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Background: Verapamil is recommended as a first-line preventive for episodic and chronic cluster headache, however, its use is limited by a wide range of adverse events. From clinical practice at a tertiary headache centre, we have observed that the initiation of verapamil may be associated with headache worsening. The aim of this service evaluation was to examine whether verapamil initiation was associated with headache worsening, and whether these exacerbations may be attributed to comorbid migraine in some patients. Methods: Patients with a diagnosis of cluster headache from June 2014 to December 2023 were identified from the tertiary headache centre at King's College Hospital, London. Data including age, sex, headache phenotype and headache frequency was collected retrospectively in a cross-sectional design through the use of clinic letters followed by a telephone interview. A Wilcoxon signed-rank test was used to compare number of cluster headache attacks per day pre- and post-verapamil administration. A negative binomial generalized linear model was used to interrogate the relationship between the number of attacks post-verapamil and age, sex, verapamil dosing, comorbid migraine and baseline number of attacks. Results: Of 168 patients included, the mean age was 31 years, 73% were male, 46% of patients had chronic cluster headache and 51% had comorbid migraine. During the latest ictal period, the median (interquartile range) frequency of cluster headache attacks per day was 3 (2–5) for the entire sample. The presence of comorbid migraine increased the likelihood of headache exacerbation by verapamil by an odds ratio of 1.616 (95% confidence interval: 1.059–2.465, χ21 = 4.955, P = 0.026). No differences were observed in the frequency of shadow attacks amongst those with comorbid migraine (n = 54/85, 64%) versus patients without migraine (n = 48/83, 58%) (Mann-Whitney U = 3728, z = 0.754, P = 0.451). No effect was seen on monthly migraine days pre- and post-verapamil administration (P = 0.141). Adverse events were reported in 62 of 109 (57%) of patients taking verapamil with the most common being PR interval prolongation (15.6%), lower limb oedema (8.3%), worsened headache (6.4%) and fatigue (6.4%). Conclusions: It is likely that the association of cluster headache and migraine is more common than generally thought and co-existence may go under-recognised. Our results show comorbid migraine increased the likelihood of headache exacerbation during the initiation of verapamil. In patients with headache worsening, a dual diagnosis of migraine alongside cluster headache should be considered. [ABSTRACT FROM AUTHOR]

Cancer pain intensity (PI) fluctuates, but the relationship between pain flares and background pain with respect to pain management is not settled. We studied how flare and background PIs corresponded with treatment results for background cancer pain. Patients admitted to an acute palliative care unit with average and/or worst PI ≥ 1 on the 11-point numeric rating scale were included. Average and worst PI at admission and average PI at discharge were collected. We examined how the difference and ratio between worst and average PI and average PI at admission, were associated with average PI development during hospitalization. Positive differences between worst and average PI at admission were defined as pain flares. Ninety out of 131 patients had pain flares. The reduction in average PI for patients with flares was 0.9 and for those without, 1.9 (p = 0.02). Patients with large worst minus average PI differences reported the least improvement, as did those with large worst/average PI ratios. Patients with pain flares and average PI ≤ 4 at admission had unchanged average PI during hospitalization, while those with pain flares and average PI > 4 experienced pain reduction (2.1, p < 0.001). Large pain flares, in absolute values and compared to background PI, were associated with inferior pain relief. [ABSTRACT FROM AUTHOR]

