Headache Trigger Research Articles

Relief Following Chronic Stress Augments Spreading Depolarization Susceptibility in Familial Hemiplegic Migraine Mice

Cortical spreading depolarization (CSD) is the electrophysiological substrate of migraine aura, and a putative trigger of trigeminovascular activation and migraine headache. Many migraineurs report stress or relief after a stress triggers an attack. We tested whether various stress conditions might modulate CSD susceptibility and whether this is dependent on genetic factors. Male and female wild type and familial hemiplegic migraine type1 (FHM1) knock-in mice heterozygous for the S218L missense mutation were subjected to acute or chronic stress, or chronic stress followed by relief (36 h). Acute stress was induced by restraint and exposure to bright light and white noise (3 h). Chronic stress was induced for 28 days by two cycles of repeated exposure of mice to a rat (7 days), physical restraint (3 days), and forced swimming (3 days). Electrical CSD threshold and KCl-induced (300 mM) CSD frequency were determined in occipital cortex in vivo at the end of each protocol. Relief after chronic stress reduced the electrical CSD threshold and increased the frequency of KCl-induced CSDs in FHM1 mutants only. Acute or chronic stress without relief did not affect CSD susceptibility in either strain. Stress status did not affect CSD propagation speed, duration or amplitude. In summary, relief after chronic stress, but not acute or chronic stress alone, augments CSD in genetically susceptible mice. Therefore, enhanced CSD susceptibility may explain why, in certain patients, migraine attacks typically occur during a period of stress relief such as weekends or holidays.

Psychological Sleep Interventions for Migraine and Tension-Type Headache: A Systematic Review and Meta-Analysis

Disordered sleep, poor sleep quality, and insufficient or excessive sleep duration are known triggers of primary and secondary headaches. Given this, it is plausible that improving sleep will subsequently reduce headache activity. We report a systematic review of the literature, examining studies utilising psychological sleep interventions for the treatment of migraine and tension-type headache. PubMed, EMBASE, CINAHL, PsycINFO, and Cochrane Central were searched, using terms pertaining to psychological sleep interventions and headaches. Meta-analysis was performed for two outcome measures; headache frequency, and headache intensity. 103 studies were retrieved, of which 55 were duplicates. After completing reviews, three studies were retained. An additional eligible study was published after the initial search, and was found via monthly update searches, resulting in a total of four included studies. The effects of psychological sleep interventions (and in one study, combined with drug therapy) significantly reduced headache frequency and headache intensity. Three studies improved various sleep outcomes such as duration, efficiency, and excessive sleepiness. Psychological sleep interventions improve headache frequency and sleep, however there is conflicting evidence for the effect on headache intensity between studies. Limitations include the small number of studies conducted to date. Despite this, the notable improvements in headaches and sleep achieved after psychological sleep interventions indicates further research on this promising topic is warranted.

Headache Triggers as Surprise.

To examine the hypothesis that surprising experiences of headache triggers are associated with daily headache activity. Little is known about the specific environmental or behavioral interactions that might trigger a headache attack in a prone individual. We propose that headache trigger exposures can be usefully characterized, not only by their mechanisms of action, but also on the degree of "surprise" they present to the individual. This hypothesis is based on elements of information theory: that unusual events and experiences carry more information than common events and experiences and that headache attacks are associated with reactions to uncommon or unexpected biopsychosocial exposures. A secondary analysis of the Headache Prediction Study, this prospective cohort study followed N=95 individuals with episodic migraine who contributed 4195 days of diary data. Information was collected on daily levels of several common headache triggers: number of caffeinated beverages, number of alcoholic beverages, stress (Daily Stress Inventory), and mood disturbance (Profile of Mood States). The probability of observing variations in each trigger was used to estimate the "surprisal" of experiencing each trigger, and this information, measured in bits, was used to predict headache attacks. Participants experienced a headache attack on 1613 of 4195 days (38.5%). Each of the triggers was modestly related to the probability of experiencing a future headache in a complex manner that involved interactions between current headache status, current levels of the trigger, and lagged (previous) levels of the trigger. However, when expressed as a surprisal, the associations were simplified and strengthened. For example, each of the individual trigger surprisals exhibited a meaningful association with the development of a future headache attack (expressed as a 1 SD change in surprisal), with odds ratios ranging from a low of 1.11 (95%CI: 1.00 to 1.24) for alcohol to a high of 1.30 (95%CI: 1.14 to 1.46) for stress. The individual surprisals could be summed for total trigger surprise and exhibited a reliable association with new onset headache, OR 1.35 (95%CI: 1.17 to 1.49). This score exhibited superior discrimination between headache and non-headache days from all of the individual triggers (ignoring base rate, AUC: 0.61; AUC: 0.71 with base rate). Diverse headache triggers can be uniformly described using their probability distributions. Rare values of headache triggers, or surprising values, were found to have consistent associations with headache activity across a variety of triggers. This finding, if validated in external data using other triggers, has potential to be used to conceptualize the influence of a wide range of headache triggers.

