You are here

  • Home
  • Archive
  • Volume 3, Issue 7
  • Potentially traumatic interpersonal events, psychological distress and recurrent headache in a population-based cohort of adolescents: the HUNT study

Article Text

Article menu
XML
Epidemiology
Research
Potentially traumatic interpersonal events, psychological distress and recurrent headache in a population-based cohort of adolescents: the HUNT study
  1. Synne Øien Stensland1,2,
  2. Grete Dyb1,2,
  3. Siri Thoresen1,
  4. Tore Wentzel-Larsen1,3,
  5. John-Anker Zwart2,4
  1. 1Norwegian Centre for Violence and Traumatic Stress Studies, Oslo, Norway
  2. 2Faculty of Medicine, University of Oslo, Oslo, Norway
  3. 3Centre for Child and Adolescent Mental Health, Eastern and Southern, Norway, Oslo, Norway
  4. 4Department of Neurology/FORMI, Ullevål sykehus, Oslo University Hospital, Oslo, Norway
  1. Correspondence to Dr Synne Øien Stensland; synne.stensland{at}nkvts.unirand.no

Abstract

Objectives Recurrent headache co-occurs commonly with psychological distress, such as anxiety or depression. Potentially traumatic interpersonal events (PTIEs) could represent important precursors of psychological distress and recurrent headache in adolescents. Our objective was to assess the hypothesised association between exposure to PTIEs and recurrent migraine and tension-type headache (TTH) in adolescents, and to further examine the potential impact of psychological distress on this relationship.

Design Population-based, cross-sectional cohort study. The study includes self-reported data from youth on exposure to potentially traumatic events, psychological distress and a validated interview on headache.

Setting The adolescent part of the Nord-Trøndelag Health Study 2006–2008 (HUNT), conducted in Norway.

Participants A cohort of 10 464 adolescents were invited to the study. Age ranged from 12 to 20 years. The response rate was 73% (7620), of whom 50% (3832) were girls.

Main outcome measures Data from the headache interview served as the outcome. Recurrent headache was defined as headache recurring at least monthly during the past year, and was subclassified into monthly, weekly and daily complaints. Subtypes were classified as TTH, migraine, migraine with TTH and/or non-classifiable headache, in accordance with the International Classification of Headache Disorders criteria, second edition.

Results Multiple logistic regression analysis, adjusted for sociodemographics, showed consistently significant associations between exposure to PTIEs and recurrent headache, regardless of the frequency or subtype of headache. Increasing exposure to PTIEs was associated with higher prevalence of recurrent headache, indicating a dose–response relationship. The strength of associations between exposure to PTIEs and all recurrent headache disorders was significantly attenuated when psychological distress was entered into the regression equation.

Conclusions The empirical evidence of a strong and cumulative relationship between exposure to PTIEs, psychological distress and recurrent headache indicates a need for the integration of somatic and psychological healthcare services for adolescents in the prevention, assessment and treatment of recurrent headache. Prospective studies are needed.

  • Public Health

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

https://doi.org/10.1136/bmjopen-2013-002997

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Article summary

    Article focus

    • The main focus was to examine, in a population-based cohort of adolescents, the associations between exposure to potentially traumatic interpersonal events (PTIEs) and migraine and tension-type headaches (TTHs), meeting the International Classification of Headache Disorders, second edition (ICHD-II) criteria.

    • Further, we aimed to assess the impact of psychological distress on the relationship between PTIEs and recurrent headache.

    Key messages

    • Our study suggests a strong and consistent relationship between exposure to PTIEs and prevalence of ICHD-II defined migraine and TTH in a population-based cohort study of adolescents.

    • Exposure to increasing numbers of types of PTIEs was consistently associated with higher prevalence of all assessed subtypes and frequencies of headache, indicating a dose–response relationship.

    • Adolescents exposed to PTIEs reported higher levels of psychological distress than their non-victimised peers. Further, adjustment for experienced psychological distress consistently and significantly attenuated strength of associations between PTIEs and recurrent headache.

    Strengths and limitations of this study

    • The strengths of this study were the large sample size, the overall high-participation rate and the use of a validated headache interview, based on the ICHD (II) criteria and the opportunity to assess the impact of multiple PTIEs and confounding factors within a population-based cohort of adolescents.

    • The retrospective, cross-sectional study design did not allow for causal inference, or differentiation between mediational and confounding effects. Findings should be interpreted within the given constraints of the study.

    Recurrent headache is the most common pain condition during adolescence, and is associated with limitations in everyday life, affecting school functioning and relationships with family and peers.1 ,2 Prepubertal onset of headache, high pain intensity, migraine and co-occurring psychological distress is related to chronification and disability in childhood and adolescence.1 ,3 ,4 Further, headache-related disability at diagnosis seems to be predictive of headache-related functional impairment decades later.5

    From early childhood to adolescence, there is a marked increase in the prevalence of headache, which is accompanied by an emerging discrepancy between genders. Prevalence tend to stabilise in boys, and increase gradually throughout adolescence in girls.6

    Primary tension-type and migraine headaches are by far the most frequent subtypes of recurrent headache in adolescence.6 Secondary headaches are consequents upon other conditions, such as medication overuse,7 infection or trauma. Primary and secondary headaches often partly overlap.8 The aetiological factors, and pathways leading to the onset and chronification of headache disorders, are largely unknown,9 yet recognised as multifactorial, including heredity, age and sex, somatic, psychological and behavioural disorders,10 ,11 head injuries,12 unfavourable lifestyle (such as smoking, inactivity13 and inadequacy of sleep1) and lack of social and economic resources within families, in schools and societies.14–16 Despite distinguishing features related to migraine headaches, the primary headaches may in part share pathophysiological mechanisms, related to the chronification of disorders,9 ,17 reflected in an observed continuum of clinical severity, ranging from tension-type complaints, through migraine,18 to combined migraine with tension-type headache (TTH).19

