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IntroductionHeadaches comprise 8-14% of total presentations to acute services. Secondary headaches cause greater morbidity and mortality (1,2,3). A five-question tool previously showed utility in identifying secondary headache (1). We present a preliminary revalidation analysis with unilateral headache as an added feature.MethodsA six-week retrospective review of headache patients attending neuro-SDEC at UCLH. Six parameters: thunderclap headache, focal neurological symptoms, focal neurological signs, systemic symptoms, unilateral headache, age greater than 50, were assessed. Multiple triggers of the tool were reviewed.Results62 patients were included. 69% had primary headache & 31% had secondary headache. The tool positively identified 74% of secondary headache (sensitivity: 74%, specificity: 40%). With removal of the least specific question, focal symptoms, sensitivity was 69% & specificity 53%. Unilateral headache was not correlated to headache type. The most specific question was focal signs (specificity: 94%, accuracy: 76%). Multiple triggers improved specificity to 81%.ConclusionFocal symptoms had the least diagnostic utility with focal neurological signs the most. Unilateral headache had no additive effect. Multiple triggers improved specificity. Seasonal sinusitis prevalence may have contributed to secondary headache percentage. Further data collection to expand the cohort, correlation plot analysis, and modification for potential clinical use, is being undertaken.a.dethabrew@nhs.net

BackgroundAcute trigeminal autonomic cephalalgia (TAC) headache service is a rapid access consultation service for patients with TAC headaches offering urgent advice and treatment. We aimed to evaluate the effectiveness of this service.MethodsData from successive consultations (n=419) in the acute TAC headache service from 19/02/2018 to 29/07/2024 were collected from clinic letters as part of a service evaluation. Data were summarized as percentages or as medians with interquartile ranges.ResultsData from 419 consultations of 190 patients were analyzed. Their median age was 49 years (IQR: 38-58) and 67% were male. The highest number of referrals were received in March (11.5%) and November (9.8%) and 19% were for patients new to the service. The majority had cluster headache (79%), followed by other primary headaches (20%) and secondary headaches (1%).Interventions included treatment revisions (51%), greater occipital nerve (GON) injections (13%), a combination of GON injection and treatment revisions (24%) or advice alone (11%). Interventions were effective in 62% of the reviews.ConclusionAn acute TAC headache service is an effective service for patients with primary headache disorders, especially for cluster headache, which can provide urgent support during bouts of headache minimizing the need to visit the emergency department.pubuduamarasena07@gmail.com

Consumption of caffeine in the diet, both daily and occasional, has a significant biological effect on the nervous system. Caffeine, through various and not yet fully investigated mechanisms, affects headaches. This is especially noticeable in migraine. In other headaches such as hypnic headache, post-dural puncture headache and spontaneous intracranial hypotension, caffeine is an important therapeutic agent. In turn, abrupt discontinuation of chronically used caffeine can cause caffeine-withdrawal headache. Caffeine can both relieve and trigger headaches.

Alcohol is a widely consumed beverage worldwide, and headaches, including migraine, tension-type headache (TTH), and other primary headaches, are common in the general population. Although epidemiological studies have shown a correlation between alcohol consumption and headaches, the specific pathophysiological mechanism of this headache remains unknown. We reviewed articles deemed relevant to the issue of alcohol as a trigger for various headaches, those that discussed alcohol consumption in these patient groups, and those that addressed the pathophysiological and clinical aspects of alcohol and headache. The review concluded that alcohol affects both migraine and non-migraine headaches. Alcohol-induced headache, classified as a secondary headache, is a throbbing, bilateral headache that is exacerbated by physical activity and is precipitated by alcohol consumption. TTH can be precipitated by alcohol consumption, and patients with TTH have more alcohol-related problems than those with migraine. Cluster headaches (CH) are often triggered by alcohol, but surprisingly, many CH patients consume alcohol, even during attacks. The relationship between alcohol and migraine is complex. Numerous components of alcoholic beverages can influence pain triggering and are responsible for migraine attacks. Red wine is one of the most frequently cited triggers for migraine attacks, a finding not always confirmed by the few prospective studies. However, there is no safe dose of alcohol, and therefore avoidance should be recommended.

