Abstract
Objective:
To examine longitudinal associations between parent factors (parent headache frequency and disability, protective parenting behaviors, parent catastrophizing) with adolescent headache-related disability and headache frequency over six months.
Background:
Theoretical models propose bi-directional, longitudinal relationships between parent factors and adolescent headache. Few studies have examined this using prospective study designs.
Design and Methods:
Participants were a cohort of 239 youth ages 11-17 years with recurrent migraine (with and without aura; chronic migraine) or tension-type headache (episodic and chronic) and their parents recruited from a pediatric neurology clinic and the community who completed assessments at baseline and 6-month follow-up.
Results:
After controlling for demographic and clinical covariates, we found that every point increase in baseline protective parenting behavior corresponded with a 2.19 point increase in adolescent headache frequency at follow-up (p = .026, 95% CI [.27, 4.10]). Similarly, every point increase in baseline parent catastrophizing corresponded with a .93-point increase in adolescent headache-related disability (p =.029, 95% CI [.09, 1.77]) and a .13-point increase in adolescent headache frequency (p = .042, 95% CI [.01, .25]) at follow-up. We also found support for the reverse association, where every point increase in baseline adolescent headache-related disability predicted a .03-point increase in parent catastrophizing (p =.016, 95% CI [.01, .05]) and a .02-point increase in protective parenting behavior (p = .009, 95% CI [.01, .03]) at follow-up. The remaining bi-directional, longitudinal associations tested between parent factors and adolescent headache were not statistically significant.
Conclusion:
Findings suggest that family-based psychological interventions targeting modifiable adolescent and parent factors may lead to improvements in adolescent headache-related disability and reductions in adolescent headache frequency.
Keywords: headache, migraine, longitudinal, family, parent, pediatric
Introduction
Headache is the most common pain complaint in childhood, with 10-12% of youth reporting high frequency migraine or tension-type headache (greater than 10 headache days/ month)1, 2. The prevalence of migraine peaks during adolescence and continues to increase into adulthood 3-5. Migraine is more common in females than males, as well as among offspring of parents with migraine 6. Frequent headache can impact nearly every aspect of daily life for youth and adults, including impairments in school/work, decreased participation in physical activities, poor quality of life, and increased anxiety and depressive symptoms 7-10. Parents of youth with recurrent headache commonly report high rates of emotional distress, family conflict, and financial burden 11-15. Pediatric headache also exerts a considerable burden on society, with an estimated annual economic cost of $1.1 billion annually in the United States16. Identifying modifiable psychosocial factors that influence headache during adolescence is critical for developing interventions to improve quality of life and functioning in youth and families.
Palermo, Valrie & Karlson (2014)17 proposed a conceptual model describing parental influences on adolescent adaptation to recurrent headache. In this model, parent factors (parental headache frequency and headache-related disability, parenting behaviors, parental distress) are hypothesized to influence and be influenced by adolescent headache frequency and headache-related disability. Research on parent factors in youth with headache and other chronic pain conditions has evaluated some of these theoretical pathways, primarily using cross-sectional study designs. For example, it is widely recognized that youth with high frequency headache often have at least one parent with headache18-20. Other cross-sectional studies have found that adolescent pain severity and pain-related disability are greater when parents report more frequent protective parenting behaviors (e.g., allowing avoidance of undesired activities due to headache, repeated check-ins about headache symptoms) and greater parental pain catastrophizing (e.g., negative thoughts and feelings about their adolescent’s pain)14, 15, 21-25.
We are aware of only two studies that have examined longitudinal associations between parent factors and adolescent adaptation to pain. Both studies enrolled youth with mixed chronic pain and demonstrated that more frequent protective parenting behaviors and greater parental distress about the adolescent’s pain at baseline were associated with less improvement in adolescent disability over short-term (4-month) 26 and long-term (12-month) follow-ups27. Little is known about whether adolescent and parent factors influence one another over time in pediatric headache. This information is critical to determine the optimal role of parents in the treatment of pediatric headache.
