The Effects of Recovery Sleep on Experimental Pain

Recent research suggests that recovery sleep (RS) has the potential to restore pain sensitivity and modulation after hyperalgesia due to preceding sleep deprivation. However, it has not yet been systematically examined whether the restoration of these pain parameters is driven by sleep characteristics of RS. Thus, the present study assessed changes in experimental pain during RS after total sleep deprivation (TSD) to test whether RS parameters predicted the restoration of the pain system. Thirty healthy participants completed one night of habitual sleep, one night of TSD and a subsequent recovery night. At-home sleep during baseline and recovery was assessed using portable polysomnography and a questionnaire. Before and after each night pressure pain thresholds (PPTs), temporal pain summation (TSP) and conditioned pain modulation (CPM) were assessed. PPTs decreased after TSD and increased following RS, indicating a restoration of pain sensitivity after hyperalgesia. RS characteristics did not predict this restoration, suggesting other mechanisms (eg, changes in serotonergic activity) underlying the observed pain changes. TSP indicated a lack of effect of experimental sleep manipulations on excitatory processes whereas CPM lacked sufficient reliability to investigate inhibitory processes. Thus, results indicate moderate effects of sleep manipulations on pain sensitivity, but not on pain modulation.PerspectiveThis article highlights the potential of recovery sleep to let pain thresholds return to normal following their decrease after a night of total sleep deprivation. In contrast, endogenous pain modulation (temporal pain summation, conditioned pain modulation) was not affected by sleep deprivation and recovery sleep.     

One night of total sleep deprivation promotes a state of generalized hyperalgesia: A surrogate pain model to study the relationship of insomnia and pain

Sleep disturbances are highly prevalent in chronic pain patients. Understanding their relationship has become an important research topic since poor sleep and pain are assumed to closely interact. To date, human experimental studies exploring the impact of sleep disruption/deprivation on pain perception have yielded conflicting results. This inconsistency may be due to the large heterogeneity of study populations and study protocols previously used. In addition, none of the previous studies investigated the entire spectrum of nociceptive modalities. To address these shortcomings, a standardized comprehensive quantitative sensory protocol was used in order to compare the somatosensory profile of 14 healthy subjects (6 female, 8 male, 23.5 ± 4.1 year; mean ± SD) after a night of total sleep deprivation (TSD) and a night of habitual sleep in a cross-over design. One night of TSD significantly increased the level of sleepiness (P < 0.001) and resulted in higher scores of the State Anxiety Inventory (P < 0.01). In addition to previously reported hyperalgesia to heat (P < 0.05) and blunt pressure (P < 0.05), study participants developed hyperalgesia to cold (P < 0.01) and increased mechanical pain sensitivity to pinprick stimuli (P < 0.05) but no changes in temporal summation. Paradoxical heat sensations or dynamic mechanical allodynia were absent. TSD selectively modulated nociception, since detection thresholds of non-nociceptive modalities remained unchanged. Our findings show that a single night of TSD is able to induce generalized hyperalgesia and to increase State Anxiety scores. In the future, TSD may serve as a translational pain model to elucidate the pathomechanisms underlying the hyperalgesic effect of sleep disturbances.     

Investigation of pain sensitivity following 3 nights of disrupted sleep in healthy individuals

Background

Poor quality sleep is a common complaint among people with chronic pain. The co-occurrence of poor sleep quality and chronic pain often comes with increased pain intensity, more disability and a higher cost of healthcare. Poor sleep has been suggested to affect measures of peripheral and central pain mechanisms. To date, sleep provocations are the only models proven to affect measures of central pain mechanisms in healthy subjects. However, there are limited studies investigating the effect of several nights of sleep disruption on measures of central pain mechanisms.

Methods

The current study implemented three nights of sleep disruption with three planned awakenings per night in 30 healthy subjects sleeping at home. Pain testing was conducted at the same time of day at baseline and follow-up for each subject. Pressure pain thresholds were assessed bilaterally on the infraspinatus and gastrocnemius muscles. Using handheld pressure algometry, suprathreshold pressure pain sensitivity and area were also investigated on the dominant infraspinatus muscle. Cuff-pressure pain detection and tolerance thresholds, temporal summation of pain and conditioned pain modulation were investigated using cuff-pressure algometry.

