Chronic Post-traumatic Headache Research Articles

Repeat mild traumatic brain injuries (RmTBI) modify nociception and disrupt orexinergic connectivity within the descending pain pathway

Repeat mild traumatic brain injuries (RmTBI) result in substantial burden to the public health system given their association with chronic post-injury pathologies, such as chronic pain and post-traumatic headache. Although this may relate to dysfunctional descending pain modulation (DPM), it is uncertain what mechanisms drive changes within this pathway. One possibility is altered orexinergic system functioning, as orexin is a potent anti-nociceptive neuromodulator. Orexin is exclusively produced by the lateral hypothalamus (LH) and receives excitatory innervation from the lateral parabrachial nucleus (lPBN). Therefore, we used neuronal tract-tracing to investigate the relationship between RmTBI and connectivity between lPBN and the LH, as well as orexinergic projections to a key site within the DPM, the periaqueductal gray (PAG). Prior to injury induction, retrograde and anterograde tract-tracing surgery was performed on 70 young-adult male Sprague Dawley rats, targeting the lPBN and PAG. Rodents were then randomly assigned to receive RmTBIs or sham injuries before undergoing testing for anxiety-like behaviour and nociceptive sensitivity. Immunohistochemical analysis identified distinct and co-localized orexin and tract-tracing cell bodies and projections within the LH. The RmTBI group exhibited altered nociception and reduced anxiety as well as a loss of orexin cell bodies and a reduction of hypothalamic projections to the ventrolateral nucleus of the PAG. However, there was no significant effect of injury on neuronal connectivity between the lPBN and orexinergic cell bodies within the LH. Our identification of structural losses and the resulting physiological changes in the orexinergic system following RmTBI begins to clarify acute post-injury mechanistic changes that drive may drive the development of post-traumatic headache and the chronification of pain.

Tension-type Headache and Migraine as Manifestations of Chronic Post-Traumatic Headache: Case Report

Introduction: A subsequent headache that appears within seven days of a head injury is referred to as a post-traumatic headache (PTHA) (or after regaining consciousness after the head trauma). If a post-traumatic headache lasts longer than three months after the injury, it is referred to as chronic or chronic post-traumatic headache (CPTHA). Case Report: A 17-year-old male comes to the neurology outpatient clinic with complaints of headache. The headache has been felt since 3 months ago, 3 days after the patient suffered a blow to his left head from falling from a chair. At that time, the patient fainted about 15 minutes later; the patient regained consciousness and had no complaints. Pain is felt on the left side of the head, throbbing, mild-moderate intensity, and feels heavier when there is a loud sound or seeing a too-bright light. Discussion: Like other primary headaches, post-traumatic headache is diagnosed clinically. Laboratory and routine diagnostic imaging studies are unnecessary and have minimal clinical utility. Brain MRI did not reveal any structural changes in patients with PTHA following injury. Conclusion: Chronic post-traumatic headaches often occur after brain injury, especially after minimally traumatic brain injury. The clinical picture is variable and may be similar to tension-type headaches and/or migraines.

Tension-type Headache and Migraine as Manifestations of Chronic Post-Traumatic Headache