(173) Information Theory and Headache Triggers

Approximately 90% of individuals with headache believe there is at least one trigger, or causal factor, of their headache attacks. The list of headache triggers is extensive, but little is known about how individuals develop such beliefs. The aim of this secondary analysis was to evaluate the degree of information, measured using Shannon entropy, that headache triggers contain and to examine the relationship between joint entropy (i.e., triggers and headache activity) and trigger beliefs. We hypothesized that as information about a headache trigger increased (i.e., an individual was exposed to more states of the trigger), the strength of belief about the trigger also would increase. In a computer-based task, N = 300 participants rated the strength of the relationship between triggers and headaches. For each trigger, participants were asked to rate how often they encountered the trigger and how likely it was to cause a headache on a 0 to 10 scale. Headache triggers contained a wide range of information with binary (i.e., presence or absence) triggers containing between 0.01 and 1 bit of information while continuously scaled triggers (e.g., stress) contained more than 10 bits of information. Each bit of joint information was associated with an 18.4% (95CI: 10.9% to 25.9%) increase in perceived potency of the trigger. However, there was a statistically significant trigger x information interaction (p

Is There Support for the Paradigm 'Spinal Posture as a Trigger for Episodic Headache'? A Comprehensive Review.

The International Classification of Headache Disorders provides an extensive framework to classify headaches. Physiotherapy is indicated if neuromusculoskeletal dysfunctions are involved in the pathophysiology. Maladaptive postures seem a dominant trigger in tension-type and cervicogenic headache. Yet, outcomes following physiotherapy vary. The absence of protocol studies to identify determinants concerning the role of spinal posture in headache might explain such variability. Hence, multi-dimensional profiling of patients with headache based on interactions between spinal posture, psychosocial and lifestyle factors might be essential. Therefore, the aim of this paper was to perform a comprehensive review to find support for the paradigm of spinal posture triggering episodic headache based on a multi-dimensional view on tension-type and cervicogenic headache including modern pain neuroscience. A review was conducted to support spinal posture-induced episodic headache. Pubmed, Web of Science, Pedro and the Cochrane database were explored based on the following 'Mesh' or 'Topics': 'Headache', 'Posture', 'Spine', 'Psychosocial', 'Lifestyle'. The contemporary review of neuroanatomical, biomechanical and non-nociceptive pathways, with integration of modern pain neuroscience in tension-type and cervicogenic headache, supports spinal posture as a trigger for episodic headache. Maladaptive postures can activate C1-C3 nociceptors. Convergence with trigeminal afferents at the trigeminocervical nucleus could explain spinal headache. Interactions with psychosocial and lifestyle factors might contribute to peripheral and central sensitisation. Neuroanatomical, biomechanical and non-nociceptive pathways seem to justify profiling patients based on a postural trigger. Further research is needed to determine the contribution of postural dysfunctions in headache and the effect of specific interventions.

Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer's Disease.