    Recently, researchers have explored the potential role of negative life events on the development of psychosomatic outcomes, including headache, in adolescence. Positive associations have been found between a range of childhood adversities and headache, including economic hardship,16 parental separation,20 poor family environment or neglect,21 and potentially traumatic events such as disaster,22 exposure to abuse23 ,24 and bullying.25 A recent population-based study of adolescents has suggested a dose–response relationship between frequency of childhood physical abuse and severe headaches, including migraine,23 supported by findings from a large convenience sample study of adults,26 and a multicentre study of adult migraineurs, alike.27 Despite these suggestive findings, the evidence for an association between exposure to childhood trauma and recurrent headache is currently debated.28

    The association between adverse experiences and mood and anxiety disorders in adolescents, however, is thoroughly documented.29 Exposure to severe family adversity, or potentially traumatic interpersonal events (PTIEs), especially early exposure to abuse or neglect30 witnessing domestic violence,31 exposure to bullying32 or sexually related victimisation,33 is recognised as particularly detrimental and associated with prolonged trajectories and comorbidity.25 ,34 A steady aggravation of psychological distress is further documented in relation to exposure to multiple types of PTIEs.35 Findings from high-exposure populations suggest that exposure to PTIEs will, regardless of psychological vulnerability, lead to psychological distress of clinical significance in anyone, although the thresholds vary individually.34 ,36 These main trends seem to be similar for both sexes.37

    During childhood, PTIE-exposure is generally evenly distributed, followed by emerging sex-related discrepancies in patterns of distribution of PTIEs during adolescence. Adolescent girls continuously experience more sexually related and close-network PTIEs, while boys gradually get more exposed to all other types of single events. Post-traumatic stress reactions are generally reported 2–3 times more often by adolescent girls, in comparison to boys.37

    Current epidemiological evidence of a gradual increase in risk of exposure to PTIEs throughout childhood and adolescence,33 strongly associated with the onset of psychological distress,30 which again often co-occurs with emerging recurrent headaches,4 implies possible shared causal pathways.38 We therefore need to study associations between the exposure to PTIEs, psychological distress and recurrent headache in adolescents.28 The present study was designed to acquire knowledge of associations between exposure to PTIEs and International Classification of Headache Disorders criteria, second edition (ICHD-II) defined migraine and TTH, in a population-based cohort of adolescents. The impact of psychological distress upon the relationship between exposure to PTIEs and recurrent headache was tested specifically.

    Methods

    The Young-HUNT 3 Study (http://www.ntnu.edu/hunt/inenglish) is a population-based, cross-sectional cohort study of Norwegian youth in Nord-Trøndelag county, conducted between 2006 and 2008, in which 10 464 adolescents were invited to participate.39 The study, which comprises a general health questionnaire, a clinical assessment and a headache interview, was approved by the Norwegian Regional Committee for Medical and Health Research Ethics. Inclusion was based on written consent from participants aged 16 years and older and from parents for those under 16, in accordance with Norwegian law.

    Participants

    In 2006, there were 128 694 inhabitants in Nord-Trøndelag. Over 95% were ethnic Norwegians, the workforce was generally well educated and unemployment was less than 3%. All adolescents in the county, within an age-range qualifying for attendance in junior or senior high school, were invited to the study. Of the 10 464 invited adolescents, 5614 were students in junior high, 4357 in senior high and 493 adolescents were not in school. Most adolescents were from 13 through 18 years of age, although age ranged from 12 to 20 years. Non-participation was mainly due to the lack of enrolment, absenteeism or participation in class activities outside school. In total, 8200 (78%) adolescents completed the general health questionnaire: more specifically 85% (4749) of the junior high students, 77% (3336) of the senior high students and 23% (115) of the adolescents not in school. Further, a total of 73% (7620) also completed the interview on headache.

    During a school lesson, students completed a self-administered questionnaire containing over 100 health-related and lifestyle-related questions, including items on potentially traumatic events, psychological distress and post-traumatic stress reactions, in addition to background information on family structure and family economy (http://www.ntnu.edu/hunt/data/que). Within 1 month of completion of the questionnaire, a validated semistructured clinical headache interview was conducted.40

    Recurrent headache

    All adolescents were asked if they had experienced recurring headache not caused by a cold (infection) or illness within the past 12 months. ‘Yes’ responders were read two descriptive texts of prototypic symptoms for TTH and migraine. They were asked if they recognised either, both or neither descriptions as resembling their own complaints. Thus, the interview differentiated between three types of headache: tension-type and/or migraine and/or non-classifiable headache. The frequency of recurrent headache was labelled as monthly (1–3 days/month), weekly (1–4 days/week) and daily (>4 days/week). Adolescents reporting ‘no recurrent headache’ and ‘headache less than monthly’ were defined as having ‘no recurrent headache’, whereas all other headache frequencies were referred to as ‘recurrent headache’. This recognition-based headache assessment has previously been validated against extensive semistructured interviews by neurologists,40 in accordance with ICHD-II.8

    Sociodemography

    Information on sex was drawn from the Norwegian National Population Registry, whereas age was calculated by subtracting the date of birth from the date of completion of the questionnaire. The sociodemographic variable ‘family structure’ was computed from 12 self-reported items on cohabitants, and was dichotomised into ‘living with both parents’ versus ‘other’ family structures, such as; living with a single parent, step-parents, foster parents or without guardians.20 ,33 The variable ‘family economy’, based on a self-reported estimation of family affordance in comparison with most others, categorised as ‘above average’, ‘average’ and ‘below average’, represented the socioeconomic situation, as inequalities in family affluence have previously been shown to be strongly related to inequalities in adolescent health.16

    Potentially traumatic interpersonal events

    In this study, PTIEs were defined as social interactions where an individual is subjected to intentional threats, use of physical force or power, which may cause immediate or long-term adverse health outcomes. Exposure encompasses direct and indirect (witnessing) subjection to PTIEs. A number of potentially traumatic events were screened for, among which we identified five items as being PTIEs. The items were introduced using the following question: Have you ever experienced any of these events? Select one of the following response options: ‘No’, ‘Yes, during the past year’ or ‘Yes, during lifetime’. The PTIE-related questions in our study were formulated as follows: (1) been subjected to violence (beaten or injured), (2) seen others being subjected to violence, (3) been subjected to unpleasant/disagreeable sexual acts by someone approximately your own age, (4) been subjected to unpleasant/disagreeable sexual acts by an adult and (5) been threatened or physically harassed by fellow students at school over a period of time. These items were dichotomised into ‘No, not experienced’ and ‘Yes, during lifetime’ (combining the two original ‘yes’ categories).