Results

Temporal summation of pain was significantly facilitated (p = 0.022), suprathreshold pain areas (p = 0.005) and intensities (p < 0.05) were significantly increased, and all pressure pain thresholds were decreased (p < 0.005) after sleep disruption compared to baseline.

Conclusions

The current study found that three consecutive nights of sleep disruption at home induced pressure hyperalgesia and increased measures of pain facilitation in healthy subjects, which is consistent with previous findings.

Significance

Poor quality of sleep is often experienced by patients with chronic pain, with the most common complaint being nightly awakenings. This exploratory study is the first to investigate changes in measures of central and peripheral pain sensitivity in healthy subjects after sleep disruptions for three consecutive nights without any restrictions on total sleep time. The findings suggest that disruptions to sleep continuity in healthy individuals can induce increased sensitivity to measures of central and peripheral pain sensitization.     

Sleep Fragmentation Hypersensitizes Healthy Young Women to Deep and Superficial Experimental Pain

The effect of sleep deprivation on pain sensitivity has typically been studied using total and partial sleep deprivation protocols. These protocols do not mimic the fragmented pattern of sleep disruption usually observed in individuals with clinical pain conditions. Therefore, we conducted a controlled experiment to investigate the effect of sleep fragmentation on pain perception (deep pain: forearm muscle ischemia, and superficial pain: graded pin pricks applied to the skin) in 11 healthy young women after 2 consecutive nights of sleep fragmentation, compared with a normal night of sleep. Compared with normal sleep, sleep fragmentation resulted in significantly poorer sleep quality, morning vigilance, and global mood. Pin prick threshold decreased significantly (increased sensitivity), as did habituation to ischemic muscle pain (increased sensitivity), over the course of the 2 nights of sleep fragmentation compared with the night of normal sleep. Sleep fragmentation did not increase the maximum pain intensity reported during muscle ischemia (no increase in gain), and nor did it increase the number of spontaneous pains reported by participants. Our data show that sleep fragmentation in healthy, young, pain-free women increases pain sensitivity in superficial and deep tissues, indicating a role for sleep disruption, through sleep fragmentation, in modulating pain perception.

Modulation of central pain mechanisms using high-definition transcranial direct current stimulation: A double-blind,sham-controlled study

Background

The use of high-definition transcranial direct current stimulation (HD-tDCS) has shown analgesic effects in some chronic pain patients, but limited anti-nociceptive effects in healthy asymptomatic subjects.

Methods

This double-blinded sham-controlled study assessed the effects of HD-tDCS applied on three consecutive days on central pain mechanisms in healthy participants with (N = 40) and without (N = 40) prolonged experimental pain induced by intramuscular injection of nerve growth factor into the right hand on Day 1. Participants were randomly assigned to Sham-tDCS (N = 20 with pain, N = 20 without) or Active-tDCS (N = 20 with pain, N = 20 without) targeting simultaneously the primary motor cortex and dorsolateral prefrontal cortex for 20 min with 2 mA stimulation intensity. Central pain mechanisms were assessed by cuff algometry on the legs measuring pressure pain sensitivity, temporal summation of pain (TSP) and conditioned pain modulation (CPM), at baseline and after HD-tDCS on Day 2 and Day 3. Based on subject's assessment of received HD-tDCS (sham or active), they were effectively blinded.

Results

Compared with Sham-tDCS, Active-tDCS did not significantly reduce the average NGF-induced pain intensity. Tonic pain-induced temporal summation at Day 2 and Day 3 was significantly lower in the NGF-pain group under Active-tDCS compared to the pain group with Sham-tDCS (p ≤ 0.05). No significant differences were found in the cuff pressure pain detection/tolerance thresholds or CPM effect across the 3 days of HD-tDCS in any of the four groups.