Mast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. Mast cell activation-dependent inflammatory mediators augment stress associated pain and neuroinflammation. Stress is the second most common trigger of headache due to mast cell activation. Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that affects more women than men and woman’s increased susceptibility to chronic stress could increase the risk for AD. Modern life-related stress, social stress, isolation stress, restraint stress, early life stress are associated with an increased level of neurotoxic beta amyloid (Aβ) peptide. Stress increases cognitive dysfunction, generates amyloid precursor protein (APP), hyperphosphorylated tau, neurofibrillary tangles (NFTs), and amyloid plaques (APs) in the brain. Stress-induced Aβ persists for years and generates APs even several years after the stress exposure. Stress activates hypothalamic-pituitary adrenal (HPA) axis and releases corticotropin-releasing hormone (CRH) from hypothalamus and in peripheral system, which increases the formation of Aβ, tau hyperphosphorylation, and blood-brain barrier (BBB) disruption in the brain. Mast cells are implicated in nociception and pain. Mast cells are the source and target of CRH and other neuropeptides that mediate neuroinflammation. Microglia express receptor for CRH that mediate neurodegeneration in AD. However, the exact mechanisms of how stress-mediated mast cell activation contribute to the pathogenesis of AD remains elusive. This mini-review highlights the possible role of stress and mast cell activation in neuroinflammation, BBB, and tight junction disruption and AD pathogenesis.

Relating Photophobia, Visual Aura, and Visual Triggers of Headache and Migraine.

This study investigated a potential association between visual factors and symptoms related to migraine. It was predicted that photophobia and visual aura would be positively associated with interictal light sensitivity and visual headache triggers (flicker, glare, and eyestrain), and that these 2 visual symptoms would also be associated. Previous studies have found independent neurophysiological associations between several visual factors and symptoms related to headache disorders. Many of these connections appear to be associated with increased cortical hypersensitivity, a phenomenon that might be in part due to repeated avoidance and reduced tolerance to triggers. If true, and if associations between visual factors and symptoms can be established, this may have implications for an exposure-based treatment for migraine symptoms. Four hundred and ninety-one participants (411 female, 80 male) were recruited through Griffith University (AUS), Headache Australia, Pain Australia, and through social media. Participants were grouped based on the presence of headache disorder symptoms and the presence or absence of photophobia and/or visual aura. A cross-sectional online survey design was utilized to gather information pertaining to interictal light sensitivity, visual triggers, and visual symptoms. With respect to interictal light sensitivity and photophobia, a significant difference (P < .001, eta squared [η2 ] = 0.084) was found between the 3 groups, where headache disorder participants with photophobia (group A1; mean [M] = 2.5, standard deviation [SD] = 0.97) reported significantly greater light sensitivity than participants with headache disorder and no photophobia (A2; M=1.68, SD = 0.62) and control group participants (A3; M=1.82, SD = 0.85). This pattern was repeated for participants reporting flicker as a headache trigger (P < .001, η2 = 0.061), with group A1 (M=2.45, SD = 1.24) significantly higher than groups A2 (M=1.68, SD = 0.83) and A3 (M=1.68, SD = 0.89), and was also seen for glare as a headache trigger (P < .001, η2 = 0.092), with group A1 (M=2.92, SD = 0.96) significantly higher than A2 (M=2.31, SD = 0.89) and A3 (M=2.09, SD = 0.93). This pattern of results was not replicated for headache disorder participants with and without visual aura. A significant association (P < .001) was found between photophobia and visual aura in headache disorder participants based on a chi-square test of independence, with 86/136 participants reporting either both or neither visual symptom. This study supports a link between certain visual phenomena in headache disorder populations, and supports future research into exposure-based treatments for migraine symptoms.

Headache Trigger Sensitivity and Avoidance after Mild Traumatic Brain Injury.