Introduction: A subsequent headache within seven days of a head injury (or after regaining consciousness after the head trauma)is referred to as a post-traumatic headache (PTHA); it is referred to as chronic or chronic post-traumatic headache (CPTHA) if it lasts longer than three months after the injury. Case : A 17-year-old male with headache since 3 months ago, 3 days after suffered a blow to his left head from falling from a chair. At that time, the patient fainted for about 15 minutes but had no complaints after regained consciousness. Pain is felt on the left side of the head, throbbing, mild-moderate intensity, and feels heavier with a loud sound or a too-bright light. Discussion: Post-traumatic headache is clinically diagnosed. Laboratory and routine diagnostic imaging studies are unnecessary and have minimal clinical utility. Conclusion: Chronic post-traumatic headaches often occur, especially after minimally traumatic brain injury. The clinical picture is variable and may be similar to tension-type headaches and/or migraines. Pendahuluan: Nyeri kepala dalam tujuh hari setelah cedera kepala atau setelah sadar kembali dari trauma kepala disebut nyeri kepala pasca-trauma (post-traumatic headache/PTHA); disebut sakit kepala pasca-trauma kronis atau kronis (CPTHA) jika berlangsung lebih dari tiga bulan setelah cedera. Kasus: Seorang laki-laki berusia 17 tahun dengan keluhan nyeri kepala sejak 3 bulan, 3 hari setelah kepala kiri terbentur karena jatuh dari kursi. Saat itu, pasien pingsan sekitar 15 menit, tidak ada keluhan setelah sadar. Nyeri dirasakan di sisi kiri kepala, berdenyut, intensitas ringan-sedang, terasa lebih berat jika ada suara keras atau cahaya terlalu terang. Diskusi: Nyeri kepala pasca-trauma didiagnosis secara klinis. Laboratorium dan studi pencitraan diagnostik rutin tidak diperlukan dan memiliki utilitas klinis minimal. Simpulan: Nyeri kepala pasca-trauma kronis sering terjadi, terutama setelah cedera otak traumatis minimal. Gambaran klinisnya bervariasi dan dapat mirip nyeri kepala tipe tegang dan/atau migrain

Post-traumatic headache: Pathophysiology and management - A review

Background Post-traumatic headache (PTH) is a common secondary headache due to traumatic brain injury. In the past, significant research has been conducted to understand the pathophysiology and treatment options for PTH. However, PTH still lacks evidence-based treatment, and most of the management depends on the primary phenotype observed in the patient. Objective The main objective of this review is to provide a single reference that covers the current understanding of the pathophysiology and the treatment options available for PTH. Methods A detailed literature search on PubMed was performed, and a narrative review was prepared. Results The pathophysiology of PTH is multifactorial. Acute PTH may be attributed to increased peripheral pain sensitization with impaired pain inhibiting pathways. Chronic or persistent PTH may be due to a chronic inflammatory response and peripheral as well as central sensitization. The mechanism responsible for the transition of acute to persistent PTH is unknown. The migraine-like phenotype is reported to be the most prevalent headache type seen in PTH. New targets for preventive treatment have been identified in recent years, such as neuropeptides like calcitonin-gene-related peptide (CGRP), nitric oxide, and glutamate. The preventive pharmacological and non-pharmacological strategies employed for migraine (e.g. anti-CGRP monoclonal antibodies, onabotulinumtoxinA, physical therapy, cognitive and behavioral treatment, and neurostimulation techniques) have shown in preliminary studies that they are potentially efficacious, but large, randomized, double blind, placebo controlled trials are needed to further establish these as treatment options for PTH. Conclusions The lack of evidence-based treatment for PTH has created a need for future large trials to confirm the safety and efficacy of the currently employed treatments.

Retrospective analysis of adult chronic post-traumatic headache with respect to the intracranial pressure and the characteristic of headache

Chronic post-traumatic headache (CPTH) is a life disturbing disorder with many symptoms (JAMA 2008; 300: 71–9) and yet the characteristic of the headache is still unclear. We have reported the possibility of increased intracranial pressure (ICP) in adult CPTH (Eur J Med Res 2007; 12: 246–54)). The main purpose of this study is to elucidate the intracranial pressure (ICP) and the characteristic of the headache.