Conclusion

HD-tDCS reduced the facilitation of TSP caused by tonic pain suggesting that efficacy of HD-tDCS might depend on the presence of sensitized central pain mechanisms.     

Further evidence of the positive effects of an educational and physical program on headache, neck and shoulder pain in a working community

In a controlled trial to evaluate the effectiveness of a simple educational and physical program administered to a large cohort of public servants, we previously found that 6 months following treatment the monthly frequency of headache and neck and shoulder pain and drug intake was reduced by 40% in the experimental compared with controls. These results were stable at a 12-month follow up. The program consists of brief shoulder and neck exercises to be performed several times a day, a relaxation exercise, and instructions on how to reduce parafunction and hyperfunction of the craniofacial and neck muscles during the day. The purpose of this work was to investigate whether the data previously obtained could be confirmed also in the group of 192 subjects that served as controls in first phase of the study and received the intervention in the second phase of the study. The primary endpoint was the change in frequency of headache and neck and shoulder pain expressed as the number of days per month with pain, and as the proportion of subjects with a ≥50% reduction of frequency (responder rate) at the last 2 months of the 6-month intervention period compared to the 2 months preceding the intervention (baseline). The number of days of analgesic drug consumption was also recorded. Days per month with headache at the baseline and at the end of intervention period were 6.40 and 4.58 (mean change −1.81, p < 0.0001), respectively; days with neck and shoulder pain were 7.48 and 6.18 (mean change −1.30, p = 0.0179); days of analgesic consumption were 1.67 and 1.17 (mean change −0.50, p = 0.0222). The responder rate was 42.3% for headache, 42% for neck and shoulder pain and 58.3% for drug consumption. In conclusion, this study adds further evidence on the efficacy of our program and its high acceptability in a large, unselected, working population.     

Long-Term Benefits of an Educational and Physical Program on Headache, and Neck and Shoulder Pain, in a Working Community

We previously published the results of a controlled trial that showed the efficacy of a workplace educational and physical program in reducing headache, and neck and shoulder pain. Participants recorded daily pain episodes in diaries; after 2 months of baseline observation, the program was administered to the intervention arm only, and comparison with the control arm was performed at month 8. The objective of the present study was to confirm the long-term (14 months from the beginning of the study) benefit of the program in the intervention arm of the study (192 office employees). Outcome measures of the present analyses were: 1) the number of days/month with headache, and neck and shoulder pain; 2) the frequency of days with analgesic drug consumption; 3) the proportion of subjects with 4 or more days/month with headache or neck and shoulder pain at baseline who achieved a ≥50% reduction in pain (responder rate). Days/month with headache decreased from 5.50 at baseline (months 1–2) to 3.11 at months 13–14 (P < .001); from 6.79 to 3.88 (P < .001) for neck and shoulder pain; and from 1.72 to 0.86 (P < .001) for analgesic consumption. Responder rates were 58.8% (95%CI = 47.1–70.5) for headache, 60.9% (49.4–72.4) for neck and shoulder pain, and 68.2 % (48.7–87.6) for drug consumption. These results confirm that the program may be effective at long term.

Perspective

This article presents the results at long term of an educational and physical program in reducing headache, and neck and shoulder pain, in a working community. Since the benefits remained stable for a considerable period of time, a randomized trial is ongoing to confirm these results on a larger, less-selected working population.     

Increased pain sensitivity is not a risk factor but a consequence of frequent headache: a population-based follow-up study

Altered pain sensitivity is believed to play an important role for chronification of headache. It has however mainly been evaluated in highly selected patients from headache clinics and never in longitudinal studies. The present study is a 12-year follow-up of a population-based study of primary headache disorders and pain perception, combining a diagnostic headache interview with examination of muscle tenderness and measurement of pressure pain thresholds in 1000 subjects drawn randomly from the general population in Denmark. The aim of the study was to explore the cause–effect relationship between the increased pain sensitivity and the development of headache. The pressure pain thresholds were normal at baseline but had decreased at follow-up in subjects who developed chronic tension-type headache over the 12-year period (p = 0.025). In subjects who developed frequent episodic tension-type headache the tenderness was normal at baseline but had increased at follow-up (p < 0.01) while the pain thresholds were normal both at baseline and at follow-up. The findings demonstrate that increased pain sensitivity is a consequence of frequent tension-type headache, not a risk factor, and support that central sensitization plays an important role for the chronification of tension-type headache.     