    Psychological distress

    General psychological distress was measured by a five-item, short-version instrument, named SCL-5, modified from the 25-item Hopkins's Symptom Checklist (HSCL) subscale on anxiety and depression, measured on a four-point Likert scale.41 The derived items were introduced as follows: Below is a list of some problems and complaints. Have you been bothered by any of this during the last 14 days? (select one alternative: 1=‘not bothered’, 2=‘a little bothered’, 3=‘quite bothered’ and 4=‘very bothered’) ‘Been constantly afraid or anxious’, ‘Felt tense, distressed or restless’, ‘Felt hopeless when you think about the future’, ‘Felt dejected or sad’ and ‘Worried too much about different things?’ A mean score ranging from 1 to 4 was computed. SCL-5 has previously been validated as a screening instrument for mental illness or psychological distress.42

    Adolescents reporting one or more PTIEs were asked three yes/no questions on post-traumatic stress reactions, derived from the child version of the UCLA PTSD index for DSM-IV,43 where two items measured current intrusion or re-experience, and one measured current avoidance.

    Statistics

    Descriptive data were presented according to the frequency of recurrent headaches (table 1). Adjusted ORs and 95% CIs were obtained from logistic regression models that estimated the likelihood of experiencing recurrent headaches according to each of the four categories of exposure to PTIEs within a complete case sample of 6787/10464 (65%) adolescents (regression model 1, tables 2⇓–4).44 The number of types of PTIEs was summed for each respondent (range 0–5), and PTIE scores of 3, 4 or 5 were combined in one category (≥3). All models included age, sex, family structure and family economy as covariates, based on a priori reasoning. The main analysis of general recurrent headache was stratified according to sex (table 2).

    View this table:
    Table 1

    Headache type, sociodemographics, exposure to PTIEs, and psychological distress, by frequency of recurrent headache, in 7620 adolescents*†

    View this table:
    Table 2

    Recurrent headache in relation to exposure to PTIEs and psychological distress, by sex*†‡

    View this table:
    Table 3

    Recurrent headache by frequency, in relation to exposure to PTIEs, sex and psychological distress*†‡

    View this table:
    Table 4

    Recurrent headache by type, in relation to exposure to PTIEs, sex and psychological distress* †‡

    Furthermore, we tested whether adjustment for psychological distress significantly altered the estimated strength of associations between PTIEs and recurrent headache. The magnitude and significance of the alteration in ORs was assessed by bootstrapping, a general procedure for computing CI without making distributional assumptions.44 ,45 Specifically, we used bootstrap methods with 10 000 replicated samples to calculate bootstrap percentile 95% CIs for the ratio between ORs in the two models (OR from model 2 (OR2)/OR from model 1 (OR1). Bootstrap estimated CIs not including 1 indicated a significant difference between the two models. Estimated CIs above 1 would indicate a significant strengthening of the association, while CIs below 1 indicated attenuation in the strength of the relationship between PTIEs and recurrent headache, after adjustment for psychological distress. Lack of power, due to low numbers or measurement uncertainties, however, would make the ORs less reliable and the CIs wider, but would not make the ORs systematically closer to, or further from, the value 1.

    In supplementary logistic regression analyses, we assessed potential differences in strength of associations between exposure to PTIEs and monthly, weekly and daily headache, respectively, followed by analysis of differences in strength of associations between PTIE exposure and headache by subtypes TTH, migraine without TTH and migraine with TTH (see online supplementary tables A1 and A2 in appendix).

    Last, we performed a subgroup, multiple regression analysis, assessing the relationship between PTIEs and recurrent headache, with and without adjustment for post-traumatic stress reactions, within the1740/6787 (26%) adolescents exposed to any PTIEs. Furthermore, we repeated analysis, with inclusion of the measure for psychological distress (SCL-5). Analyses were undertaken using SPSS V.20, in combination with the program R (The R Foundation for Statistical Computing, Vienna, Austria) package boot for bootstrap calculations.

    Results

    The demographic data are displayed in table 1.

    Generally, twice as many girls as boys reported recurrent headache. Among girls, 20% reported TTH and 8% reported migraine (with or without TTH), while 11% of boys reported TTH and 3% reported migraine. Prevalence increased with age in girls, but not in boys. About two-thirds of adolescents with only TTH or migraine reported monthly recurrence, while those with combined migraine and TTH headache mostly reported weekly or daily complaints. Despite sex differences in headache prevalence, the sociodemographic distribution of recurrent headache followed similar patterns for both sexes, linking living in ‘other’ family structures and having a family economy ‘below average’ with recurrent headache.

    In the present study, 26% of girls and 33% of boys reported exposure to one or more types of PTIEs, while 4% of both sexes reported exposure to three or more types of PTIEs. Adolescents without recurrent headache reported the lowest exposure to PTIEs, with 73% reporting no exposure, 18% reporting exposure to one, and 9% reporting exposure to two or more PTIEs. Whereas the highest degree of PTIE exposure was observed among adolescents with daily headache, of whom only 55% reported no exposure, 25% reported exposure to one and 20% reported exposure to two or more PTIEs. Mean score for psychological distress was 1.49 (±0.55; SCL-5), and increasing distress was significantly associated with recurrent headache, as assessed in univariate analysis.

    A multiple logistic regression analysis, adjusted for sociodemographic factors, revealed a steady trend of increasing odds for recurrent headache with increasing exposure to PTIEs (table 2, model 1). The strength of associations between exposure to PTIEs and recurrent headache consistently and significantly decreased after psychological distress was entered into the regression equation (table 2, model 2), as assessed in the analysis of ratio of OR with bootstrap 95% CIs. Moreover, the magnitude of attenuation in ORs seemed to increase with increasing exposure to PTIEs.

