Dataset Information

Pain Catastrophizing in Childhood Migraine: An Observational Study in a Tertiary Headache Center.

ABSTRACT: Background: Migraine is the most common cause of primary headache in children leading to a decrease in the quality of life. During the last decade, pain catastrophizing construct became a major focus of interest in the study and treatment of pain. Aim of the study: To evaluate pain catastrophizing in episodic and chronic migraine children and adolescents selected in a tertiary headache Center.To test whether the children's pain catastrophizing might be associated (a) with the frequency of attacks and disability (b) with psychopathological aspects (c) with allodynia and total tenderness score as symptom of central sensitization.To test the best discriminating clinical variables and scores between episodic and chronic migraine, including pain catastrophizing. Methods: We conducted a cross sectional observational study on consecutive pediatric patients affected by migraine. We selected 190 headache patients who met the diagnostic criteria for Migraine without aura, Migraine with aura and Chronic migraine. We submitted all children to the Child version of the Pain Catastrophizing Scale (PCS-C), and to the disability scale for migraine (PedMIDAS), general quality of life estimated by children (PedsQL) and parents (PedsQL-P), anxiety and depression (SAFA-A; SAFA-D) scales. We also evaluated headache frequency and the presence and severity of allodynia and pericranial tenderness. Results: No difference was detected in Total Pain Catastrophizing score (PCS-C) between chronic and episodic migraine groups (ANOVA F = 0.59, p = 0.70); the PedMIDAS, the PedsQL-P for physical functioning and the Total Tenderness Score were discriminant variables between episodic and chronic migraine. The PCS-C was not correlated with migraine related disability as expressed by Ped MIDAS, but it was significantly correlated with general low quality of life, allodynia, pericranial tenderness, anxiety, and depression. Conclusion: Pain catastrophizing seems a mental characteristic of a clinical phenotype with psychopathological traits and enhanced expression of central sensitization symptoms. This clinical profile causes general decline in quality of life in the child judgment, with a probable parents' underestimation. In childhood age, it would not be a feature of chronic migraine, but the possibility that it could predict this evolution is consistent and worthy of further prospective evaluation.

SUBMITTER: Sciruicchio V

PROVIDER: S-EPMC6384232 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Pain Catastrophizing in Childhood Migraine: An Observational Study in a Tertiary Headache Center.

Sciruicchio Vittorio V Simeone Michele M Foschino Barbaro Maria Grazia MG Tanzi Roberta Caterina RC Delussi Marianna D MD Libro Giuseppe G D'Agnano Daniela D Basiliana Roberta R de Tommaso Marina M

Frontiers in neurology 20190215

<b>Background:</b> Migraine is the most common cause of primary headache in children leading to a decrease in the quality of life. During the last decade, pain catastrophizing construct became a major focus of interest in the study and treatment of pain. <b>Aim of the study:</b> To evaluate pain catastrophizing in episodic and chronic migraine children and adolescents selected in a tertiary headache Center.To test whether the children's pain catastrophizing might be associated (a) with the frequ ...[more]