Aims and Hypotheses
This is a secondary data analysis from a longitudinal measure validation project of psychosocial and family risk in youth with recurrent migraine and tension-type headache11. The purpose of this secondary data analysis is to examine bi-directional associations between parent factors and adolescent headache over six months. Based on the conceptual model proposed by Palermo et al. (2014)17, we hypothesized that baseline parent factors (more frequent headache, greater headache-related disability, more frequent protective parenting behaviors, and greater parental catastrophizing about the adolescent’s pain) would predict increased adolescent headache frequency and headache-related disability over 6 months after controlling for relevant demographic and clinical characteristics. We further hypothesized that the reverse direction of the association would also be found where greater adolescent headache frequency and headache-related disability at baseline would predict increased protective parenting behaviors and greater parental catastrophizing over 6 months after controlling for demographic and clinical covariates.
Methods
The Institutional Review Board at Seattle Children's Research Institute approved this study. Parents gave written informed consent and adolescents gave written assent prior to initiating any study procedures. We have published one prior manuscript from this dataset11, in which we reported the psychometric properties of the Psychosocial Assessment Tool in youth with recurrent migraine and tension-type headache. The secondary data analyses presented below are novel. Specifically, we have not previously reported on longitudinal changes in, or bi-directional associations between, adolescent headache, parenting behaviors, and parental distress.
Participants.
Participants were 239 youth and their parents enrolled in a longitudinal cohort and measure validation study examining psychosocial and family risk in pediatric headache. We report complete details on the participants, design, and procedures of this study in our previous publication11.
We recruited participants from a neurology clinic at a pediatric academic medical center in the Pacific Northwest and from the local community over a 2-year period (March 2016-May 2018). Eligibility criteria were: 1) age 11-17 years old, 2) at least 10 episodes of headache per month for more than 3 months based on a telephone-administered screening, 3) no serious comorbid medical condition (e.g., cancer, diabetes), 4) parent was the legal guardian and lived with the adolescent, 5) parent and adolescent did not have cognitive impairment, and 6) parent and adolescent both fluent in English. Additional eligibility criteria for the neurology clinic group were: 1) had completed a new patient evaluation for headache at the neurology clinic in the past month, and 2) a primary diagnosis by a headache specialist of migraine (with or without aura), chronic migraine, frequent episodic tension-type headache, or chronic tension-type headache based on ICHD-3 beta28 criteria. For participants recruited from the community, there was one additional eligibility criterion: had never received evaluation in a neurology clinic or other specialty care clinic for headache.
We recruited youth from the neurology clinic via screening clinic schedules and using postal mailings and telephone calls, and 259 families completed telephone screening. We excluded 56 families due to failure to meet inclusion criteria, 13 declined to participate, and 32 were subsequently unable to be reached to complete informed consent. We enrolled 158 participants from the neurology clinic (recruitment/enrollment rate = 61.0%, n = 158/259). We had 157 participants complete the baseline assessment, and 146 participants completed the 6-month follow-up assessment.
We recruited participants from the community via social media advertisements in the local metropolitan area for a study about adolescent headache. We had 135 families respond to our advertisements and complete telephone screening; we excluded 37 due to failure to meet eligibility criteria, 10 declined to participate, and six were subsequently unable to be reached to complete informed consent. We enrolled 82 participants from the community (recruitment/enrollment rate = 60.7%, n = 82/135). All 82 completed the baseline assessment, and 75 participants completed the 6-month follow-up assessment. Thus, our full sample included 239 families at baseline and 221 families at follow-up (attrition = 9.2%).
Procedures
At enrollment and 6-month follow-up, adolescents completed a questionnaire measure of headache-related disability followed by a 28-day headache diary. Parents reported on demographics and completed questionnaires about their own headache, parenting behaviors, and parental catastrophizing. We used a 6-month follow-up period based on International Headache Society guidelines for the timeframe most likely to capture clinical changes following headache treatment29. Participants completed all assessments electronically via RedCAP30. We compensated participants with gift cards after completion of each assessment.
Measures
Demographics.
Parents reported on parent and adolescent age, sex, race, parent education, and family income at baseline. Parents also reported on whether their adolescent was currently taking a tricyclic antidepressant (e.g., amitriptyline) or anticonvulsant (e.g., topiramate) for headache prevention.