    Similarly, the associations between exposure to PTIEs and headache by ‘monthly’, ‘weekly’ and ‘daily’ recurrence, respectively, were all significant and cumulative (model 1, table 3). For all frequencies of recurrent headache as outcomes, we observed a significant attenuation in ORs, with inclusion of psychological distress in the logistic regression analyses (model 2). We found a stronger relationship between exposure to PTIEs and weekly, or more frequent, headache, compared with monthly headache. This difference in strength of associations levelled out when adjusting for psychological distress (see online supplementary table A1).

    The association between exposure to PTIEs and subtypes of recurrent headache followed a similar consistently significant and cumulative pattern for all assessed subtypes of recurrent headache; including TTH, migraine without TTH, migraine with TTH and non-classifiable headache (model 1, table 4). Adding psychological distress in regression model 2 for all four subtypes of recurrent headache yielded a significant reduction in ORs for all analyses. The association between PTIEs and recurrent headache was significantly stronger among adolescents reporting any migraine (with or without TTH), in comparison to adolescents reporting TTH only (see online supplementary table A2). This observed difference between subtypes seemed to be mainly driven by a stronger association between exposure to PTIEs and migraine with TTH, as opposed to TTH only. We found no significant difference in associations between victimization and the two groups of migraine; migraine with TTH and migraine without TTH.

    Furthermore, in subgroup analysis investigating the impact of post-traumatic stress reactions on the relationship between exposure to PTIEs and recurrent headache, post-traumatic stress reactions independently and significantly attenuated ORs, the contribution of post-traumatic stress reactions became insignificant when we additionally adjusted for general psychological distress.

    Discussion

    To our knowledge, this is the first population-based study to comprehensively assess associations between exposure to multiple PTIEs and recurrent headache meeting the ICHD-II criteria. The study documents a strong and consistent relationship between exposure to PTIEs and recurrent headache experienced by adolescents. The association was observed for monthly, weekly and daily headache, although it was significantly stronger for weekly or more frequent. A similar, robust pattern was found between exposure to PTIEs and ICHD-II defined TTH, migraine without TTH, migraine with TTH and non-classifiable headache. Increasing exposure to PTIEs was associated with higher prevalence of all assessed frequencies and subtypes of recurrent headache, indicating a dose–response relationship. Furthermore, adjustment for psychological distress led to a consistent and significant decrease in strength of associations between exposure to PTIEs and all frequencies and subtypes of recurrent headache. Post-traumatic stress reactions seem to play a similar role, although adjustment for general distress levelled out its specific effect. This may indicate that general psychological distress, as measured within this study, encompasses post-traumatic stress reactions, as found in a recent study of comorbidity in adolescents.46

    The strengths of this study were the large sample size, the overall high participation rate, the use of a validated headache interview based on the ICHD-II criteria,40 and the opportunity to assess the impact of several types of PTIEs and confounding factors, within a population-based cohort of adolescents.

    Importantly, the retrospective, cross-sectional study design did not allow for causal inference, or differentiation between confounding and mediational effects. Findings should thus be interpreted within the given constraints of the study. The lower participation and response rate among adolescents not enrolled in school, as well as among those in senior high school compared with junior high school, represents a possible selection bias. Additionally, young adolescents, boys and adolescents not living with both parents were less likely to respond to the PTIE items. This missing pattern may represent another source of selection bias. The most prominent observed selection bias within this study is the high non-response among adolescents not enrolled in school, which may have led to an underestimation of the associations.47 Our measures of PTIEs lack event-specific information on relationship to the perpetrator, severity, frequency, duration and recency of exposure48 and commonly occurring PTIEs, such as emotional abuse, peer-relational victimisation and cyber bullying, were not addressed.49 ,50 The aforementioned uncertainties, related to the measurement of PTIEs, may have affected the observed strengths of associations. Furthermore, analysis on an additional outcome measure of headache-related functional impairment would most probably have strengthened associations.24 Despite these accounted for potential selection biases and measurement uncertainties, it is quite likely that the main findings can be generalised to other adolescent populations.

    Prevalence rates of recurrent headache, including frequencies and subtypes of complaints, were in large unchanged in comparison with national headache prevalence from 1995 to 199751 and within the lower range of aggregated international estimates.6 Further, the observed patterns of distribution of recurrent headache in this study, in relation to sex, age,6 sociodemography2 ,16 ,20 and psychological distress,2 ,4 ,10 ,19 complied with previous epidemiological documentation. Likewise, the observed prevalence of exposure to PTIEs in our study was within the lower range, and distribution followed patterns similar to those observed in comparable studies, although comparison across measures and populations is difficult.28 ,33 Regarding the levels of psychological distress, the screening estimates were in correspondence with prior national and international findings.42 ,46

    Our main findings substantiate recent but scarce evidence provided by cross-sectional population-based studies of adolescents of a significant association between exposure to PTIEs and headache. Two of these studies used the ICHD-II criteria.14 ,21 ,23 ,25 Further, results are in coherence with one population-based,52 two clinical27 ,53 and another two convenience sample26 ,54 retrospective, cross-sectional studies of adults, of which one used the ICHD-II criteria.27 Apart from one adolescent study which examined girls only,14 and the adult convenience sample study,26 the sample sizes in these studies were smaller than in the present study. Generally, the adolescent studies assessed exposure to one type of PTIEs only, while the adult studies looked specifically at child abuse and family dysfunction.

    Concerning temporality of associations, a large cohort study using follow-up data over 12 years of adolescent and adult Canadians recently found childhood adversity and depression to be significant predictors of adult migraine.38 Additionally, observational, prospective, convenience sample studies of adolescents exposed to bullying lend evidence to the more general relationship between victimisation and psychosomatic complaints, although the headache measurements in these studies were too imprecise to draw more specific conclusions of associations.49 ,55 ,56 Taken together, some evidence suggests that PTIEs may be important factors on the causal pathway leading to the onset and chronification of headache disorder.