Most patients with primary headache disorders identify environmental stimuli (e.g., visual glare), situational factors (e.g., stress), physiological states (e.g., hormones), or activities (e.g., exercise) as triggers that elicit or worsen headache episodes. Headache triggers have not been previously studied in post-traumatic headache (PTH). The present study explored the frequency of headache triggers and their avoidance in PTH. Participants with mild traumatic brain injury (TBI) were recruited from outpatient specialty clinics and completed questionnaires at or soon after their initial clinic visit. The research assessment included a list of 12 possible headache triggers where participants were asked to rate sensitivity (how often they get a headache when exposed to the trigger) and avoidance (how often they try to avoid the trigger). Enrolled participants were 40.6 years old (standard deviation [SD] = 11.8 years) on average, predominantly female (69.8%) and Caucasian (69.8%), and injured in a motor vehicle crash (47.2%) or fall (20.8%). They were assessed at 9.4 weeks (SD = 6.8) post-injury. Most patients with mild TBI in this consecutive series (82.7%) reported ongoing headaches. Mental exertion, stress, and lack of sleep were rated as the most potent headache triggers and among the most frequently avoided. Odors or foods, hunger, and weather conditions were rated as the least potent triggers. Headache trigger sensitivity and avoidance were moderately correlated (r = 0.736, p < 0.001). Headache severity was more associated with trigger sensitivity [F(2,49) = 13.45, p < 0.001] than trigger avoidance [F(2,47) = 2.97, p = 0.062]. In summary, the pattern of headache triggers in persistent PTH after mild TBI appears somewhat different from that in primary headache disorders, with mental exertion emerging as uniquely important. Pervasive avoidance of mental exertion to prevent headaches (cogniphobia) might be a worthwhile behavioral intervention target after mild TBI.

Intact mast cell content during mild head injury is required for development of latent pain sensitization: implications for mechanisms underlying post-traumatic headache.

Post-traumatic headache (PTH) is one of the most common, debilitating, and difficult symptoms to manage after a traumatic head injury. Although the mechanisms underlying PTH remain elusive, recent studies in rodent models suggest the potential involvement of calcitonin gene-related peptide (CGRP), a mediator of neurogenic inflammation, and the ensuing activation of meningeal mast cells (MCs), proalgesic resident immune cells that can lead to the activation of the headache pain pathway. Here, we investigated the relative contribution of MCs to the development of PTH-like pain behaviors in a model of mild closed-head injury (mCHI) in male rats. We initially tested the relative contribution of peripheral CGRP signaling to the activation of meningeal MCs after mCHI using a blocking anti-CGRP monoclonal antibody. We then used a prophylactic MC granule depletion approach to address the hypotheses that intact meningeal MC granule content is necessary for the development of PTH-related pain-like behaviors. The data suggest that after mCHI, ongoing activation of meningeal MCs is not mediated by peripheral CGRP signaling and does not contribute to the development of the mCHI-evoked cephalic mechanical pain hypersensitivity. Our data, however, also reveal that the development of latent sensitization, manifested as persistent hypersensitivity upon the recovery from mCHI-evoked acute cranial hyperalgesia to the headache trigger glyceryl trinitrate requires intact MC content during and immediately after mCHI. Collectively, our data implicate the acute activation of meningeal MCs as mediator of chronic pain hypersensitivity after a concussion or mCHI. Targeting MCs may be explored for early prophylactic treatment of PTH.

Red wine triggers may lead to better understanding of migraine headache: a narrative review

ABSTRACTMigraine headache is a prevalent condition that places a substantial burden on the healthcare system. It is known that certain foods, food additives, alcohol, caffeine, stress, sensory stimuli, disruptions in sleep-wake patterns, hormonal changes, and many other things may trigger migraines. Red wine is a frequently reported trigger for migraines and other headaches but it is unclear what substance(s) in red wine triggers headache and why red wine is more associated with headache than white wine, sparkling wines, or spirits. Implicated as headache triggers are biogenic amines (histamine, phenylethylamine, tyramine, and others), phenols, polyphenols, and sulfites. Enzymatic action in the metabolism of phenols and polyphenols may cause fluctuations in dopamine and serotonin levels which, in turn, have been implicated as headache triggers. The role of sulfotransferase enzymes and dopamine appears to offer a promising explanation of the red wine headache. The investigation of potential red wine triggers may better elucidate headache pathogenesis.

Entrapment Neuropathy: A Concept for Pathogenesis and Treatment of Headaches-A Narrative Review.

Entrapment neuropathy is a known cause of neurological disorders. In the head and neck area, this pathophysiological mechanism could be a trigger for headache. Over the last few decades, injection of botulinum toxin type A in the muscles that are causing the compression as well as surgical decompression have proved to be effective treatment methods worldwide for large numbers of patients with daily headaches. In particular the entrapment of the supraorbital nerves in the glabellar musculature and the occipital nerves in the neck musculature are triggers for headache disorders for which many patients are still seeking an effective treatment. This article reviews the literature and aims to bring the concept of neural entrapment to the attention of a wider audience. By doing so, we hope to give more exposure to an effective and relatively safe headache treatment.