Does pain mediate the pain interference with sleep problem in chronic pain? Findings from studies for management of diabetic peripheral neuropathic pain with duloxetine

Although sleep problems are common in patients with chronic pain, it is unclear whether pain mediates (causes) impaired sleep. The relationship between pain and sleep has been difficult to investigate because of the potential confounds of depression and somnolence. This report used clinical trials data for duloxetine in the management of diabetic peripheral neuropathic pain (DPNP) to investigate the direction of this association. Data were pooled from three double-blind, randomized, placebo-controlled, 12-week trials of patients with DPNP without mood disorder (n = 1,139). DPNP patients reporting somnolence and those who were receiving sedating concomitant medications were removed from the analyses (n = 93). Efficacy measures included weekly mean scores for average daily pain severity, night pain severity, and pain interference with sleep. Duloxetine at 60 and 120 mg per day separated from placebo for average pain and night pain improvement as early as one week after treatment began, whereas sleep interference improvement separated from placebo at the three visits it was assessed (Weeks 4, 8, and 12). Change in sleep interference was moderately to strongly correlated (P < 0.001) with changes in average pain (r = 0.46) and nighttime pain severity (r = 0.53). These results confirm the association between the improvement in daily pain and nighttime pain, and improvement in sleep interference for a large population without depression or somnolence. Although this association cannot establish causality, these results provide some evidence for the possibility that pain may mediate the sleep problem associated with DPNP and perhaps chronic pain in general.     

The mediating role of pain acceptance during mindfulness-based cognitive therapy for headache

ObjectivesThis study aimed to determine if mindfulness-based cognitive therapy (MBCT) engenders improvement in headache outcomes via the mechanisms specified by theory: (1) change in psychological process, (i.e., pain acceptance); and concurrently (2) change in cognitive content, (i.e., pain catastrophizing; headache management self-efficacy).DesignA secondary analysis of a randomized controlled trial comparing MBCT to a medical treatment as usual, delayed treatment (DT) control was conducted. Participants were individuals with headache pain who completed MBCT or DT (N = 24) at the Kilgo Headache Clinic or psychology clinic. Standardized measures of the primary outcome (pain interference) and proposed mediators were administered at pre- and post-treatment; change scores were calculated. Bootstrap mediation models were conducted.ResultsPain acceptance emerged as a significant mediator of the group-interference relation (p < .05). Mediation models examining acceptance subscales showed nuances in this effect, with activity engagement emerging as a significant mediator (p < .05), but pain willingness not meeting criteria for mediation due to a non-significant pathway from the mediator to outcome. Criteria for mediation was also not met for the catastrophizing or self-efficacy models as neither of these variables significantly predicted pain interference.ConclusionsPain acceptance, and specifically engagement in valued activities despite pain, may be a key mechanism underlying improvement in pain outcome during a MBCT for headache pain intervention. The theorized mediating role of cognitive content factors was not supported in this preliminary study. A large, definitive trial is warranted to replicate and extend the findings in order to streamline and optimize MBCT for headache.     

Relapsing remitting hypnic headache responsive to indomethacin in an adolescent: a case report

Hypnic headache (HH) is a rare sleep-associated primary headache disorder that usually begins after the age of 60 years. Here we report a 19-year-old male with 4-year history of predominantly left sided HH. He is the youngest person reported who fulfills the IHS diagnostic criteria for HH. The patient had history of relapsing–remitting course. The headache occurred every night at a constant time in each relapse. It was non-throbbing, moderate to severe, for 30 min to 5 h, and usually after 3 h of sleep. The patient showed complete response to indomethacin (75 mg at bedtime). Frequent tapering of indomethacin was required to look for the remission phase.     