Adolescent headache-related disability and headache frequency.
Adolescents completed the Pediatric Migraine Disability Assessment (PedMIDAS)31, a 6-item measure where youth report the number of days they were unable participate fully in activities in their school, home, and social environments due to headache over the past three months. Responses are summed to create a total score and there are validated cut-off scores to categorize disability severity, as follows: little to none (0-10), mild (11-30), moderate (31-50), or severe (greater than 50).
Adolescents also completed a prospective 28-day online headache diary32 to measure headache frequency, which was calculated as the sum of the number of days of headache recorded.
Parent headache-related disability and headache frequency.
Parents completed the Headache Impact Test-6 (HIT-6)33, a widely used tool to assess headache-related disability in adults across work, home, and social settings. Response options are on a 5-point scale (1 = ‘never’, 5 = ‘always’). Total scores range from 36-78. There are validated cut-offs to indicate disability severity: 49 or less = little to none, 50-55 = mild, 56-59 = moderate, and 60 or more = severe.
Parents also retrospectively reported on how many days they had headache over the past three months.
Protective parenting behaviors.
Parents completed the 13-item Protect subscale from the Adult Responses to Children’s Symptoms questionnaire (ARCS)22 to assess frequency of maladaptive protective parenting behaviors (e.g., increased attention to headache, permission to avoid unpleasant activities because of headache). Parents rated how likely they are to engage in each parenting behavior on a 5-point scale (0 = ‘never’, 4 = ‘always’). Responses are averaged to provide the subscale score (range 0 to 4).
Parental catastrophizing.
Parents completed the 13-item Pain Catastrophizing Scale-Parent (PCS-P)34 to assess negative thoughts and feelings about their adolescent’s pain. Using response options on a 5-point scale (0 = ‘not at all’, 4 = ‘all the time’), parents rated the extent to which they experienced each catastrophic thought or feeling (e.g., ‘When my child is in pain, I feel like I can’t go on like this much longer’). Responses are summed to create the total score (range 0-52).
Data Analysis Plan
All analyses were performed with SPSS v.2535. Statistical significance was set at p < .05 and two-sided tests were used. First, we examined distributions of dependent variables using visual inspection of histograms and Levine’s test for variances and found that variables were normally distributed. We then calculated means and standard deviations for continuous variables, and frequency statistics for categorical variables. We used independent samples t-tests to compare baseline adolescent and parent clinical characteristics by recruitment method (neurology vs. community group).
We used MLM procedures to test our primary hypotheses regarding longitudinal associations between adolescent and parent factors. Multilevel modeling accounts for repeated measures within subjects, accommodates missing observations, and includes all available observations in the analyses. Procedures for linear growth model specifications were based on the work done by Shek and Ma36. Assessment wave (baseline, 6-month follow-up) was treated as a categorical variable and baseline values were specified as the reference point so that results were interpreted as change from baseline to 6-month follow-up.
Using MLM, we first tested the predictive effects of baseline parent factors (parent headache-related disability, parent headache frequency, protective parenting behaviors, parent catastrophizing) on adolescent headache related disability and adolescent headache frequency over the 6-month study period. We then tested baseline adolescent headache frequency and headache-related disability as predictors of protective parenting behaviors and parental catastrophizing over 6 months. In exploratory analyses, we examined these MLM models in the neurology and community groups separately. All models controlled for covariates of recruitment group (neurology vs. community), adolescent age, adolescent gender, and parent education. Baseline predictor variables and covariates were treated as fixed effects in the models. Effect sizes were calculated using Cohen’s f 2, where .02, .15, and .35 represent small, medium, and large effect sizes, respectively37.
Power Analysis
The sample size was determined based on an a priori power calculation for the primary aim of this study, which we have previously published11. For MLM analyses testing associations between parent factors and adolescent headache, our achieved sample size of 239 at enrollment and 221 at follow-up provided 97% power at the .05 significance level to detect a small effect size for fixed effects (Cohen’s f 2 = .02), A Cohen’s f 2 of .02 implies that one standard deviation increase in the predictor variable is related to .02 expected standard deviations increase in the outcome variable, controlling for covariates.