PMID: 30828315

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Project description:Obesity is related to migraine. Maladaptive pain coping strategies (eg, pain catastrophizing) may provide insight into this relationship. In women with migraine and obesity, we cross-sectionally assessed: (1) prevalence of clinical catastrophizing; (2) characteristics of those with and without clinical catastrophizing; and (3) associations of catastrophizing with headache features.Obese women migraineurs seeking weight loss treatment (n?=?105) recorded daily migraine activity for 1 month via smartphone and completed the Pain Catastrophizing Scale (PCS). Clinical catastrophizing was defined as total PCS score ?30. The six-item Headache Impact Test (HIT-6), 12-item Allodynia Symptom Checklist (ASC-12), Headache Management Self-Efficacy Scale (HMSE), and assessments for depression (Centers for Epidemiologic Studies Depression Scale) and anxiety (seven-item Generalized Anxiety Disorder Scale) were also administered. Using PCS scores and body mass index (BMI) as predictors in linear regression, we modeled a series of headache features (ie, headache days, HIT-6, etc) as outcomes.One quarter (25.7%; 95% confidence interval [CI]?=?17.2-34.1%) of participants met criteria for clinical catastrophizing: they had higher BMI (37.9?±?7.5 vs 34.4?±?5.7?kg/m(2) , P?=?.035); longer migraine attack duration (160.8?±?145.0 vs 97.5?±?75.2 hours/month, P?=?.038); higher HIT-6 scores (68.7?±?4.6 vs 64.5?±?3.9, P?<?.001); more allodynia (7.0?±?4.1 vs 4.5?±?3.5, P?<?.003), depression (25.4?±?12.4 vs 13.3?±?9.2, P?<?.001), and anxiety (11.0?±?5.2 vs 5.6?±?4.1, P?<?.001); and lower self-efficacy (80.1?±?25.6 vs 104.7?±?18.9, P?<?.001) compared with participants without clinical catastrophizing. The odds of chronic migraine were nearly fourfold greater in those with (n?=?8/29.6%) vs without (n?=?8/10.3%) clinical catastrophizing (odds ratio?=?3.68; 95%CI?=?1.22-11.10, P?=?.021). In all participants, higher PCS scores were related to more migraine days (??=?0.331, P?=?.001), longer attack duration (??=?0.390, P?<?.001), higher HIT-6 scores (??=?0.425, P?<?.001), and lower HMSE scores (??=?-0.437, P?<?.001). Higher BMI, but not higher PCS scores, was related to more frequent attacks (??=?-0.203, P?=?.044).One quarter of participants with migraine and obesity reported clinical catastrophizing. These individuals had more frequent attacks/chronicity, longer attack duration, higher pain sensitivity, greater headache impact, and lower headache management self-efficacy. In all participants, PCS scores were related to several migraine characteristics, above and beyond the effects of obesity. Prospective studies are needed to determine sequence and mechanisms of relationships between catastrophizing, obesity, and migraine.

Project description:The aim was to assess the association between objectified preoperative psychological factors and postoperative pain at the first day after otolaryngological surgery in accordance with other predictors of postoperative pain. Eighty-two (82) patients (59% male, median age 56 years) were included between January and May 2015. The psychological assessment the day before surgery included the Patient Health Questionnaire (PHQ-9), pain catastrophizing scale (PCS), State-Trait Operation Anxiety (STOA) inventory, and the resilience scale (RS-13). On first postoperative day, patients were rated their pain using the questionnaires of the German-wide project Quality Improvement in Postoperative Pain Treatment (QUIPS) including a numeric rating scale (NRS, 0-10) for determination of patient's maximal pain. QUIPS allowed standardized assessment of patients' characteristics, pain parameters, and outcome. The influence of preoperative and postoperative parameters on patients' maximal postoperative pain was estimated by univariate and multivariate statistical analysis. The mean maximal pain was 3.2?±?2.9. In univariate analysis, higher PHQ-9 score more than 4 (P = 0.010), higher STOA trait anxiety (P = 0.044), and higher STOA total score (P = 0.043) were associated to more postoperative pain. In multivariate analysis higher PHQ-9 score remained an independent predictor for severe pain (beta = 0.302; 95% confidence interval [CI]: 0.054-0.473; P = 0.014). When all parameters were included into multivariate analysis, 2 of all somatic, psychological, and treatment factors were associated with severe maximal pain: more depression (PHQ-9; beta = 0.256; 95% CI: 0.042-0.404; P = 0.017), and use of opioids in the recovery room (beta = 0.371; 95% CI: 0.108-0.481; P = 0.002). Otolaryngological surgery covers the spectrum from low to severe postoperative pain and is therefore a good model for pain management studies. A set of somatic and psychological parameters seems to allow the identification of patients with higher risk for more postoperative pain. This should help to individualize and improve the perioperative pain management.