A 4-year follow-up of patients with medication-overuse headache previously included in a randomized multicentre study

The aim of this study was to evaluate the long-term outcome in 61 patients with medication-overuse headache (MOH) who 4 years previously had been included in a randomized open-label prospective multicentre study. Sixty patients still alive after 4 years were invited to a follow-up investigation. Fifty patients (83%) participated. Sixteen visited a neurologist, 22 were interviewed through telephone, 2 gave response by a letter, and 10 were evaluated through hospital records. The influence of baseline characteristics on outcome 4 years later was evaluated by non-parametric tests. p values below 0.01 were considered significant. At follow-up, the 50 persons had a mean reduction of 6.5 headache days/month (p < 0.001) and 9.5 acute headache medication days/month (p < 0.001) compared to baseline. Headache index/month was reduced from 449 to 321 (p < 0.001). Sixteen persons (32%) were considered as responders due to a ≥50% reduction in headache frequency from baseline, whereas 17 (34%) persons met the criteria for MOH. None of the baseline characteristics consistently influenced all five outcome measures. Total Hospital Anxiety and Depression Scale (HADS) score at baseline was predictors (p < 0.005) for being a responder after 4 years. At 4 years’ follow-up, one-third of the 50 MOH patients had ≥50% reduction in headache frequency from baseline. A low total HADS score at baseline was associated with the most favorable outcome.     

Clinical features of headache patients with fibromyalgia comorbidity

Our previous study assessed the prevalence of fibromyalgia (FM) syndrome in migraine and tension-type headache. We aimed to update our previous results, considering a larger cohort of primary headache patients who came for the first time at our tertiary headache ambulatory. A consecutive sample of 1,123 patients was screened. Frequency of FM in the main groups and types of primary headaches; discriminating factor for FM comorbidity derived from headache frequency and duration, age, anxiety, depression, headache disability, allodynia, pericranial tenderness, fatigue, quality of life and sleep, and probability of FM membership in groups; and types of primary headaches were assessed. FM was present in 174 among a total of 889 included patients. It prevailed in the tension-type headache main group (35%, p < 0.0001) and chronic tension-type headache subtype (44.3%, p < 0.0001). Headache frequency, anxiety, pericranial tenderness, poor sleep quality, and physical disability were the best discriminating variables for FM comorbidity, with 81.2% sensitivity. Patients presenting with chronic migraine and chronic tension-type headache had a higher probability of sharing the FM profile (Bonferroni test, p < 0.01). A phenotypic profile where headache frequency concurs with anxiety, sleep disturbance, and pericranial tenderness should be individuated to detect the development of diffuse pain in headache patients.     

Sleep deprivation and its effects on object-selective attention

Sleep deprivation (SD) affects attention but it is an open question as to whether all subtypes of attention are similarly affected. We investigated the effects of 24 h of total SD on object-selective attention. 26 healthy, young adults viewed quartets of alternating faces or place scenes and performed selective judgments on faces only, scenes only or both faces and scenes. Volunteers underwent fMRI following a normal night of sleep and again following approximately 24 h of total sleep deprivation in a counterbalanced fashion. Sleep deprivation resulted in slower and less accurate picture classification as well as poorer recognition memory for scenes. Attention strongly modulated activation in the Parahippocampal Place Area (PPA). Task-related activation in the fronto-parietal cortex and PPA was reduced in SD, but the relative modulation of PPA activation by attention was preserved. Psychophysiological interaction between the left intra-parietal sulcus and the PPA that was clearly present after a normal night of sleep was reduced below threshold following SD suggesting that PPI may be a more sensitive method of detecting change in selective attention. Sleep deprivation may affect object-selective attention in addition to exerting a task-independent deficit in attention.     

Nitroglycerin‐induced changes in facial skin temperature: ‘cold nose’ as a predictor of headache?