Missing Data
Missing data across measures were minimal (range .01%-5%). We had 239 participants complete our baseline assessment; the number of participants with missing data on measures used in analyses ranged from 3-6. We had 221 participants complete our follow-up assessment; the number of participants with missing data on measures used in analyses ranged from 5-12. We used all available data in analyses without imputation.
Results
Participant Characteristics
Adolescent and parent demographic and clinical characteristics are in Tables 1 and 2. Youth were on average 14 years old (SD = 1.9) and predominantly Caucasian (82.7%, 198/239). Headache diagnosis per ICHD-3beta24 criteria were available for adolescents in the neurology group, most had diagnoses of chronic migraine (58.0%, 91/157) or chronic tension-type headache (26.8%, 42/157). Adolescents had an average 13.6 headache days per month (SD = 7.8) and the majority (67.8% 162/239) had moderate to severe headache-related disability. We examined differences in adolescent headache frequency and disability by recruitment group (neurology versus community). As expected, at baseline adolescents from neurology clinic had greater headache-related disability (M = 82.6, SD = 73.7 vs. M = 62.7, SD = 57.8, p = .001) and more frequent headache (M = 14.7, SD = 8.3 vs. M = 11.5, SD =6.5, p = .001) compared to adolescents from the community. At enrollment, we found that none of the adolescents in the community group were prescribed a tricyclic antidepressant or anticonvulsant for headache prevention, whereas 35.0% (55/157) of youth in the neurology group were prescribed one or both of these medications to treat headache (p < .001).
Table 1.
Adolescent and Parent Baseline Characteristics by Recruitment Method
| Total (n = 239 dyads) |
Neurology (n = 157 dyads) |
Community (n = 82 dyads) |
|
|---|---|---|---|
| Adolescent characteristics | |||
| Age, M (SD) | 14 years, 7 mos (1.9) | 14 years, 9 mos (1.9) | 14 years, 3 mos (1.9) |
| Sex, % female | 66.8 | 68.2 | 64.2 |
| Race, % | |||
| Caucasian | 82.7 | 80.3 | 87.2 |
| African American | 1.8 | 2.0 | 1.3 |
| Pacific Islander | 0.9 | 1.4 | 0.0 |
| Asian | 2.2 | 3.4 | 0.0 |
| Native American/Alaska Native | 4.9 | 5.4 | 3.8 |
| Other | 7.6 | 7.5 | 7.7 |
| HA diagnosis, % | |||
| Migraine (w/ or w/out aura) | -- | 13.5 | -- |
| Chronic migraine | -- | 57.9 | -- |
| Frequent episodic tension-type | -- | 1.7 | -- |
| Chronic tension-type | -- | 26.9 | -- |
| Preventive medication, % * | |||
| Tricyclic antidepressant | 6.3 | 9.5 | 0.0 |
| Anticonvulsant | 12.9 | 19.1 | 0.0 |
| Parent characteristics | |||
| Age, M (SD) | 44 years (6.0) | 45 years (6.0) | 42 years (5.8) |
| Sex, % female | 94.0 | 92.4 | 97.5 |
| Education, % | |||
| High school education or less | 7.3 | 7.9 | 6.2 |
| Some college | 24.9 | 21.7 | 30.9 |
| College degree | 43.3 | 46.1 | 38.3 |
| Graduate degree | 24.5 | 24.3 | 24.7 |
| Annual household income, % | |||
| <$10,000-29,999 | 10.5 | 12.4 | 7.4 |
| $30,000-69,999 | 26.5 | 25.4 | 28.4 |
| $70,000-100,999 | 21.1 | 17.8 | 27.2 |
| >$100,999 | 41.9 | 44.5 | 37.0 |
| HA frequency/month, M (SD)* | 11.5 (18.0) | 9.5 (16.4) | 15.3 (20.2) |
| None, % | 17.7 | 21.2 | 11.1 |
| 1-9 days/month, % | 69.4 | 69.5 | 69.1 |
| 10+ days/month, % | 12.9 | 9.3 | 19.8 |
| HA disability, M (SD)* | 49.9 (10.4) | 48.0 (9.8) | 53.7 (10.4) |
| Little to none, % | 49.6 | 58.3 | 33.3 |
| Mild, % | 16.4 | 15.9 | 17.3 |
| Moderate, % | 11.6 | 10.6 | 13.6 |
| Severe, % | 22.4 | 15.2 | 35.8 |
Note.