Intracranial pressure in adolescent chronic post-traumatic headache and its treatment

Intracranial pressure in adolescent chronic post-traumatic headache and its treatment

Incidence (2008-2015) of post-traumatic headaches in United States military personnel

ABSTRACT Objective: To conduct a descriptive transversal study to evaluate the incidence and demographic characteristics of post-traumatic headache using data from the Defense Medical Epidemiology Database. Methods: A retrospective cohort study was conducted of data from 2008 to 2015 based on the International Classification of Diseases codes for both acute and chronic post-traumatic headache. Results: A total of 17,010 new cases of post-traumatic headaches were diagnosed among active duty military personnel. Reported incidence rates of post-traumatic headaches in the military increased 29-fold over the timeframe analyzed. Males enlisted in the Army were more likely to be diagnosed with post-traumatic headaches than females (O/E = 0.76), other branches, and officers. Conclusion: Findings of this study indicate that there is a significant incidence of post-traumatic headaches in the U.S. military. However, the incidence rates of post-traumatic headaches in the military are much lower than what was expected considering the number of traumatic brain injuries in the United States military reported by the Department of Defense for the same period. Additional research is needed to further evaluate these differences and the impact of PTHs on military personnel.

Increase in trigeminal ganglion neurons that respond to both calcitonin gene-related peptide and pituitary adenylate cyclase-activating polypeptide in mouse models of chronic migraine and posttraumatic headache.

A large body of animal and human studies indicates that blocking peripheral calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide (PACAP) signaling pathways may prevent migraine episodes and reduce headache frequency. To investigate whether recurring migraine episodes alter the strength of CGRP and PACAP signaling in trigeminal ganglion (TG) neurons, we compared the number of TG neurons that respond to CGRP and to PACAP (CGRP-R and PACAP-R, respectively) under normal and chronic migraine-like conditions. In a mouse model of chronic migraine, repeated nitroglycerin (NTG) administration significantly increased the number of CGRP-R and PACAP-R neurons in TG but not dorsal root ganglia. In TG neurons that express endogenous αCGRP, repeated NTG led to a 7-fold increase in the number of neurons that respond to both CGRP and PACAP (CGRP-R&PACAP-R). Most of these neurons were unmyelinated C-fiber nociceptors. This suggests that a larger fraction of CGRP signaling in TG nociceptors may be mediated through the autocrine mechanism, and the release of endogenous αCGRP can be enhanced by both CGRP and PACAP signaling pathways under chronic migraine condition. The number of CGRP-R&PACAP-R TG neurons was also increased in a mouse model of posttraumatic headache (PTH). Interestingly, low-dose interleukin-2 treatment, which completely reverses chronic migraine-related and PTH-related behaviors in mouse models, also blocked the increase in both CGRP-R and PACAP-R TG neurons. Together, these results suggest that inhibition of both CGRP and PACAP signaling in TG neurons may be more effective in treating chronic migraine and PTH than targeting individual signaling pathways.

Mild traumatic brain injury is associated with effect of inflammation on structural changes of default mode network in those developing chronic pain

BackgroundMild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up.MethodsSeventy-seven mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54 (70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). Forty-two matched healthy controls completed the same protocol at T-1 once.ResultsAt baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01–0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury.ConclusionThe findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.Trial registrationClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.

Identifying oxidized lipid mediators as prognostic biomarkers of chronic posttraumatic headache.

Chronic posttraumatic headache (PTH) is among the most common and disabling sequelae of traumatic brain injury (TBI). Current PTH treatments are often only partially effective and have problematic side effects. We previously showed in a small randomized trial of patients with chronic nontraumatic headaches that manipulation of dietary fatty acids decreased headache frequency, severity, and pain medication use. Pain reduction was associated with alterations in oxylipins derived from n-3 and n-6 fatty acids, suggesting that oxylipins could potentially mediate clinical pain reduction. The objective of this study was to investigate whether circulating oxylipins measured in the acute setting after TBI could serve as prognostic biomarkers for developing chronic PTH. Participants enrolled in the Traumatic Head Injury Neuroimaging Classification Protocol provided serum within 3 days of TBI and were followed up at 90 days postinjury with a neurobehavioral symptom inventory (NSI) and satisfaction with life survey. Liquid chromatography-tandem mass spectrometry methods profiled 39 oxylipins derived from n-3 docosahexaenoic acid (DHA), and n-6 arachidonic acid and linoleic acid. Statistical analyses assessed the association of oxylipins with headache severity (primary outcome, measured by headache question on NSI) as well as associations between oxylipins and total NSI or satisfaction with life survey scores. Among oxylipins, 4-hydroxy-DHA and 19,20-epoxy-docosapentaenoate (DHA derivatives) were inversely associated with headache severity, and 11-hydroxy-9-epoxy-octadecenoate (a linoleic acid derivative) was positively associated with headache severity. These findings support a potential for DHA-derived oxylipins as prognostic biomarkers for development of chronic PTH.