    Among the relationships observed between exposure to PTIEs and the main subtypes of headache, migraine was most strongly linked to exposure. The observed stronger association between PTIEs and migraine, as opposed to TTH, seemed to be explained in large by the stronger association between exposure to PTIEs and combined headache (migraine with TTH). This may indicate that exposure to PTIEs predisposes to more severe and complex head pains,57 reflecting a pattern similar to that observed in the relationship between PTIE-exposure and comorbidity of psychiatric disorders.29 Such an interpretation complies with previous findings that migraines in general and combined migraines specifically tend to be clinically more severe and disabling, compared to TTH only.18 ,19 On the other hand, the observed discrepancies in strength of associations may be an artefact of underlying chronification of complaints, as migraine with TTH was more often experienced weekly or daily, as opposed to migraine or TTH only, which mostly recurred monthly.

    Our findings suggest that psychological distress may play an important role as a confounder or as a mediator. A mediating role would comply with current pathophysiological understanding, where violence as an environmental stressor may acutely or over time overwhelm, exhaust and further dysregulate the stress response system.58 Pathological effects such as recurrent headache, though initially induced by external trauma, may largely be related to persistence of physiological distress, functioning as an internal stressor that triggers cerebral sensitisation and hypersensitivity through alterations of shared neuroendoimmunological pathways of emotion and pain, which in turn may lead to hyperalgesia and chronification of headache disorders.3 ,9 ,17 ,59 Future interdisciplinary studies need to explore these suggested mechanisms to delineate aetiological pathways and further enable tailored interventions.

    Sex differences in the strength of associations between PTIEs and recurrent headache may be related to the gender-biased qualitative differences of reported PTIEs, such as girls being more prone to sexual abuse and exposure within their social networks.37 Such exposure is associated with worse health outcomes, which are possibly related to the developmental stage at the time of abuse, proximity to the perpetrator and the persistence and severity of the abuse.31 ,60 Other possible mechanisms may be related to developmental biological differences, or sociocultural gender role expectations affecting reaction patterns,61 predisposing girls to internalising as opposed to externalising behaviour, which in turn increases their susceptibility to experiencing persistent chronic pain.62

    Conclusion and implications

    Our main findings comply with essential features of current theoretical models of developmental psychopathology,63 recurrent pain62 and chronic paediatric headache3 ,17 ,64 that underscore the need for a biopsychosocial approach to understand adverse-health outcomes in childhood. Knowing that recurrent headaches are among the most common causes of disability in adults and adolescents alike,1 ,18 substantiated empirical evidence of a strong, consistent and cumulative relationship between exposure to PTIEs, psychological distress and recurrent headache, regardless of subtype, demands further investigation.23 We are currently at a stage where we recognise that childhood victimisation and adversities do little good for psychological and somatic health and development, and yet we lack valid, distinct and precise knowledge to guide public health interventions and clinical practice. Thus, primarily there is a need for more comprehensive, interdisciplinary research, preferably prospective, using valid measurements of risk factors and clinically applicable outcome measures, aiming to identify underlying gene–environment interplay or biopsychosocial causal pathways as targets of tailored prevention and intervention. Second, from a more general public health perspective, the observed dependency between exposure to PTIEs and highly prevalent psychological and somatic conditions challenges the traditional dichotomisation of health services, requiring the establishment and maintenance of low threshold, local-health services directed towards adolescents that integrate and accommodate psychological and somatic needs.64–67

    Acknowledgments

    We would like to thank the adolescents participating in the HUNT Study and the HUNT research centre for their collaboration. Further, we would like to thank Professor Dean Kilpatrick for his valuable comments on the manuscript.