Comparison between neurology and community groups significant at p < .05
Table 2.
Adolescent Headache and Parent Factors at Baseline and 6-month Follow-up by Recruitment Method.
| Baseline | 6-month follow-up | |||||
|---|---|---|---|---|---|---|
| Total n = 239 |
Neurology n = 157 |
Community n = 82 |
Total n = 221 |
Neurology n = 146 |
Community n = 75 |
|
| Adolescent headache | ||||||
| Headache frequency/28 days | 13.6 (7.8) | 14.7 (8.3) | 11.5 (6.5) | 12.7 (8.0) | 13.4 (8.3) | 11.2 (7.0) |
| Headache disability, M (SD) | 75.8 (69.2) | 82.6 (73.7) | 62.7 (57.8) | 51.3 (66.0) | 58.0 (75.2) | 38.6 (41.3) |
| Little to none, % | 10.5 | 8.0 | 15.4 | 27.1 | 28.6 | 24.3 |
| Mild, % | 21.5 | 20.0 | 24.4 | 27.6 | 24.1 | 34.3 |
| Moderate, % | 17.1 | 16.0 | 19.2 | 15.3 | 15.0 | 15.7 |
| Severe, % | 50.9 | 56.0 | 41.0 | 30.0 | 32.3 | 25.7 |
| Parent factors | ||||||
| Protective parenting behaviors, M (SD) | 1.7 (0.6) | 1.7 (0.6) | 1.7 (0.7) | 1.6 (0.6) | 1.6 (.6) | 1.7 (0.6) |
| Parent catastrophizing, M (SD) | 18.3 (9.8) | 19.2 (9.8) | 16.5 (9.7) | 16.6 (10.2) | 17.1 (10.1) | 15.7 (10.4) |
Most parents had completed a college degree (68.2%, 163/239) and average annual household income was ≥ $70,000 (63.1%, 151/239). Parental headache was common with 69.0% (161/233) reporting 1-9 headache days per month and 12.8% (30/233) reporting 10+ headache days per month (see Table 1). We found that 50.2% of parents (117/233) reported moderate to severe headache-related disability at baseline. Parents from the community had more frequent headache than parents from the pediatric neurology clinic (M = 15.3, SD = 20.2 versus M = 9.5, SD = 16.4, p = .019), as well as more severe headache-related disability (M = 53.7, SD = 10.4 versus M = 48.0, SD = 9.8, p < .001). We did not find any other statistically significant differences in adolescent or parent characteristics between the neurology and community groups.
Persistence of Adolescent Headache over 6 months
We used MLM procedures to examine stability of adolescent headache from baseline to 6-month follow-up, controlling for recruitment group (neurology vs. community). Adolescent headache frequency was stable across the 6-month period (b = −.40, p = .109, 95% CI [−.89, .09 ]), while adolescent headache-related disability decreased over time (b = −24.28, p = <.001). However, moderate to severe headache-related disability was still present in nearly half of adolescents at follow-up (45%, 100/221). We found the same pattern of results when we examined the neurology and community groups separately. Table 2 shows means and standard deviations for adolescent headache frequency and disability at baseline and 6-month follow-up.
Predictive Effects of Baseline Parent Factors on Adolescent Headache over 6 months
We first tested the predictive effects of baseline parent factors on adolescent headache-related disability and adolescent headache frequency over the 6-month study period (see Table 3).
Table 3.