Purpose of Review Tension-type headaches (TTH) significantly diminish patients’ quality of life and increase absenteeism, thereby imposing a substantial economic burden. Animal models are essential tools for studying disease mechanisms and drug development. However, until now, little focus has been placed on summarizing the animal models of TTH and associated mechanistic studies. This narrative review discusses the current animal models of TTH and related mechanistic studies to provide insights into the pathophysiological mechanisms of and treatments for TTH. Recent Findings The primary method for constructing an animal model of TTH involves injecting a solution of pain relievers, such as adenosine triphosphate, nerve growth factor, or a high concentration of salt solution, into the neck to initiate harmful cervical muscle responses. This model enables the examination of the interaction between peripheral muscles and central sensitization, which is crucial for understanding the pathophysiology of TTH. Mechanistic studies based on this model have investigated the effect of the P2X receptor antagonist, P2X7 receptor blockade, the P2Y1 receptor agonist 2-MESADP, P2Y1 receptor antagonist MRS2179, nitric oxide synthase inhibitors, and acetylsalicylic acid. Summary Despite notable advancements, the current model of TTH has limitations, including surgical complexity and the inability to replicate chronic tension-type headache (CTTH). To gain a more comprehensive understanding and develop more effective treatment methods, future studies should focus on simplifying surgical procedures, examining other predisposing factors, and establishing a model for chronic TTH. This will offer a deeper insight into the pathophysiological mechanism of TTH and pave the way for improved treatment approaches.

Cluster headache is a debilitating primary headache disorder that affects approximately 0.1% of the population worldwide. Cluster headache attacks involve severe unilateral pain in the trigeminal distribution together with ipsilateral cranial autonomic features and a sense of agitation. Acute treatments are available and are effective in just over half of the patients. Until recently, preventive medications were borrowed from non-headache indications, so management of cluster headache is challenging. However, as our understanding of cluster headache pathophysiology has evolved on the basis of key bench and neuroimaging studies, crucial neuropeptides and brain structures have been identified as emerging treatment targets. In this Review, we provide an overview of what is known about the pathophysiology of cluster headache and discuss the existing treatment options and their mechanisms of action. Existing acute treatments include triptans and high-flow oxygen, interim treatment options include corticosteroids in oral form or for greater occipital nerve block, and preventive treatments include verapamil, lithium, melatonin and topiramate. We also consider emerging treatment options, including calcitonin gene-related peptide antibodies, non-invasive vagus nerve stimulation, sphenopalatine ganglion stimulation and somatostatin receptor agonists, discuss how evidence from trials of these emerging treatments provides insights into the pathophysiology of cluster headache and highlight areas for future research.In this Review, Wei and Goadsby discuss the pathophysiology of cluster headache, the treatments available and their mechanisms, and the insights being provided by results from trials of emerging treatments, which indicate mechanistic differences between episodic and chronic cluster headache.

Background The Global Campaign against Headache has pioneered evaluation of the prevalence and impact of headache on the preceding day (“headache yesterday”) as a new approach to the estimation of headache-attributed burden, avoiding recall error. We report its application in Karnataka State, southern India. Methods In a door-to-door survey, biologically unrelated adults (aged 18–65 years) were randomly sampled from urban and rural areas in and around Bengaluru and interviewed by trained researchers using a validated, structured questionnaire. Enquiry into headache applied ICHD-II diagnostic criteria and included questions about headache on the day preceding the interview (headache yesterday [HY]). Results There were 2329 participants (participation proportion 92.6 %; males 1141 [49.0 %], females 1188 [51.0 %]; mean age 38.0 [±12.7] years; 1103 [47.4 %] from rural areas, 1226 [52.6 %] urban). HY was reported by 138 participants (males 33 [2.9 %], females 105 [8.8 %]): the 1-day prevalence of headache was 5.9 %. Mean duration of HY was 7.0 ± 8.5 h, so that 1.7 % of the population (5.9 % * 7.0/24), on average, had headache at any moment in time yesterday. Mean intensity on a scale of 1–3 was 2.0 [±0.8]. Lost productivity due to HY was reported by 83.3 % of participants with HY: 37.7 % able to do less than half of what they had planned and 13.0 % able to do nothing. Productivity loss at population level (being the productivity loss within the entire adult population, every single day, attributable to headache) was 3.0 %. Conclusions This method of enquiry, free from recall error, confirmed a very high level of headache-attributed burden in Karnataka: previous estimates based on 3-month recall may even have been too low. Until another study is done in the country, these are the best data for all India. They demonstrate need for action nationwide to mitigate this burden, and correct action will ultimately almost certainly be cost-saving.