    References

    1. ↵
      1. Roth-Isigkeit A,
      2. Thyen U,
      3. Stöven H,
      4. et al
      . Pain among children and adolescents: restrictions in daily living and triggering factors. Pediatrics 2005;115: e152–62.
      OpenUrlAbstract/FREE Full Text
    2. ↵
      1. King S,
      2. Chambers CT,
      3. Huguet A,
      4. et al
      . The epidemiology of chronic pain in children and adolescents revisited: a systematic review. Pain 2011;152:2729–38.
      OpenUrlCrossRefPubMedWeb of Science
    3. ↵
      1. Seshia SS,
      2. Wang SJ,
      3. Abu-Arafeh I,
      4. et al
      . Chronic daily headache in children and adolescents: a multi-faceted syndrome. Can J Neurol Sci 2010;37:769–78.
      OpenUrlPubMed
    4. ↵
      1. Dunn KM,
      2. Jordan KP,
      3. Mancl L,
      4. et al
      . Trajectories of pain in adolescents: a prospective cohort study. Pain 2011;152:66–73.
      OpenUrlCrossRefPubMed
    5. ↵
      1. Brna P,
      2. Dooley J,
      3. Gordon K,
      4. et al
      . The prognosis of childhood headache: a 20-year follow-up. Arch Pediatr Adolesc Med 2005;159:1157–60.
      OpenUrlCrossRefPubMedWeb of Science
    6. ↵
      1. Jensen R,
      2. Stovner LJ
      . Epidemiology and comorbidity of headache. Lancet Neurol 2008;7:354–61.
      OpenUrlCrossRefPubMedWeb of Science
    7. ↵
      1. Dyb G,
      2. Holmen TL,
      3. Zwart JA
      . Analgesic overuse among adolescents with headache: the Head-HUNT-Youth Study. Neurology 2006;66:198–201.
      OpenUrlCrossRef
    8. ↵
      1. Olesen J
      . The international classification of headache disorders, 2nd edition (ICHD-II). Rev Neurol (Paris) 2005;161:689–91.
      OpenUrlPubMed
    9. ↵
      1. Kelman L
      . The biological basis of headache. [Review]. Expert Rev Neurother 2011;11:363–78.
      OpenUrlPubMedWeb of Science
    10. ↵
      1. Strine TW,
      2. Okoro CA,
      3. McGuire LC,
      4. et al
      . The associations among childhood headaches, emotional and behavioral difficulties, and health care use. Pediatrics 2006;117:1728–35.
      OpenUrlAbstract/FREE Full Text
    11. ↵
      1. Lateef TM,
      2. Merikangas KR,
      3. He J,
      4. et al
      . Headache in a national sample of American children: prevalence and comorbidity. J Child Neurol 2009;24:536–43.
      OpenUrlAbstract/FREE Full Text
    12. ↵
      1. Seifert TD,
      2. Evans RW
      . Posttraumatic headache: a review. Curr Pain Headache Rep 2010;14:292–8.
      OpenUrlCrossRefPubMedWeb of Science
    13. ↵
      1. Robberstad L,
      2. Dyb G,
      3. Hagen K,
      4. et al
      . An unfavorable lifestyle and recurrent headaches among adolescents: the HUNT study. Neurology 2010;75:712–17.
      OpenUrlCrossRef
    14. ↵
      1. Ghandour RM,
      2. Overpeck MD,
      3. Huang ZJ,
      4. et al
      . Headache, stomachache, backache, and morning fatigue among adolescent girls in the United States: associations with behavioral, sociodemographic, and environmental factors. Arch Pediatr Adolesc Med 2004;158:797–803.
      OpenUrlCrossRefPubMedWeb of Science
    15. ↵
      1. Lewandowski AS,
      2. Palermo TM,
      3. Stinson J,
      4. et al
      . Systematic review of family functioning in families of children and adolescents with chronic pain. J Pain 2010;11:1027–38.
      OpenUrlCrossRefPubMedWeb of Science
    16. ↵
      1. Holstein BE,
      2. Currie C,
      3. Boyce W,
      4. et al
      . Socio-economic inequality in multiple health complaints among adolescents: international comparative study in 37 countries. Int J Public Health 2009;54(Suppl 2):260–70.
      OpenUrlPubMedWeb of Science
    17. ↵
      1. Borsook D,
      2. Maleki N,
      3. Becerra L,
      4. et al
      . Understanding migraine through the lens of maladaptive stress responses: a model disease of allostatic load. Neuron 2012;73:219–34.
      OpenUrlCrossRefPubMedWeb of Science
    18. ↵
      1. Merikangas KR,
      2. Cui L,
      3. Richardson AK,
      4. et al
      . Magnitude, impact, and stability of primary headache subtypes: 30 year prospective Swiss cohort study. BMJ 2011;343:d5076.
      OpenUrlAbstract/FREE Full Text
    19. ↵
      1. Waldie KE,
      2. Poulton R
      . The burden of illness associated with headache disorders among young adults in a representative cohort study. Headache 2002;42:612–19.
      OpenUrlCrossRefPubMedWeb of Science
    20. ↵
      1. Bugdayci R,
      2. Ozge A,
      3. Sasmaz T,
      4. et al
      . Prevalence and factors affecting headache in Turkish schoolchildren. Pediatr Int 2005;47:316–22.
      OpenUrlCrossRefPubMedWeb of Science
    21. ↵
      1. Juang KD,
      2. Wang SJ,
      3. Fuh JL,
      4. et al
      . Association between adolescent chronic daily headache and childhood adversity: a community-based study. Cephalalgia 2004;24:54–9.
      OpenUrlAbstract/FREE Full Text
    22. ↵
      1. Hensley L,
      2. Varela RE
      . PTSD symptoms and somatic complaints following Hurricane Katrina: the roles of trait anxiety and anxiety sensitivity. J Clin Child Adolesc Psychol 2008;37:542–52.
      OpenUrlPubMed
    23. ↵
      1. Fuh JL,
      2. Wang SJ,
      3. Juang KD,
      4. et al
      . Relationship between childhood physical maltreatment and migraine in adolescents. Headache 2010;50:761–8.
      OpenUrlCrossRefPubMedWeb of Science
    24. ↵
      1. Zafar M,
      2. Kashikar-Zuck SM,
      3. Slater SK,
      4. et al
      . Childhood abuse in pediatric patients with chronic daily headache. Clin Pediatr (Phila) 2012;51:590–3.
      OpenUrlFREE Full Text
    25. ↵
      1. Luntamo T,
      2. Sourander A,
      3. Rihko M,
      4. et al
      . Psychosocial determinants of headache, abdominal pain, and sleep problems in a community sample of Finnish adolescents. Eur Child Adolesc Psychiatry 2012;21:301–13.
      OpenUrlCrossRefPubMedWeb of Science
    26. ↵
      1. Anda R,
      2. Tietjen G,
      3. Schulman E,
      4. et al
      . Adverse childhood experiences and frequent headaches in adults. Headache 2010;50:1473–81.
      OpenUrlCrossRefPubMedWeb of Science
    27. ↵
      1. Tietjen GE,
      2. Brandes JL,
      3. Peterlin BL,
      4. et al
      . Childhood maltreatment and migraine (part I). Prevalence and adult revictimization: a multicenter headache clinic survey. Headache 2010;50:20–31.
      OpenUrlCrossRefPubMedWeb of Science
    28. ↵
      1. Norman RE,
      2. Byambaa M,
      3. De R,
      4. et al
      . The long-term health consequences of child physical abuse, emotional abuse, and neglect: a systematic review and meta-analysis. PLoS Med 2012;9:e1001349.
      OpenUrlCrossRefPubMed
    29. ↵
      1. Ford JD,
      2. Elhai JD,
      3. Connor DF,
      4. et al
      . Poly-victimization and risk of posttraumatic, depressive, and substance use disorders and involvement in delinquency in a national sample of adolescents. J Adolesc Health 2010;46:545–52.
      OpenUrlCrossRefPubMedWeb of Science
    30. ↵
      1. McLaughlin K,
      2. Greif Green J,
      3. Gruber MJ,
      4. et al
      . Childhood adversities and first onset of psychiatric disorders in a national sample of us adolescents. Arch Gen Psychiatry 2012;69:1151–60.
      OpenUrlCrossRefPubMedWeb of Science
    31. ↵
      1. Zinzow HM,
      2. Ruggiero KJ,
      3. Resnick H,
      4. et al
      . Prevalence and mental health correlates of witnessed parental and community violence in a national sample of adolescents. J Child Psychol Psychiatry 2009;50:441–50.
      OpenUrlCrossRefPubMedWeb of Science
    32. ↵
      1. Fisher HL,
      2. Moffitt TE,
      3. Houts RM,
      4. et al
      . Bullying victimisation and risk of self harm in early adolescence: longitudinal cohort study. BMJ 2012;344:e2683.
      OpenUrlAbstract/FREE Full Text
    33. ↵
      1. Finkelhor D,
      2. Ormrod RK,
      3. Turner HA
      . Lifetime assessment of poly-victimization in a national sample of children and youth. Child Abuse Negl 2009;33:403–11.
      OpenUrlCrossRefPubMedWeb of Science
    34. ↵
      1. Jonson-Reid M,
      2. Kohl PL,