Multilevel Modeling (MLM) Analyses Evaluating Baseline Parent Factors as Predictors of Adolescent Headache at 6-month Follow-up, and Baseline Adolescent Headache as Predictors of Parent Factors at 6-month Follow-up in the Full Sample.
| Adolescent Headache at 6-month follow-up | ||||||
|---|---|---|---|---|---|---|
| Model 1 | Adolescent headache-related disability | Adolescent headache frequency | ||||
| Parent Factors at Baseline | beta | p | 95% CI | beta | p | 95% CI |
| Protective parenting behaviors | 4.91 | 0.451 | [−0.79, 17.73] | 2.19 | 0.026 | [0.27, 4.10] |
| Parental catastrophizing | 0.93 | 0.029 | [0.09, 1.77] | 0.13 | 0.042 | [0.01, 0.25] |
| Parent headache-related disability | 0.68 | 0.199 | [−0.36, 1.71] | 0.04 | 0.521 | [−0.19, 0.09] |
| Parent headache frequency | 0.13 | 0.598 | [−0.34 , 0.60] | 0.05 | 0.090 | [−0.01, 0.12] |
| Parent Factors at 6-month follow-up | ||||||
| Model 2 | Protective parenting behaviors | Parental catastrophizing | ||||
| Adolescent Headache at Baseline | beta | p | 95% CI | beta | p | 95% CI |
| Headache-related disability | 0.02 | 0.009 | [0.01, 0.03] | 0.03 | 0.016 | [0.01, 0.05] |
| Headache frequency | 0.001 | 0.535 | [−0.02, 0.01] | 0.02 | 0.856 | [−0.17, 0.20] |
Note. Predictors in Model 1 included baseline protective parenting behaviors, parental catastrophizing, parent headache-related disability, and parent headache frequency as predictors of adolescent headache related disability and adolescent headache frequency over the 6-month study period. Predictors in Model 2 included baseline adolescent headache-related disability and headache frequency. All analyses controlled for recruitment group (neurology clinic vs. community), adolescent gender, adolescent age, and parent education.
Predicting longitudinal adolescent headache-related disability.
In support of our hypothesis, greater parental catastrophizing at baseline was a significant predictor of greater adolescent headache-related disability at follow-up. Every point increase in parental catastrophizing (range 0-52) corresponded with a .93-point increase over time in the adolescent headache-related disability score which was a small effect size (p = .029, 95% CI [.09, 1.77], f 2 = .02). Contrary to our expectation, parent headache frequency, parent headache-related disability, and protective parenting behaviors at baseline were not significant predictors of longitudinal adolescent headache-related disability. In exploratory analyses, we found the same pattern of results within the neurology sub-group. None of the parent factors had significant predictive effects in the community sub-group.
Predicting longitudinal adolescent headache frequency.
Consistent with our hypothesis, more frequent protective parenting behavior and greater parental catastrophizing at baseline were significant predictors of increased adolescent headache frequency over time. Protective parenting behavior was the strongest predictor. Every point increase in protective parenting behavior at baseline (range 0-4), corresponded with a 2.19 increase in longitudinal adolescent headache frequency which was a medium effect size (p = .026, 95% CI [.27, 4.10], f 2 = .28). The predictive effect of parental catastrophizing was smaller. Every point increase in parent catastrophizing at baseline (range 0-52) corresponded with a .13-point increase in adolescent headache frequency over time which was a small effect size (p = .042, 95% CI [.01, .25], f 2 = .02). Contrary to our expectation, parent headache frequency and parent headache-related disability were not significant predictors of longitudinal adolescent headache frequency in the full sample. In exploratory analyses, we found that none of the parent factors had significant predictive effects on adolescent headache frequency when we examined the neurology and community groups separately.
Predictive Effects of Baseline Adolescent Headache on Parent Factors over 6 months
We then tested the reverse direction of association to evaluate predictive effects of baseline adolescent headache-related disability and adolescent headache frequency on maladaptive protective parenting behaviors and parental catastrophizing over the 6-month study period (see Table 3).
Predicting longitudinal parenting behaviors.
As expected, every point increase in adolescent headache-related disability at baseline (range 0-90) was associated with a .02-point increase in protective parenting behavior over time which was a small effect size (p = .009, 95% CI [.01, .03], f 2 = .02). In exploratory analyses, we found the same pattern in the neurology sub-group. Adolescent headache-related disability did not have a significant predictive effect on longitudinal parenting behaviors in the community sub-group.