Chronic Post Traumatic Headaches Unresponsive to Medication Management

Chronic post traumatic headaches (PTH) are being more frequently seen in military medicine due to the increasing prevalence of patients suffering from explosive related head injuries. Data from recent wars in the Middle East have shown a higher proportion of traumatic brain injuries (TBI) caused by blast-related and explosive injuries. Patients who have served in military combat operations in the middle-east have a higher chance to develop PTH related to TBIs. These patients can be difficult to manage as there are limited medication options for the treatment of these headaches in patients. This brief report describes 2 patients who suffered from chronic PTH who failed a multitude of medication management.

Ensuring and maintaining brain health of the combat sport athlete

Professional boxing and mixed martial arts (MMA) are popular sports with high risk for both acute and chronic traumatic brain injury (TBI). Acute catastrophic neurological injuries include subdural hematoma (SDH), epidural hematoma (EDH), subarachnoid hemorrhage (SAH), intracranial hemorrhage (ICH) and second-impact syndrome (SIS). Late-life neuropsychologic sequelae of repeated brain injury include chronic traumatic encephalopathy (CTE), dementia pugilistica, chronic post-concussion syndrome, posttraumatic dementia, posttraumatic cognitive impairment, posttraumatic Parkinsonism and chronic posttraumatic headache. Urgent measures are needed to ensure and maintain the brain health of the combat sport athlete. In the commentary that follows, some of these measures are discussed.

Low-dose interleukin-2 reverses behavioral sensitization in multiple mouse models of headache disorders.

Headache disorders are highly prevalent and debilitating, with limited treatment options. Previous studies indicate that many proinflammatory immune cells contribute to headache pathophysiology. Given the well-recognized role of regulatory T (Treg) cells in maintaining immune homeostasis, we hypothesized that enhancing Treg function may be effective to treat multiple headache disorders. In a mouse model of chronic migraine, we observed that repeated nitroglycerin (NTG, a reliable trigger of migraine in patients) administration doubled the number of CD3 T cells in the trigeminal ganglia without altering the number of Treg cells, suggesting a deficiency in Treg-mediated immune homeostasis. We treated mice with low-dose interleukin-2 (ld-IL2) to preferentially expand and activate endogenous Treg cells. This not only prevented the development of NTG-induced persistent sensitization but also completely reversed the established facial skin hypersensitivity resulting from repeated NTG administration. The effect of ld-IL2 was independent of mouse sex and/or strain. Importantly, ld-IL2 treatment did not alter basal nociceptive responses, and repeated usage did not induce tolerance. The therapeutic effect of ld-IL2 was abolished by Treg depletion and was recapitulated by Treg adoptive transfer. Furthermore, treating mice with ld-IL2 1 to 7 days after mild traumatic brain injury effectively prevented as well as reversed the development of behaviors related to acute and chronic post-traumatic headache. In a model of medication overuse headache, Ld-IL2 completely reversed the cutaneous hypersensitivity induced by repeated administration of sumatriptan. Collectively, this study identifies ld-IL2 as a promising prophylactic for multiple headache disorders with a mechanism distinct from the existing treatment options.

Behavioral treatment for post-traumatic headache after mild traumatic brain injury: Rationale and case series.