Hypnotherapy or transcendental meditation versus progressive muscle relaxation exercises in the treatment of children with primary headaches: a multi-centre, pragmatic, randomised clinical study

Many children suffer from headaches. Since stress may trigger headaches, effective techniques to cope with stress are needed. We investigated the effectiveness of two mind-body techniques, transcendental meditation (TM) or hypnotherapy (HT), and compared them with progressive muscle relaxation (PMR) exercises (active control group). Children (9–18 years) suffering from primary headaches more than two times per month received either TM (N = 42), HT (N = 45) or PMR (N = 44) for 3 months. Primary outcomes were frequency of headaches and ≥ 50% reduction in headaches at 3 and 9 months. Secondary outcomes were adequate relief, pain coping, anxiety and depressive symptoms, somatisation and safety of treatment. Groups were comparable at baseline. Headache frequency was significantly reduced in all groups from 18.9 days per month to 12.5 and 10.5 at respectively 3 and 9 months (p < 0.001), with no significant differences between the groups. Clinically relevant headache reduction (≥ 50%) was observed in 41% and 47% of children at 3 and 9 months respectively, with no significant differences between the groups. No differences were observed in secondary outcome measures between the intervention groups. No adverse events were reported.Conclusion: All three techniques reduced primary headache in children and appeared to be safe.Trial registration: NTR 2955, 28 June 2011 (www.trialregister.nl)What is Known:• Stress may be an important trigger for both tension type headache and migraine in children.• Good data are lacking on the effect of transcendental meditation, hypnotherapy or progressive muscle relaxation as possible stress-reducing therapies in children with primary headaches.What is New:• Three non-pharmacological techniques, i.e., transcendental meditation, hypnotherapy and progressive muscle relaxation exercises, all result in a clinically significant reduction of headaches and use of pain medication.• No large differences between the three techniques were found, suggesting that children can choose either one of the three techniques based on personal preferences.

Headache Trigger Sensitivity and Avoidance after Concussion

Headache Trigger Sensitivity and Avoidance after Concussion

Long-Term Depression Induced by Optogenetically Driven Nociceptive Inputs to Trigeminal Nucleus Caudalis or Headache Triggers.

The peripheral trigeminovascular pathway mediates orofacial and craniofacial pain and projects centrally to the brainstem trigeminal nucleus caudalis (TNc). Sensitization of this pathway is involved in many pain conditions, but little is known about synaptic plasticity at its first central synapse. We have taken advantage of optogenetics to investigate plasticity selectively evoked at synapses of nociceptive primary afferents onto TNc neurons. Based on immunolabeling in the trigeminal ganglia, TRPV1-lineage neurons comprise primarily peptidergic and nonpeptidergic nociceptors. Optical stimulation of channelrhodopsin-expressing axons in the TRPV1/ChR2 mouse in TNc slices thus allowed us to activate a nociceptor-enriched subset of primary afferents. We recorded from lamina I/II neurons in acutely prepared transverse TNc slices, and alternately stimulated two independent afferent pathways, one with light-activated nociceptive afferents and the other with electrically-activated inputs. Low-frequency optical stimulation induced robust long-term depression (LTD) of optically-evoked EPSCs, but not of electrically-evoked EPSCs in the same neurons. Blocking NMDA receptors or nitric oxide synthase strongly attenuated LTD, whereas a cannabinoid receptor 1 antagonist had no effect. The neuropeptide PACAP-38 or the nitric oxide donors nitroglycerin or sodium nitroprusside are pharmacologic triggers of human headache. Bath application of any of these three compounds also persistently depressed optically-evoked EPSCs. Together, our data show that LTD of nociceptive afferent synapses on trigeminal nucleus neurons is elicited when the afferents are activated at frequencies consistent with the development of central sensitization of the trigeminovascular pathway.SIGNIFICANCE STATEMENT Animal models suggest that sensitization of trigeminovascular afferents plays a major role in craniofacial pain syndromes including primary headaches and trigeminal neuralgia, yet little is known about synaptic transmission and plasticity in the brainstem trigeminal nucleus caudalis (TNc). Here we used optogenetics to selectively drive a nociceptor-enriched population of trigeminal afferents while recording from superficial laminae neurons in the TNc. Low-frequency optical stimulation evoked robust long-term depression at TRPV1/ChR2 synapses. Moreover, application of three different headache trigger drugs also depressed TRPV1/ChR2 synapses. Synaptic depression at these primary afferent synapses may represent a newly identified mechanism contributing to central sensitization during headache.