Purpose of the Review Traumatic brain injury (TBI) is a major public health concern in the USA and worldwide. Sleep disruption and headaches are two of the most common problems reported by patients after TBI. In this manuscript, we review the current knowledge regarding the relation between post-traumatic sleep disruption and headaches. We also describe the role of the glymphatic system as a potential link between TBI, sleep, and headaches. Recent Findings Recent studies show a reciprocal relation between post-traumatic sleep disruption and headaches: patients with sleep disruption after TBI report more headaches, and post-traumatic headaches are a risk factor for developing disrupted sleep. Despite this clinical association, the exact mechanisms linking post-traumatic sleep disruption and headaches are not well understood. The glymphatic pathway, a newly described brain–wide network of perivascular spaces that supports the clearance of interstitial solutes and wastes from the brain, is active primarily during sleep, and becomes dysfunctional after TBI. We propose a model where changes in glymphatic function caused by TBI and post-traumatic sleep disruption may impair the clearance of neuropeptides involved in the pathogenesis of post-traumatic headaches, such as CGRP. Summary The relation between TBI, post-traumatic sleep disruption, and post-traumatic headaches, although well documented in the literature, remains poorly understood. Dysfunction of the glymphatic system caused by TBI offers a novel and exiting explanation to this clinically observed phenomenon. The proposed model, although theoretical, could provide important mechanistic insights to the TBI-sleep-headache association.

Background: Mindfulness-based therapy (MBT) has been demonstrated to be effective for reducing chronic pain symptoms; however, the use of MBT for Chronic Tension-Type Headache (CTH) exclusively has to date not been examined. Typically, MBT for chronic pain has involved an 8-week program based on Mindfulness Based Stress Reduction. Recent research suggests briefer mindfulness-based treatments may be effective for chronic pain. Aims: To conduct a pilot study into the efficacy of brief MBT for CTH. Method: We conducted a randomized controlled trial of a brief (6-session, 3-week) MBT for CTH. Results: Results indicated a significant decrease in headache frequency and an increase in the mindfulness facet of Observe in the treatment but not wait-list control group. Conclusion: Brief MBT may be an effective intervention for CTH.

Postdural puncture headache (PDPH) is a debilitating, life-altering complication of the administration of obstetric spinal anesthesia (SA). The lack of evidence-based treatment for PDPH necessitates the implementation of new treatment modalities. Mirtazapine is a noradrenergic and specific serotonergic antidepressant that has been used as a prophylactic treatment for chronic tension-type headaches. Few previous studies have assessed the efficacy of sumatriptan in the treatment of PDPH. The purpose of this study was to assess the hypothesis that an adjunctive therapy that involved adding mirtazapine or sumatriptan to conventional management (CM) would be more effective in reducing the incidence of refractory PDPH after obstetric surgery under SA than would CM alone. A prospective randomized study. This study was carried out at Ain-Shams University Maternity Hospital. Two hundred and ten American Society of Anesthesiologists (ASA) physical status II  women who complained of PDPH after obstetric SA were randomly allocated to one of 3 groups. Each group consisted of 70 women. The intervention treatment for every group was continued for 3 days, as was the CM of PDPH. Every day at 8 p.m., patients in the mirtazapine group (the M-group) took 30 mg mirtazapine tablet, patients in the sumatriptan group (the S-group) took 50 mg sumatriptan tablet, and patients in the control group (the C-group) took placebo tablets. The primary outcome was the incidence of refractory headache 72 hours after the ingestion of the first dose of the intervention drugs. The incidences of side effects of the study drugs, the hospital length of stay (LOS), and the patient satisfaction score were secondary outcomes. Patients in the C-group had higher means of headache intensity, lower rates of complete response to medical treatment, more increased incidences of refractory PDPH 72 hours after intervention, and a greater need for epidural blood patches than did patients in either of the intervention groups (P < 0.001), with comparable efficacy between the M- and S-groups (P > 0.05). Incidences of nausea, vomiting, and the need for antiemetics were least frequent in the M-group (P < 0.001). More patients in the C-group had a high prevalence of photophobia and neck stiffness than did patients in the other 2 groups (P < 0.001). Meanwhile, patients in the M- and S-groups had lower hospital LOS and higher patient satisfaction scores (P < 0.001), with no significant differences between the intervention groups (P > 0.05). This was a single-center study. This study did not determine the optimal dose of mirtazapine. Adding either mirtazapine or sumatriptan to the CM of PDPH following obstetric SA was associated with lower means of headache intensities, higher rates of complete response to medical treatment, and decreased incidence of refractory headaches. As an antiemetic drug, mirtazapine was found to be effective, inexpensive, safe, well-tolerated, and capable of being used on an outpatient basis.