Headache is among the most common persistent symptoms after mild traumatic brain injury (mTBI). Currently available treatments have limited efficacy. To present a rationale for a novel behavioral treatment approach and a supporting case series with a multiple baseline design. Pervasive avoidance of common headache triggers may be maladaptive, promoting sensitization and restricting life participation. Graded exposure to triggers that are prone to sensitization (e.g., stress, light flicker, loud noise) may represent an alternative behavioral approach to treating chronic headaches after mTBI. The present study reports on a series of physician-referred patients (N = 4, aged 28-48, enrolled at 9-19 months post-injury) with persistent headache attributed to mTBI. They participated in an 8-session manualized treatment with a registered psychologist. Patients completed a daily headache diary before, during, and after treatment, as well as pre- and post-treatment assessments with a battery of questionnaires. All patients finished treatment and no adverse events were reported. Improvement was variable across measures of headache frequency/intensity, headache trigger avoidance, post-concussion symptoms, disability, and patient global impression of change. Future directions for behavioral management of headache triggers as a potential treatment for chronic post-traumatic headaches after mTBI are discussed.

Decreased grey matter volume in mTBI patients with post-traumatic headache compared to headache-free mTBI patients and healthy controls: a longitudinal MRI study.

Traumatic brain injury (TBI) occurs in 1.7 million people annually and many patients go on to develop persistent disorders including post-traumatic headache (PTH). PTH is considered chronic if it continues past 3months. In this study we aimed to identify changes in cerebral grey matter volume (GMV) associated with PTH in mild TBI patients. 50 mTBI patients (31 Non-PTH; 19 PTH) underwent MRI scans: within 10days post-injury, 1month, 6months and 18months. PTH was assessed at visit 4 by a post-TBI headache questionnaire. Healthy controls (n = 21) were scanned twice 6months apart. Compared to non-PTH, PTH patients had decreased GMV across two large clusters described as the right anterior-parietal (p = 0.012) and left temporal-opercular (p = 0.027). Compared to healthy controls non-PTH patients had decreased GMV in the left thalamus (p = 0.047); PTH patients had decreased GMV in several extensive clusters: left temporal-opercular (p = 0.003), temporal-parietal (p = 0.041), superior frontal gyrus (p = 0.008) and right middle frontal/superior frontal gyrus (0.004) and anterior-parietal (p = 0.003). Differences between PTH and non-PTH patients were most striking at early time points. These early changes may be associated with an increased risk of PTH. Patients with these changes should be monitored for chronic PTH.

Early prophylactic treatment reduces development of chronic post traumatic headache after concussion

BackgroundHeadaches after concussion are common, potentially debilitating, and long lasting. There are currently no guidelines on the treatment of post traumatic headaches (PTH). The aim of this study is to investigate the effects of early prophylactic pharmacologic treatment on the development of chronic post traumatic headaches (cPTH) in adolescent and adult concussion patients.MethodsPatients were retrospectively enrolled from the patient population at the Barrow Concussion and Brain Injury Center (Phoenix, AZ) from the previous 5 years. Males and females ages 13 and older with a diagnosis of PTH attributed to mild head injury based on ICHD2 criteria who were offered a headache prophylactic medication were included. Patients were divided into 3 groups: those who did not take treatment (Untreated), those who took nortriptyline (Nor), and those who took topiramate (Top). Groups were subdivided into those that developed cPTH and those who did not (ncPTH). The average time from injury to start of treatment (SoT) in days were analyzed using t-tests within and between groups.ResultsOne hundred twenty patients met inclusion criteria for the study (Untreated = 36, Top = 46, Nor = 38). Overall, 64 of 120 patients met criteria for cPTH (53%). SoT and development of cPTH is significant overall (35 vs 23, p< 0.001). SoT is significant for Untreated (NcPTH 14.4 vs cPTH 35.6, p = 0.001) and Top (NcPTH 23.9 vs cPTH 35.5, p = 0.002), but not for Nor (NcPTH 31.9 vs cPTH 34.0, p = 0.372). For NcPTH there is a significant difference between SoT for Untreated and Top (14.4 vs 23.9, p = 0.04) and Untreated vs Nor (14.4 vs 31.9, p = 0.002), but not Top and Nor (23.9 vs 31.9, p = 0.09). For cPTH there is no difference for SoT between groups.ConclusionEarly intervention with nonpharmacologic treatments and topiramate is associated with reduced development of cPTH.