Sleep and Migraine: Assessment and Treatment of Comorbid Sleep Disorders.

The relationship of sleep and migraine is unequivocal and familiarity with the nature and magnitude of these associations may inform clinical practice. Recent prospective, longitudinal, and time-series analysis has begun to unravel the magnitude and temporal patterns of sleep and migraine. Prospective evidence has shown that sleep variables can trigger acute migraine, precede and predict new onset headache by several years, and indeed, sleep disturbance and snoring are risk factors for chronification. The presence of a sleep disorder is associated with more frequent and severe migraine and portends a poorer headache prognosis. Interestingly, the disorders linked to migraine are quite varied, including insomnia, snoring and obstructive sleep apnea, restless legs, circadian rhythm disorders, narcolepsy, and others. Insomnia is by far the most common sleep disorder in headache patients. In fact, the majority of patients with chronic migraine presenting for treatment have insomnia. Despite a rapidly expanding literature, very few controlled treatment studies have been published to guide clinical practice. This paper focuses on clinical assessment and treatment of sleep disorders. An algorithm is presented for sleep disorders management in the migraine patient, which highlights major sleep disorders and psychiatric comorbidity. Diagnostic procedures are recommended that are conducive to clinical practice. Suggested tools include the sleep history, screening mnemonics, prediction equation, and sleep diary. New developments in treatment have produced abbreviated and cost-effective therapies for insomnia and obstructive sleep apnea that may reach a larger population. Revisions in the diagnostic manuals for sleep and headache disorders enhance recognition of sleep-related headache. Recommendations include behavioral sleep regulation, shown in recent controlled trials to decrease migraine frequency, management for sleep apnea headache, cognitive behavioral therapy (CBT) for insomnia abbreviated for the physician practice setting, sleep-related headache trigger, and others. There is no empirical evidence that sleep evaluation should delay or supersede usual headache care. Rather, sleep management is complimentary to standard headache practice.

Clinical and polysomnographic characteristics in patients with morning headache

Background: The relation between headaches and sleep disorders are complex and heavily questioned. However, there is still controversy about this interrelationship. Objective: To describe the clinical and polysomnographic characteristics of patients with morning headache, and to compare them with patients without morning headaches. Methods: Prospective study between April and August 2009. One hundred and eight patients were included consecutively and by convenience. All patients were submitted to polysomnography and were distributed in the group with headache (group 1) or the group without headache (group 2). Results: Morning headache was reported by 33 (30.6%) patients, 17 (51.5%, p = 0.02) women. The clinical characteristics in the group of morning headache were 42.4% with disease in upper respiratory system, 72.7% with anxiety, 45% with headache in general, 54% with neurocognitive symptoms, 81.2% reported non restorative sleep and 60.6% had insomnia (all p&lt; 0.05). Among the polysomnographic features surveyed, the only variable that showed statistical significance was wake after sleep onset. Almost 43% (vs. 20%) of patients with morning headaches were in normal range. Conclusions: It was not possible to conclude that the presence of the increase apnea/hypopnea indices, desaturation relevant and intermittent and disruption of sleep patterns are sufficient to modulate, by itself, the occurrence of morning headaches. Sleep disorders can act as a trigger for morning headaches in susceptible individuals with specific clinical profile