Nitroglycerin (NTG) often induces headaches when used to treat cardiac diseases. Such property of NTG has been widely used in modelling of migraine‐like headaches. However, background reasons, predisposing to the development of NTG‐headache, are less studied. The main aim of our study was to find, using NTG model, easily accessible markers of the vascular changes associated with headache. Because changes in the blood flow alter the local skin temperature (Tsk), we studied the relationship between the regional changes in the facial Tsk and NTG‐induced headaches. Tsk was measured with infrared thermography in 11 healthy women during 3 h after sublingual NTG administration. NTG caused headache in five women, and four of them were the first‐degree relatives of migraine patients. Notably, before NTG administration, subjects in the headache group had lower Tsk values, especially in the nose area, than women in the pain‐free group (n = 6). NTG‐induced headache was associated with a long‐lasting increase of Tsk over the baseline. In sharp contrast, in the pain‐free group, the Tsk reduced and returned rapidly to the baseline. Thus, the low baseline level and greater increase of regional Tsk correlated with the incidence of headache that supports a role of greater vascular changes in headache happening on the basis of the dissimilarities in vascular tone. An easily accessible phenomenon of ‘cold nose’ may indicate background vascular dysfunctions in individuals with predisposition to headache. Facial infrared thermography, coupled with NTG administration, suggests a novel temporally controlled approach for non‐invasive investigation of vascular processes accompanying headaches.     

Pain Expectancy and Positive Affect Mediate the day-to-day Association Between Objectively Measured Sleep and Pain Severity Among Women With Temporomandibular Disorder

The majority of individuals with temporomandibular disorders (TMD) experience sleep disturbance, which can maintain and exacerbate chronic pain. However, the factors underlying the sleep-pain link have not been fully elucidated, especially beyond the laboratory. Sleep deprivation can induce threat interpretation bias, as well as impairment in positive affective functioning. Using both actigraphy and daily diaries, we examined whether morning pain expectancy and positive affect mediate the association between previous night's sleep disturbance and next-day overall pain severity. Total sleep time (TST) was selected as the primary measure of sleep. The sample included 144 women (mean age = 36 [SD = 11.1]) with TMD who displayed at least subclinical insomnia. Sleep was assessed for 14 days using actigraphy which was validated by concurrent sleep diaries. Daily diary assessments of pain-related experiences and affective states were conducted twice per day (ie, once upon participants’ waking and the other prior to going to sleep) for the same 14-day period. Multilevel structural equation modeling revealed that both morning pain expectancy (95% CI: -.0004, -.00003) and positive affect (95% CI: -.0005, -.000001) mediated the association between previous night's TST and next-day's overall pain severity, such that shorter previous night TST was associated with higher next-morning pain expectancy and lower positive affect, which in turn were associated with a greater level of next-day's overall pain severity while controlling for morning pain severity. Reducing exaggerated daily pain expectancy and up-regulating positive affect may be important intervention targets for disengaging the sleep-pain link among individuals with co-occurring TMD and sleep disturbance.PerspectiveThe daily link between previous night sleep duration and next day pain severity is mediated by morning pain expectancy and positive affect among women with temporomandibular disorder and sleep disturbance. Reducing pain expectancy and increasing positive affect may serve an important role in improving self-management of chronic pain.     

Botulinum toxin type-A in the prophylactic treatment of medication-overuse headache: a multicenter,double-blind,randomized, placebo-controlled,parallel group study

Medication-overuse headache (MOH) represents a severely disabling condition, with a low response to prophylactic treatments. Recently, consistent evidences have emerged in favor of botulinum toxin type-A (onabotulinum toxin A) as prophylactic treatment in chronic migraine. In a 12-week double-blind, parallel group, placebo-controlled study, we tested the efficacy and safety of onabotulinum toxin A as prophylactic treatment for MOH. A total of 68 patients were randomized (1:1) to onabotulinum toxin A (n = 33) or placebo (n = 35) treatment and received 16 intramuscular injections. The primary efficacy end point was mean change from baseline in the frequency of headache days for the 28-day period ending with week 12. No significant differences between onabotulinum toxin A and placebo treatment were detected in the primary (headache days) end point (12.0 vs. 15.9; p = 0.81). A significant reduction was recorded in the secondary end point, mean acute pain drug consumption at 12 weeks in onabotulinum toxin A-treated patients when compared with those with placebo (12.1 vs. 18.0; p = 0.03). When we considered the subgroup of patients with pericranial muscle tenderness, we recorded a significant improvement in those treated with onabotulinum toxin A compared to placebo treated in both primary (headache days) and secondary end points (acute pain drug consumption, days with drug consumption), as well as in pain intensity and disability measures (HIT-6 and MIDAS) at 12 weeks. Onabotulinum toxin A was safe and well tolerated, with few treatment-related adverse events. Few subjects discontinued due to adverse events. Our data identified the presence of pericranial muscle tenderness as predictor of response to onabotulinum toxin A in patients with complicated form of migraine such as MOH, the presence of pericranial muscle tenderness and support it as prophylactic treatment in these patients.     