Behavioral Therapies and Mind-Body Interventions for Posttraumatic Headache and Post-Concussive Symptoms: A Systematic Review.

There are no clear guidelines on how to treat posttraumatic headache (PTH) or post-concussive symptoms (PCS). However, behavioral interventions such as cognitive behavioral therapy, biofeedback, and relaxation are Level-A evidence-based treatments for headache prevention. To understand how to develop and study further mind-body interventions (MBIs) and behavioral therapies for PTH and PCS, we developed the following question using the PICO framework: Are behavioral therapies and MBIs effective for treating PTH and PCS? We conducted a systematic search of 3 databases (Medline, PsycINFO, and EMBASE) for behavioral interventions and MBIs with the subject headings and keywords for PTH, concussion, and traumatic brain injury (TBI). Inclusion criteria were (1) randomized controlled trials, (2) the majority of the intervention had to be behavioral or mind-body therapy focused, (3) the majority of the participants (>50%) had to have had a mild TBI (not a moderate or severe TBI), (4) published in a peer-reviewed publication, and (5) meeting pre-specified primary and/or secondary outcomes. Primary outcome(s): whether there was a significant change in concussion symptom severity (yes/no) based on the symptom severity checklist/scale used, whether there was a 50% reduction in headache days and/or disability; secondary outcome(s): sleep variables, cognitive complaints, depression, and anxiety. The search identified 917 individual studies. Two independent reviewers screened citations and full-text articles independently. Nineteen articles were pulled for full article review. Seven articles met the final inclusion criteria. The systematic review was registered in Prospero (CRD42017070072). Overall, there was vast heterogeneity across the studies, making it difficult to fully assess efficacy. The heterogeneity ranged from differences in patient populations, the timing of when the interventions were initiated, the types of intervention implemented, and the measures used to assess outcomes. Seven studies were identified as meeting final inclusion criteria, resulting in a total of 1108 adult participants ranging from 18 to 80. Sixty-nine percent were male. Of the 7 studies, 3 were focused on military staff (retired and active). Time post-injury for inclusion into the studies varied from 48 hours post-injury to more than 2 years post-injury. One of the 7 studies did not include time post-TBI in the inclusion criteria. Two studies recruited patients who had visited their emergency departments, 4 of the studies recruited subjects through outpatient referrals, and 1 study recruited patients who had been in a prior traffic accident with resulting chronic PTH directly from a headache center. Group cognitive behavioral therapy (CBT) sessions and telephonic counseling or communication were common intervention methods used in the studies, with group CBT being used in 2 of the studies and telephonic counseling being used in 3. Other intervention methods used included individual CBT, cognitive training, psychoeducation, and computer-based and/or therapist-directed cognitive rehabilitation. Many of the interventions offered vastly different methods of delivery of intervention and doses of intervention. Many of the negative studies were done after an extended duration post-injury (>1-year posttraumatic brain injury [TBI]). In addition, the participants were lumped together regardless of their pre-concussion comorbidities, their mechanism of injury, their symptoms, and the duration from injury to the start of the intervention. The mass heterogeneity found between the studies led to inconclusive findings. Thus, there are various considerations for the design of the intervention for future behavioral/MBI studies for PTH and concussion that must be addressed before the leading question of this review may be effectively answered.