Contrary to our hypothesis, baseline adolescent headache frequency did not have a significant predictive effect on longitudinal parenting behaviors in the full sample or the two subgroups.
Predicting longitudinal parent catastrophizing.
In support of our hypothesis, we found that greater adolescent headache-related disability at baseline had a small, significant predictive effect on increased parental catastrophizing over time. Every point increase in baseline adolescent headache-related disability (range 0-90) was associated with a .03-point increase in longitudinal parent catastrophizing, which was a small effect size (p = .016, 95% CI [.01, .05], f 2 = .04). In exploratory analyses, we found the same pattern of results in the neurology sub-group. Adolescent headache-related disability did not have a significant predictive effect on longitudinal parent catastrophizing in the community sub-group.
Contrary to our hypothesis, baseline adolescent headache frequency did not have a significant predictive effect on longitudinal parent catastrophizing in the full sample or the two sub-groups.
Discussion
To our knowledge, this report is the first longitudinal evaluation of bi-directional associations between parent factors and adolescent headache. Consistent with our hypothesis and the conceptual model put forth by Palermo and colleagues17, we found that more frequent maladaptive protective parenting behaviors and greater parental catastrophizing at baseline predicted increased adolescent headache frequency at 6-month follow-up. Greater parental catastrophizing at baseline, but not protective parenting behaviors, also predicted increased adolescent headache-related disability at 6-month follow-up. We also found support for the reverse association where greater adolescent headache-related disability, but not headache frequency, at baseline predicted increased parental catastrophizing and protective parenting behaviors at 6-month follow-up. Effect sizes were generally small to moderate. These findings indicate that parental catastrophizing and maladaptive protective parenting behavior may increase the risk for poor headache outcomes for adolescents, and that caring for an adolescent with headache may increase the risk for poor behavioral and mental health outcomes for parents.
Numerous prior studies have demonstrated cross-sectional associations between parent and adolescent functioning in youth chronic and recurrent pain12, 14, 15, 22-25, 34, but very few have examined these associations prospectively26, 27. The two prior longitudinal studies which evaluated families of youth with mixed chronic pain found that higher baseline parental distress and protective parenting behaviors increased risk for poor response to treatment 26, 27. Our study extends this limited body of research to families of youth with recurrent headache, and to our knowledge, is the first to provide evidence in support of the theory that associations between parent functioning and adolescent headache are longitudinal and bi-directional17. Indeed a cyclical relationship may exist, whereby caring for an adolescent with recurrent headache increases parental distress/maladaptive parenting behaviors, which exacerbates adolescent cognitions and behaviors known to worsen headache (e.g., poor emotion regulation, poor sleep habits, reduced physical activity 38, 39), that in turn maintains adolescent headache and perpetuates parental distress and maladaptive parenting behaviors. Based on this conceptual model, we argue that psychological treatment directly targeting parental distress and parenting behaviors has the potential to improve outcomes for youth with recurrent headache.
There is growing evidence to support adolescent-focused cognitive-behavioral therapy (CBT) for pain management as a first line treatment for pediatric headache41-43. However, existing CBT protocols for pediatric headache aim to increase adolescent pain coping skills and do not address the psychosocial treatment needs of parents44. We propose that families with parents experiencing elevated pain catastrophizing and/or maladaptive protective parenting behaviors may benefit from evidence-based behavioral interventions that directly target these treatment needs. For example, Problem Solving Skills Training (PSST) delivered only to parents has demonstrated efficacy for reducing parental distress and reducing maladaptive protective parenting behaviors in a variety of pediatric populations including chronic pain45-47. We need research to determine whether combining adolescent-focused CBT for pain management with parent-focused PSST could enhance outcomes for youth with headache. It is possible that the synergy between the two interventions could produce more powerful and longer-lasting effects than either intervention alone, particularly for adolescents at increased risk for poor long-term adaptation to headache.