      3. Drake B
      . Child and adult outcomes of chronic child maltreatment. Pediatrics 2012;129:839–45.
      OpenUrlAbstract/FREE Full Text
    35. ↵
      1. Copeland WE,
      2. Keeler G,
      3. Angold A,
      4. et al
      . Traumatic events and posttraumatic stress in childhood. Arch Gen Psychiatry 2007;64:577–84.
      OpenUrlCrossRefPubMedWeb of Science
    36. ↵
      1. Neuner F,
      2. Schauer M,
      3. Karunakara U,
      4. et al
      . Psychological trauma and evidence for enhanced vulnerability for posttraumatic stress disorder through previous trauma among West Nile refugees. BMC Psychiatry 2004;4:34.
      OpenUrlCrossRefPubMed
    37. ↵
      1. Tolin DF,
      2. Foa EB
      . Sex differences in trauma and posttraumatic stress disorder: a quantitative review of 25 years of research. Psychol Bull 2006;132:959–92.
      OpenUrlCrossRefPubMedWeb of Science
    38. ↵
      1. Modgill G,
      2. Jette N,
      3. Wang JL,
      4. et al
      . A population-based longitudinal community study of major depression and migraine. Headache 2012;52:422–32.
      OpenUrlCrossRefPubMedWeb of Science
    39. ↵
      1. Holmen TL,
      2. Bratberg G,
      3. Krokstad S,
      4. et al
      . Cohort profile of the Young-HUNT Study, Norway: a population-based study of adolescents. Int J Epidemiol 2013;1–9.
    40. ↵
      1. Zwart JA,
      2. Dyb G,
      3. Stovner LJ,
      4. et al
      . The validity of ‘recognition-based’ headache diagnoses in adolescents. Data from the Nord-Trondelag Health Study 1995–97, Head-HUNT-Youth. Cephalalgia 2003;23:223–9.
      OpenUrlAbstract/FREE Full Text
    41. ↵
      1. Tambs K,
      2. Moum T
      . How well can a few questionnaire items indicate anxiety and depression? Acta Psychiatr Scand 1993;87:364–7.
      OpenUrlCrossRefPubMedWeb of Science
    42. ↵
      1. Strand BH,
      2. Dalgard OS,
      3. Tambs K,
      4. et al
      . Measuring the mental health status of the Norwegian population: a comparison of the instruments SCL-25, SCL-10, SCL-5 and MHI-5 (SF-36). Nord J Psychiatry 2003;57:113–18.
      OpenUrlCrossRefPubMedWeb of Science
    43. ↵
      1. Rodriguez N,
      2. Steinberg A,
      3. Pynoos RS
      . UCLAs PTSD-index for DSM IV (revision 1). UCLA Trauma Psychiatry Service, 1999.
    44. ↵
      1. Kenny DA
      . Mediation. Secondary Mediation 2012.
    45. ↵
      1. Efron B,
      2. Tibshirani RJ
      . An introduction to the bootstrap. Monographs on statistics and applied probability 57. Chapman and Hall/CRC, 1994.
    46. ↵
      1. Kessler RC,
      2. Avenevoli S,
      3. McLaughlin KA,
      4. et al
      . Lifetime co-morbidity of DSM-IV disorders in the US national comorbidity survey replication adolescent supplement (NCS-A). Psychol Med 2012;42:1997–2010.
      OpenUrlCrossRefPubMed
    47. ↵
      1. De Ridder KA,
      2. Pape K,
      3. Johnsen R,
      4. et al
      . School dropout: a major public health challenge: a 10-year prospective study on medical and non-medical social insurance benefits in young adulthood, the Young-HUNT 1 Study (Norway). J Epidemiol Community Health 2012;66:995–1000.
      OpenUrlAbstract/FREE Full Text
    48. ↵
      1. Scott-Storey K
      . Cumulative abuse: do things add up? An evaluation of the conceptualization, operationalization, and methodological approaches in the study of the phenomenon of cumulative abuse. Trauma Violence Abuse 2011;12:135–50.
      OpenUrlAbstract/FREE Full Text
    49. ↵
      1. Nixon CL,
      2. Linkie CA,
      3. Coleman PK,
      4. et al
      . Peer relational victimization and somatic complaints during adolescence. J Adolesc Health 2011;49:294–9.
      OpenUrlCrossRefPubMedWeb of Science
    50. ↵
      1. Suzuki K,
      2. Asaga R,
      3. Sourander A,
      4. et al
      . Cyberbullying and adolescent mental health. Int J Adolesc Med Health 2012;24:27–35.
      OpenUrlPubMed
    51. ↵
      1. Zwart JA,
      2. Dyb G,
      3. Holmen TL,
      4. et al
      . The prevalence of migraine and tension-type headaches among adolescents in Norway. The Nord-Trondelag Health Study (Head-HUNT-Youth), a large population-based epidemiological study. Cephalalgia 2004;24:373–9.
      OpenUrlAbstract/FREE Full Text
    52. ↵
      1. Bonomi AE,
      2. Cannon EA,
      3. Anderson ML,
      4. et al
      . Association between self-reported health and physical and/or sexual abuse experienced before age 18. Child Abuse Negl 2008;32:693–701.
      OpenUrlCrossRefPubMedWeb of Science
    53. ↵
      1. Gerber MR,
      2. Fried LE,
      3. Pineles SL,
      4. et al
      . Posttraumatic stress disorder and intimate partner violence in a women's headache center. Women Health 2012;52:454–71.
      OpenUrl
    54. ↵
      1. Audi CA,
      2. Segall-Corrêa AM,
      3. Santiago SM,
      4. et al
      . Adverse health events associated with domestic violence during pregnancy among Brazilian women. Midwifery 2012;28:416–21.
      OpenUrlWeb of Science
    55. ↵
      1. Rigby K
      . Peer victimisation at school and the health of secondary school students. Br J Educ Psychol 1999;69(Pt 1):95–104.
      OpenUrlCrossRefPubMedWeb of Science
    56. ↵
      1. Fekkes M,
      2. Pijpers FI,
      3. Fredriks AM,
      4. et al
      . Do bullied children get ill, or do ill children get bullied? A prospective cohort study on the relationship between bullying and health-related symptoms. Pediatrics 2006;117:1568–74.
      OpenUrlAbstract/FREE Full Text
    57. ↵
      1. Tietjen GE,
      2. Brandes JL,
      3. Peterlin BL,
      4. et al
      . Childhood maltreatment and migraine (part III). Association with comorbid pain conditions. Headache 2010;50:42–51.
      OpenUrlCrossRefPubMed
    58. ↵
      1. Danese A,
      2. McEwen BS
      . Adverse childhood experiences, allostasis, allostatic load, and age-related disease. Physiol Behav 2012;106:29–39.
      OpenUrlCrossRefPubMedWeb of Science
    59. ↵
      1. Macdonald G,
      2. Leary MR
      . Why does social exclusion hurt? The relationship between social and physical pain. Psychol Bull 2005;131:202–23.
      OpenUrlCrossRefPubMedWeb of Science
    60. ↵
      1. Costello EJ,
      2. Erkanli A,
      3. Fairbank JA,
      4. et al
      . The prevalence of potentially traumatic events in childhood and adolescence. J Trauma Stress 2002;15:99–112.
      OpenUrlCrossRefPubMedWeb of Science
    61. ↵
      1. Rutter M,
      2. Caspi A,
      3. Moffitt TE
      . Using sex differences in psychopathology to study causal mechanisms: unifying issues and research strategies. J Child Psychol Psychiatry 2003;44:1092–115.
      OpenUrlCrossRefPubMedWeb of Science
    62. ↵
      1. Asmundson GJG,
      2. Katz J
      . Understanding the co-occurrence of anxiety disorders and chronic pain: state-of-the-art. Depress Anxiety 2009;26:888–901.
      OpenUrlCrossRefPubMedWeb of Science
    63. ↵
      1. Pynoos RS,
      2. Steinberg AM,
      3. Piacentini JC
      . A developmental psychopathology model of childhood traumatic stress and intersection with anxiety disorders. Biol Psychiatry 1999;46:1542–54.
      OpenUrlCrossRefPubMedWeb of Science
    64. ↵
      1. Seshia SS,
      2. Phillips DF,
      3. Von Baeyer CL
      . Childhood chronic daily headache: a biopsychosocial perspective. Dev Med Child Neurol 2008;50:541–5.
      OpenUrlCrossRefPubMedWeb of Science
    65. ↵
      1. Shonkoff JP,
      2. Boyce WT,
      3. MB S
      . Neuroscience, molecular biology, and the childhood roots of health disparities: building a new framework for health promotion and disease prevention. JAMA 2009;301:2252–59.
      OpenUrlCrossRefPubMedWeb of Science
    66. ↵
      1. Russ S,
      2. Garro N,
      3. Halfon N
      . Meeting children's basic health needs: from patchwork to tapestry. Child Youth Serv Rev 2010;32:1149–64.
      OpenUrl
    67. ↵
      1. Goodman A,
      2. Joyce R,
      3. Smith JP
      . The long shadow cast by childhood physical and mental problems on adult life. Proc Natl Acad Sci USA 2011;108:6032–7.
      OpenUrlAbstract/FREE Full Text