Project description:BackgroundVariability in patients' postoperative pain experience and response to treatment challenges effective pain management. Variability in pain reflects individual differences in inhibitory pain modulation and psychological sensitivity, which in turn may be clinically relevant for the disposition to acquire pain. The aim of this study was to investigate the effects of conditioned pain modulation and situational pain catastrophizing on postoperative pain and pain persistency.MethodsPreoperatively, 42 healthy males undergoing funnel chest surgery completed the Spielberger's State-Trait Anxiety Inventory and Beck's Depression Inventory before undergoing a sequential conditioned pain modulation paradigm. Subsequently, the Pain Catastrophizing Scale was introduced and patients were instructed to reference the conditioning pain while answering. Ratings of movement-evoked pain and consumption of morphine equivalents were obtained during postoperative days 2-5. Pain was reevaluated at six months postoperatively.ResultsPatients reporting persistent pain at six months follow-up (n = 15) were not significantly different from pain-free patients (n = 16) concerning preoperative conditioned pain modulation response (Z = 1.0, P = 0.3) or level of catastrophizing (Z = 0.4, P = 1.0). In the acute postoperative phase, situational pain catastrophizing predicted movement-evoked pain, independently of anxiety and depression (β = 1.0, P = 0.007) whereas conditioned pain modulation predicted morphine consumption (β = -0.005, P = 0.001).ConclusionsPreoperative conditioned pain modulation and situational pain catastrophizing were not associated with the development of persistent postoperative pain following funnel chest repair. Secondary outcome analyses indicated that conditioned pain modulation predicted morphine consumption and situational pain catastrophizing predicted movement-evoked pain intensity in the acute postoperative phase. These findings may have important implications for developing strategies to treat or prevent acute postoperative pain in selected patients. Pain may be predicted and the malfunctioning pain inhibition mechanism as tested with CPM may be treated with suitable drugs augmenting descending inhibition.

Project description:BACKGROUND:Migraine has many presumed comorbidities which have rarely been compared between samples with and without migraine. Examining the association between headache pain intensity and monthly headache day (MHD) frequency with migraine comorbidities is novel and adds to our understanding of migraine comorbidity. METHODS:The MAST Study is a prospective, web-based survey that identified US population samples of persons with migraine (using modified International Classification of Headache Disorders-3 beta criteria) and without migraine. Eligible migraine participants averaged ≥1 MHDs over the prior 3 months. Comorbidities "confirmed by a healthcare professional diagnosis" were endorsed by respondents from a list of 21 common cardiovascular, neurologic, psychiatric, sleep, respiratory, dermatologic, pain and medical comorbidities. Multivariable binary logistic regression calculated odds ratios (OR) and 95% confidence intervals for each condition between the two groups adjusting for sociodemographics. Modeling within the migraine cohort assessed rates of conditions as a function of headache pain intensity, MHD frequency, and their combination. RESULTS:Analyses included 15,133 people with migraine (73.0% women, 77.7% White, mean age 43 years) and 77,453 controls (46.4% women, 76.8% White, mean age 52 years). People with migraine were significantly (P < 0.001) more likely to report insomnia (OR 3.79 [3.6, 4.0]), depression (OR 3.18 [3.0, 3.3]), anxiety (OR 3.18 [3.0 3.3]), gastric ulcers/GI bleeding (OR 3.11 [2.8, 3.5]), angina (OR 2.64 [2.4, 3.0]) and epilepsy (OR 2.33 [2.0, 2.8]), among other conditions. Increasing headache pain intensity was associated with comorbidities related to inflammation (psoriasis, allergy), psychiatric disorders (depression, anxiety) and sleep conditions (insomnia). Increasing MHD frequency was associated with increased risk for nearly all conditions and most prominent among those with comorbid gastric ulcers/GI bleeding, diabetes, anxiety, depression, insomnia, asthma and allergies/hay fever. CONCLUSIONS:In regression models controlled for sociodemographic variables, all conditions studied were reported more often by those with migraine. Whether entered into the models separately or together, headache pain intensity and MHD frequency were associated with increased risk for many conditions. Future work is required to understand the causal sequence of relationships (direct causality, reverse causality, shared underlying predisposition), the potential confounding role of healthcare professional consultation and treatment, and potential detection bias.