It is important to acknowledge that there is room to improve standard care for pediatric headache. In our sample, adolescent headache frequency did not change during the study period and a substantial proportion of youth (45%) continued to endorse moderate to severe headache-related disability at 6-month follow-up. This pattern was the same for youth in the neurology and community groups, which suggests that severe headache can persist for many youth even after establishing care in a neurology clinic. Other longitudinal cohort studies of youth with recurrent headache have reported similar findings 48, 49. A next step in this line of research will be to determine whether we can improve pediatric headache treatment by screening for parental distress and maladaptive protective parenting behaviors, and delivering family-based interventions that address both adolescent and parent psychosocial treatment needs.
We also were interested in evaluating whether parental headache frequency and headache-related disability influence adolescent adaptation to headache. Prior studies have found that youth report more frequent and more disabling pain when one or both parents have chronic pain40. We found that headache was common among parents in our sample, and that 50% of parents reported moderate to severe headache-related disability. Contrary to our expectation, however, parental headache frequency and headache-related disability at baseline were not significant predictors of adolescent headache at 6-month follow-up. It is possible that parental distress and parenting behaviors have a stronger influence on adolescent adaptation to headache relative to parental headache symptoms. However, it is also important to note that our measurements of parental headache frequency and disability were retrospective, which is not ideal. A future direction for research is to determine whether parent and adolescent headache symptoms are temporally associated, which could be accomplished using validated, prospective assessment tools of headache symptoms (e.g., daily headache diary) administered to adolescents and their parents over the same 28-day assessment window.
A unique feature of our study is that we recruited families from a neurology clinic and from the community. In exploratory analyses, we found that the pattern of associations identified in the full sample was generally replicated in the neurology group but not the community group. As we reported previously11, adolescents in the neurology group had greater headache-related disability and more frequent headache compared to the community group. It is possible that associations between parent factors and adolescent headache are stronger in treatment-seeking families, and/or in families of youth with more severe headache. However, due to the relatively small sample size of the community group, these exploratory analyses must be interpreted cautiously. Research is needed to evaluate associations between parent factors and adolescent headache in families from a wider variety of settings (e.g., recruited from schools, community, primary care, general neurology clinics, multidisciplinary headache clinics) and with a broader range of headache frequency and disability.
There are several additional limitations to consider when interpreting results from this study. Although associations between parent factors and adolescent headache were statistically significant, the effect sizes were small to medium and should be interpreted with appropriate caution. From a clinical perspective, our findings suggest that patients in families with high parental distress and/or frequent protective parenting behaviors may benefit from intervention that addresses the psychosocial treatment needs of parents. However, further research is needed to replicate and extend our findings. For example, there are other modifiable bio-behavioral factors that can influence adolescent adaptation to headache but are not targeted in standard CBT for pain management intervention (e.g., insomnia symptoms, adolescent mental health comorbidities) and this warrants further study.
It is also important to note that this report is a secondary data analysis and so there are limitations that are inherent to the study design and sample characteristics. For example, our study design used two assessment time points. We need longitudinal studies with more frequent measurements to understand trajectories of change in adolescent and parent functioning over time and to describe intra-individual and inter-individual changes in adolescent adaptation to headache. In addition, our sample was predominantly Caucasian and middle class, which reflects our local demographics. Parents in the community group had more frequent and more severe headache than parents in the neurology clinic group, which could indicate a potential selection bias in the community group. Research is needed to replicate these findings in families representing varying sociodemographic backgrounds, with a broader range of headache symptoms, and from a wider variety of recruitment settings.
Conclusion
On average, most youth in our sample had high frequency and severely disabling headache that persisted over the 6-month study period. This is consistent with other longitudinal studies which have found that up to 75% of youth with migraine or tension-type headache continue to have headache over the following months to years48, 49, even with neurology evaluation and treatment. There is a clear need for innovative approaches to psychosocial screening and intervention for this patient population. In our study, we identified parent catastrophizing and protective parenting behaviors as potentially modifiable factors that can both influence and be influenced by adolescent headache over time. Screening for parent distress and protective parenting behaviors, and delivering family-based psychosocial interventions targeting adolescent and parent treatment needs is deserving of further attention by clinicians and researchers.
Acknowledgments
Financial Support: NIH/NINDS Grant No. K23NS089966 (PI: Law).
Footnotes
Conflict of Interest Statement: No conflict.
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