headache have high levels of psychiatric comorbidity. The hypothesis of a shared biologic predisposition between migraine and depression has been suggested on the basis of similarities in the biologic aspects (role of serotonergic system) [57,58]. Of absolute importance is that the prevalence of migraine is highest in patients who are referred for affective disorders in an open psychiatric ward for unipolar (46%) and bipolar (44%) disorders; within bipolar disorders, migraine predominates in bipolar II disorder (77%) versus bipolar I disorder (14%) [59]. This
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aspect supports the possibility of shared causal conditions. The probability of an incidental association between migraine and comorbid psychiatric disorders has been ruled out; consequently, the following related issues need to be examined closely and several points need to be explained. 1. Direction of the relationship (Is migraine caused by or the cause of anxiety and mood disorders? Is migraine associated with anxiety and mood disorders, but an unrelated result of factors other than itself? Is the comorbid association related to a specific moment in a patient’s life?) 2. Pathophysiologic mechanisms (What are the main factors involved? Are there shared common biologic, genetic, environmental, or psychologic processes to migraine and psychiatric disorders? What is the relative weight of each factor?) 3. Diagnostic consequences (Does migraine that is associated with psychiatric comorbidity differ from migraine occurring alone? Should we make an additional differentiation in migraine subtypes according to the presence of psychiatric comorbidity?) 4. Therapeutic lines (How is treating migraine associated with psychiatric comorbidity?) 5. Influences on the outcome (What is the effect of psychiatric comorbidity on the evolution of migraine? What is the role of the age of onset, gender, distressing life events, and personality characteristics?) These issues are applicable to the co-occurrence of psychiatric disorders in patients without migraine. The understanding of the mechanisms involved in neurologic and psychiatric disorders may lead to an understanding of respective pathophysiologic mechanisms [60].
Chronic Daily Headache and Psychiatric Comorbidity The studies on CDH have been performed almost entirely by the clinical population [61,62••]. The low prevalence of CDH in the general population may explain the difficulty of finding results when using nonclinical samples; doubts remain on likely biases of the findings (the so-called Berkson’s bias). The prevalence of psychiatric disorders is highest in patients with CDH than in other patients with headache. Estimates of the prevalence of psychiatric comorbidity in patients with CDH range from 64% to 66.1% [63,64] to 90% [65] (mostly anxiety and mood disorders), with higher rates in women with CDH than in men [66,67]. In general, chronic pain is related to the co-occurrence of depression and anxiety, opening the door to diagnostic [68], treatment [69], and etiologic [70,71] issues.
Studies that observe patients with CDH are not always easy to compare when trying to understand the adoption of different systems of classification. Some studies deal with CDH on the basis of a high frequency of crises or on the analysis of severe headache without migrainous features (not based on IHS criteria). However, these studies contribute to stress the highest (or similar) occurrence of psychiatric disorders in CDH than in migraine. Major depression is three times more prevalent in people with migraine and in people with severe headaches compared with healthy subjects [72]. Frequency of headache, but not headache severity, seems to be related to depression, anxiety, and a high disability rate [73]. Similar findings concern the occurrence of panic disorder, which is related to migraine headache and to severe headache without migrainous features [74••]. There have been attempts to find specific relationships between CDH subtypes and different psychiatric disorders. Patients with transformed migraine seem to have a higher rate of psychiatric comorbidity (57% have major depression, 11% have dysthymia, 30% have panic disorder, and 8% have generalized anxiety disorder) than those with chronic tension-type headache (51% have major depression, 8% have dysthymia, 22% have panic disorder, and 1% have generalized anxiety disorder) [75]. Another study [63] found the highest prevalence of psychiatric disorders in patients with co-existing migraine and chronic tension-type headache (72.2%) compared with chronic migraine (70.3%) and chronic tension-type headache (50%). Other studies [76,77] did not find significant differences in the association between anxiety or depression and other psychopathologic symptoms according to CDH subtypes (chronic tension-type headache, migraine plus chronic tension-type headache, and transformed migraine). However, these promising studies lack comparable diagnostic systems for the classification of CDH and psychiatric disorders, so their results may be unclear. Psychiatric comorbidity may represent an obstacle for the effectiveness of drugs in the treatment of headache [37]. In fact, the occurrence of psychiatric disorders may cause physicians to address treatment by joining pharmacologic and nonpharmacologic therapies. This makes a multidisciplinary approach from diagnosis to therapy important for patients with CDH. Psychiatric comorbidity should be analyzed carefully in the diagnostic process so that the best treatment options are chosen. A psychologic evaluation is the conditio qua non for a complete framework of patients with CDH and for tailoring the treatment according to the peculiarities of the case [78,79]. Pharmacologic and nonpharmacologic therapies should be combined in the treatment of CDH [80,81]. However, evidence-based data on nonpharmacologic therapies are needed, although well-done studies have been performed for adults, children, and adolescents [82–84]. Studies should be conducted to evaluate the effectiveness of certain therapies
Psychiatric Comorbidity in Chronic Daily Headache • Guidetti and Galli
and the different applications according to different CDH types and comorbid disorders. Antidepressants have been the most widely studied medications in the prophylactic therapy of CDH [85]; however, the method of action is unknown and likely unrelated to the antidepressive action. The understanding of factors involved in the chronicization and prognosis of headache is another aspect that should be analyzed. The role of analgesic overuse can not explain every case of CDH; this has been demonstrated by the large percentage of small children or adolescents with onset CDH. Psychiatric disorders seem to be related to the chronicization of headache [38,39], resulting in the need to assess and treat psychiatric comorbidity from an early age.
Conclusions The etiology, pathophysiology, diagnosis, treatment, and prognosis of CDH present many questions that need answers. Psychiatric comorbidity seems to be cross-related to each of these dimensions. The knowledge of the mechanisms involved in the etiology, pathophysiology, diagnosis, treatment, and prognosis of CDH may provide new insights into the role that psychiatric disorders may play in influencing each domain.
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