Spontaneous cervicocephalic arterial dissection with headache and neck pain as the only symptom

Background and objective  

Cervicocephalic arterial dissection can cause both ischemic stroke and hemorrhagic stroke. However, spontaneous cervicocephalic arterial dissection presenting only with headache and neck pain has rarely been reported. The clinical features of patients with spontaneous cervicocephalic arterial dissection presenting only with headache and neck pain were investigated.     

Stress and sleep duration predict headache severity in chronic headache sufferers

The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (<15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (?15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n = 33) and chronic tension-type headache (n = 22) sufferers. Patients completed the Daily Stress Inventory and recorded headache and sleep variables using a daily sleep/headache diary. Stress ratings, duration of previous nights’ sleep, and headache severity were modeled using a series of linear mixed models with random effects to account for individual differences in observed associations. Models were displayed using contour plots. Two consecutive days of either high stress or low sleep were strongly predictive of headache, whereas 2 days of low stress or adequate sleep were protective. When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days, denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.     

16th European Headache Congress 2022 meeting abstracts

Background

Initial evidence have shown the short-term efficacy of sTMS in the acute and preventive treatment of migraine. It is unknown whether this treatment approach in the long-term is effective and well tolerated in difficult-to-treat migraine.

Methods

This is a prospective, single centre, open-label, real-world analysis conducted in difficult-to-treat patients with high-frequency episodic migraine (HFEM) and chronic migraine (CM) with and without medication overuse headache (MOH), who were exposed to sTMS therapy. Patients responding to a three-month sTMS treatment, continued the treatment and were assessed again at month 12. The cut-off outcome for treatment continuation was reduction in the monthly moderate to severe headache days (MHD) of at least 30% (headache frequency responders) and/or a?≥?4-point reduction in headache disability using the Headache Impact test-6 (HIT-6) (headache disability responders).

Results

One hundred fifty-three patients were included in the analysis (F:M?=?126:27, median age 43, IQR 32.3–56.8). At month 3, 93 out of 153 patients (60%) were responders to treatment. Compared to baseline, the median reduction in monthly headache days (MHD) for all patients at month 3 was 5.0?days, from 18.0 (IQR: 12.0–26.0) to 13.0?days (IQR: 5.75–24.0) (P =?0.002, r =???0.29) and the median reduction in monthly migraine days (MMD) was 4.0?days, from 13.0 (IQR: 8.75–22.0) to 9.0 (IQR: 4.0–15.25) (P =?0.002, r =???0.29). Sixty-nine out of 153 patients (45%) reported a sustained response to sTMS treatment at month 12. The percentage of patients with MOH was reduced from 52% (N =?79/153) at baseline to 19% (N =?29/153) at month 3, to 8% (N =?7/87) at month 12. There was an overall median 4-point reduction in HIT-6 score, from 66 (IQR: 64–69) at baseline to 62 at month 3 (IQR: 56–65) (P <?0.001, r =???0.51). A total of 35 mild/moderate adverse events were reported by 23 patients (15%). One patient stopped sTMS treatment due to scalp sensitivity.

Conclusions

This open label analysis suggests that sTMS may be an effective, well-tolerated treatment option for the long-term prevention of difficult-to-treat CM and HFEM.