Abstract Introduction Different definitions of breakthrough pain (BTP) influence the observed BTP prevalence. This study examined BTP prevalence variability due to use of different cutoffs for controlled background pain, different assessment periods for background pain, and difference between worst and average pain intensity (PI). Methods Cancer patients from the EPCRC-CSA study who reported flare-ups of pain past 24 h were potential BTP cases. BTP prevalence was calculated for different cutoffs for background PI on numeric rating scales (NRS 0–10) for the past week, past 48 and past 24 h period. Furthermore, BTP cases were categorized based on the difference between maximum and average PI past 24 h (range, 0 to > 2 points, NRS 0–10). Results Of 696 respondents, 302 patients (43.4%) reported pain flares the past 24 h. The BTP prevalence when using a defined background PI ≤ 4 for the past week was 19.8%. This number varied for different defined cutoffs for background PI. Actual background PI and BTP prevalence also varied between the assessment periods “past week”, “past 48 h”, and “past 24 h” (PI 4.0, 3.6, and 3.4; BTP prevalence 19.8, 22.7, and 24.9% for background PI ≤ 4). For patients with background PI ≤ 4 past week, 105 had a difference between maximum and average PI ≥ one point and 48 had a difference > two points. Conclusions The reported BTP prevalence is dependent on the cutoff for background PI in the BTP definition, population background PI during the assessment period, and defined cutoff for the difference between worst and average PI. Funding NTNU, Norwegian University of Science and Technology.

Introduction: Different definitions of breakthrough pain (BTP) influence the observed BTP prevalence. This study examined BTP prevalence variability due to use of different cutoffs for controlled background pain, different assessment periods for background pain, and difference between worst and average pain intensity (PI).Methods: Cancer patients from the EPCRC-CSA study who reported flare-ups of pain past 24 h were potential BTP cases. BTP prevalence was calculated for different cutoffs for background PI on numeric rating scales (NRS 0-10) for the past week, past 48 and past 24 h period. Furthermore, BTP cases were categorized based on the difference between maximum and average PI past 24 h (range, 0 to > 2 points, NRS 0-10).Results: Of 696 respondents, 302 patients (43.4%) reported pain flares the past 24 h. The BTP prevalence when using a defined background PI ≤ 4 for the past week was 19.8%. This number varied for different defined cutoffs for background PI. Actual background PI and BTP prevalence also varied between the assessment periods “past week”, “past 48 h”, and “past 24 h” (PI 4.0, 3.6, and 3.4; BTP prevalence 19.8, 22.7, and 24.9% for background PI ≤ 4). For patients with background PI ≤ 4 past week, 105 had a difference between maximum and average PI ≥ one point and 48 had a difference > two points.Conclusions: The reported BTP prevalence is dependent on the cutoff for background PI in the BTP definition, population background PI during the assessment period, and defined cutoff for the difference between worst and average PI.Funding: NTNU, Norwegian University of Science and Technology. [ABSTRACT FROM AUTHOR]

Abstract: Endothelin-1 (ET-1) may be involved in driving pain in patients with advanced cancer. However, a few studies focus on the role of ET-1 in breakthrough pain (BP). The aim of this pivotal study was to explore the correlation between the plasma (ET-1) level and BP intensity. A total of 40 patients were enrolled in the study, and they were divided into two groups: BP group and non-BP group. Moreover, 20 healthy adults were used as the normal control group. Pain intensity was measured using visual analog scale (VAS) scores of 1–10. Plasma ET-1 levels were detected by an ET radioimmunoassay kit. Subsequently, the correlation of ET-1 level with the VAS score and cancer types was analyzed by Pearson’s correlation coefficient. The plasma ET-1 level in the BP group (35.31±8.02 pg/mL) was higher than that in the non-BP group (29.51±6.78 pg/mL) and the normal control group (24.77±10.10 pg/mL, P,0.05). In addition, the VAS score in the BP group (7.45±0.82) was higher than that in the non-BP group (2.80±1.23, P,0.05). The plasma ET-1 level was positively correlated with the VAS score of the BP group (Pearson’s r=0.42). There was no significant correlation between the plasma ET-1 level and VAS score of the non-BP group (Pearson’s r=−0.22) or/and cancer types (P.0.05). The elevated plasma ET-1 levels were positively related to BP, and targeting ET-1 may provide a novel pain-reducing therapeutic treatment in BP. [ABSTRACT FROM AUTHOR]