    Supplementary materials

    • Supplementary Data

      This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

      Files in this Data Supplement:

    Footnotes

    • Contributors SØS carried out the data processing, analysed the data, and drafted and revised the paper. She is the guarantor. GD and J-AZ contributed to the integration of the headache interview, measures of victimisation and post-traumatic distress in the Young-HUNT3 Study. GD and ST wrote the original study protocol, applied for and received the grant for the study and further participated in the epidemiological modelling, analysis and writing of the manuscript. TW-L contributed to the statistical analysis. J-AZ participated in the design of the study and helped to write the manuscript. All authors have read and approved the final version of the manuscript.

    • Funding This work was supported by the Norwegian Centre for Violence and Traumatic Stress Studies and received a grant from The Norwegian Council for Mental Health, The Norwegian Extra Foundation for Health and Rehabilitation, grant number 2009/2/0023. The Nord-Trøndelag Health Study (The HUNT Study), which is a collaboration between the HUNT Research Centre (Faculty of Medicine, Norwegian University of Science and Technology NTNU), Nord-Trøndelag County Council, Central Norway Health Authority and the Norwegian Institute of Public Health, planned, organised and financed the data collection.

    • Competing interests None.

    • Ethics approval Inclusion was based on written consent from participants aged 16 years and older and from parents for those under 16, in accordance with Norwegian law. This study was approved by the Norwegian Regional Committee for Medical and Health Research Ethics.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data sharing statement Data are available from the HUNT study http://www.huntbiosciences.com/Cohorts/Diabetes/The-HUNT-Bio-And-Databank. The general health questionnaire and headache interview used in the study are accessible from the HUNT Bio-And-Databank (http://www.ntnu.edu/hunt/data/que).