Significance of fatigue in patients with migraine

Fatigue is often stated as a headache trigger or migraine-specific symptom. We investigated predictors of fatigue and its impact on quality of life (QOL) in patients with migraine. Patients with migraine were recruited from a headache clinic and completed psychosomatic instruments, including the 12-item Allodynia Symptom Checklist (ASC-12), the Migraine Disability Assessment Scale (MIDAS), the Patients Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), the Epworth Sleepiness Scale (ESS), the Insomnia Severity Index (ISI), the Fatigue Severity Scale (FSS), and Migraine-Specific Quality of Life Questionnaire (MSQ). Two hundreds twenty-six patients with migraine were eligible for the study. Pathologic fatigue was manifested in 133 patients (58.8%). The FSS score was significantly associated with age, age of onset, the Visual Analog Scale (VAS) depicting headache intensity, photophobia, phonophobia, and the scores of the ASC-12, the MIDAS, the ESS, the ISI, the PHQ-9 and the GAD-7. The strongest predictor for the FSS was the PHQ-9 (β = 0.432, p < .001), followed by age (β = −0.169, p = .002), the ISI (β = 0.151, p = .016), and the VAS (β = 0.139, p = .018). There was an inverse correlation between the FSS score and three dimensional scores of the MSQ (p < .001). Appropriate interventions for depression, insomnia, and headache intensity are likely to lessen fatigue and improve QOL.

Características clínicas e polissonográficas em pacientes com queixa de cefaleia matinal

Background: The relation between headaches and sleep disorders are complex and heavily questioned. However, there is still controversy about this interrelationship. Objective: To describe the clinical and polysomnographic characteristics of patients with morning headache, and to compare them with patients without morning headaches. Methods: Prospective study between April and August 2009. One hundred and eight patients were included consecutively and by convenience. All patients were submitted to polysomnography and were distributed in the group with headache (group 1) or the group without headache (group 2). Results: Morning headache was reported by 33 (30.6%) patients, 17 (51.5%, p = 0.02) women. The clinical characteristics in the group of morning headache were 42.4% with disease in upper respiratory system, 72.7% with anxiety, 45% with headache in general, 54% with neurocognitive symptoms, 81.2% reported non restorative sleep and 60.6% had insomnia (all p< 0.05). Among the polysomnographic features surveyed, the only variable that showed statistical significance was wake after sleep onset. Almost 43% (vs. 20%) of patients with morning headaches were in normal range. Conclusions: It was not possible to conclude that the presence of the increase apnea/hypopnea indices, desaturation relevant and intermittent and disruption of sleep patterns are sufficient to modulate, by itself, the occurrence of morning headaches. Sleep disorders can act as a trigger for morning headaches in susceptible individuals with specific clinical profile

Influences on headache trigger beliefs and perceptions.

Background Previous headache trigger studies have primarily utilized checklists to measure beliefs about triggers. While this work has defined the diversity of beliefs across headache sufferers, the strength of association and the frequency at which these triggers are encountered remain unexplored. Objective To measure the strength of association, frequency of encounter, and influences on trigger beliefs and perceptions using a laboratory assessment task. Methods This cross-sectional observational study, part of the HACOGS project, included adult current migraine, tension-type, or cluster headache sufferers. Participants rated the chances they would experience a headache if they were to encounter a specific trigger and the number of days per month they experience that trigger for 33 common triggers. Results All 300 participants contributed data on all triggers, with little missing data (1.2%). All triggers exhibited a high degree of inter-individual variability on the strength of association and encounter perceptions. Many triggers were perceived to be encountered daily (e.g., caffeine, air conditioning), and a full range of perceptions were observed for each trigger. Stress (75% chance of headache), missing a meal (60%), and dehydration (60%) were the triggers with the greatest potency beliefs. Only 8-15% of these beliefs were related to individual differences and 26-27% to the triggers themselves. Conclusions Participants expressed diverse beliefs and perceptions about the strength of many common headache triggers. Variation in these beliefs was not associated with individual differences or the triggers themselves. This finding supports the importance of measuring more than just the presence-absence of trigger beliefs.

Novel Therapeutic Targets Against Spreading Depression.

Migraine is among the most prevalent and disabling neurological diseases in the world. Cortical spreading depression (SD) is an intense wave of neuronal and glial depolarization underlying migraine aura, and a headache trigger, which has been used as an experimental platform for drug screening in migraine. Here, we provide an overview of novel therapeutic targets that show promise to suppress SD, such as acid-sensing ion channels, casein kinase Iδ, P2X7-pannexin 1 complex, and neuromodulation, and outline the experimental models and essential quality measures for rigorous and reproducible efficacy testing.