Project description:BackgroundPain catastrophizing (PC) is associated with more severe and disabling migraine attacks. However, factors that moderate this relationship are unknown. Failure of inhibitory control (IC), or the ability to suppress automatic or inappropriate responses, may be one such factor given previous research showing a relationship between higher PC and lower IC in non-migraine samples, and research showing reduced IC in migraine. Therefore, we examined whether lower IC interacts with increased PC to predict greater migraine severity as measured by pain intensity, attack frequency, and duration.MethodsWomen (n = 105) aged 18-50 years old (M = 38.0 ± 1.2) with overweight/obesity and migraine who were seeking behavioral treatment for weight loss and migraine reduction completed a 28-day smartphone-based headache diary assessing migraine headache severity. Participants then completed a modified computerized Stroop task as a measure of IC and self-report measures of PC (Pain Catastrophizing Scale [PCS]), anxiety, and depression. Linear regression was used to examine independent and joint associations of PC and IC with indices of migraine severity after controlling for age, body mass index (BMI) depression, and anxiety.ResultsParticipants on average had BMI of 35.1 ± 6.5 kg/m2and reported 5.3 ± 2.6 migraine attacks (8.3 ± 4.4 migraine days) over 28 days that produced moderate pain intensity (5.9 ± 1.4 out of 10) with duration of 20.0 ± 14.2 h. After adjusting for covariates, higher PCS total (β = .241, SE = .14, p = .03) and magnification subscale (β = .311, SE = .51, p < .01) scores were significant independent correlates of longer attack duration. IC interacted with total PCS (β = 1.106, SE = .001, p = .03) rumination (β = 1.098, SE = .001, p = .04), and helplessness (β = 1.026, SE = .001, p = .04) subscale scores to predict headache pain intensity, such that the association between PC and pain intensity became more positive at lower levels of IC.ConclusionsResults showed that lower IC interacted with higher PC, both overall and specific subcomponents, to predict higher pain intensity during migraine attacks. Future studies are needed to determine whether interventions to improve IC could lead to less painful migraine attacks via improvements in PC.

Project description:BackgroundMigraine is considered a disease with diurnal and 24 h pattern, though the existence of a prevalent circadian rhythm associated to migraine frequency and severity is still not clear. This observational cross-sectional study aimed to: 1. Assess the circadian rhythm of migraine attacks onset in a large patients' population selected in a headache center and including episodic and chronic migraine 2. Analyze the principal characteristic of the different onset time groups 3. Verify if migraine features, particularly those associated to chronic and disabling migraine, could be discriminant factors for time of onset group.MethodsWe selected 786 consecutive migraine outpatients, who correctly completed the headache diaries for 3 consecutive months and who fulfilled the diagnosis of migraine without aura-MO, migraine with typical aura alone or associated to migraine without aura - MO/MA and chronic migraine - CM. For the time of headache onset, we considered four time slots, from 6 to 12 am (morning), from 1 to 6 pm (afternoon), from 7 to 11 pm (evening), from 12 pm to 5 am (night), and an additional category named "any time". Each time slot included the 60 min preceding the next one (e.g. an onset at 12.30 am was included in 6-12 am time slot). We evaluated in all patients the pericranial tenderness, anxiety and depression tracts, headache-related disability, sleep features, quality of life, allodynia and fatigue.ResultsWe scored a total of 16,578 attacks, distributed in the entire day. The most of patients, including CM, satisfied the criteria for the "any time" onset. Night onset was significantly less represented in the MA/MO group. Patients with prevalent night onset were significantly older, with longer migraine history and shorter sleep duration. Age and illness duration were the variables discriminating the different onset time groups.ConclusionsThe most of migraine patients do not report a specific circadian profile of attacks occurrence. Frequent migraine, severe disability, psychopathological tracts as well as central sensitization signs, do not match with a specific circadian rhythm of attacks onset. Night onset migraine seems to be an age related feature, emerging in the course of the disease.

Dataset Information

Pain Catastrophizing in Childhood Migraine: An Observational Study in a Tertiary Headache Center.

Publications

Pain Catastrophizing in Childhood Migraine: An Observational Study in a Tertiary Headache Center.

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