Lifestyle modifications as therapy for medication refractory post-traumatic headache (PTHA) in the military population of Okinawa

ObjectiveOur aim was 1) to reduce disability, as characterized by headache frequency, duration and severity in patients with post-traumatic headache (PTHA), 2) to reduce the number of medical boards and work limitations in patients with post traumatic headache, and 3) to reduce use of medical resources and clinic visits related to headache or migraine.BackgroundModifiable risk factors for PTHA include stressful life event, sleep disturbances, and medication overuse. Cognitive-behavioral strategies, biofeedback, and relaxation therapy may have an important role in treatment and preventing progression to chronic post-traumatic headache (CPTHA). There is limited literature and a known practice gap for implementation of these techniques.Design/methodsAn IRB approved project focused on patients who were seen for PTHA and CPTHA. 1) Intervention consisted of lifestyle teaching, cognitive-behavioral therapy and biofeedback, supplemented by decreasing polypharmacy. 2) Patients were followed for 2 years and a retrospective review was conducted for 2 years prior to presentation. 3) Outcome measures included reduction in migraine intensity or frequency, improved quality of life, duty status, and decreased utilization of clinic visits.ResultsOver the course of one year, 221 patients were treated for migraines in the Naval Okinawa Neurology Clinic. Of these, 22 active duty service members and 3 Dependents suffered a mild TBI prior to onset. After intervention, there was a 36% decrease in PTHA frequency, 56% decrease in headache severity and 60% of patients had improved quality of life as compared to the 2 years prior to intervention. Twenty-four percent had reduction in polypharmacy. Appointment frequency for migraine decreased from an average of 6.8 to 2.6 per year.ConclusionsAn implemented program geared towards reducing polypharmacy was shown to improve safety, quality of life and reduce hospitalizations from the burden of migraines. Our systematic approach resulted in quality of life improvements and decreased use of medical resources.Trial registrationAuthors received the approval of NAVMED West, Okinawa Naval Hospital Institutional Review Board on January 13th, 2016. QI.2016.0021.

Psychological distress, neuroticism and disability associated with secondary chronic headache in the general population \u2013 the Akershus study of chronic headache

BackgroundPrimary headaches are associated with psychological distress, neuroticism and disability. However, little is known about headache-related disability and psychological distress among people with secondary chronic headaches.Methods30,000 persons aged 30–44 from the general population was screened for headache by a questionnaire. The responder rate was 71%. The International Classification of Headache Disorders with supplementary definitions for chronic rhinosinusitis and cervicogenic headache were used. The Hopkins Symptom Checklist-25 assessed high psychological distress, the Migraine Disability Assessment questionnaire assessed disability, and Eysenck Personality Questionnaire assessed neuroticism.ResultsNinety-five of the 113 eligible participants (84%) completed the self-reported questionnaire. A total of 38 people had chronic post-traumatic headache, 21 had cervicogenic headache, and 39 had headache attributed to chronic rhinosinusitis, while 9 had co-occurrence of chronic post-traumatic and cervicogenic headache. Six persons had miscellaneous secondary chronic headaches. Overall, 49% of those with secondary chronic headache reported high psychological distress, which is significantly higher than in the general population. A high level of neuroticism was significantly more common in those with secondary chronic headache than in the general population. Severe headache-related disability was reported by 69%. 92 persons were followed up after 3 years. A low headache frequency was the only significant predictor of improvement of ≥ 25% in headache days. Having post-traumatic or cervicogenic headache and not headache attributed to chronic rhinosinusitis predicted an increased risk > 25% worsening of headache days or having a severe disability at 3 years follow-up.ConclusionPsychological distress and neuroticism were more common among people with secondary chronic headache than in the general population. Only a high headache frequency was significantly associated with increased headache disability at baseline and a poor prognosis in the long term.

Strides Toward Better Understanding of Post-Traumatic Headache Pathophysiology Using Animal Models.

In recent years, the awareness of the detrimental impact of concussion and mild traumatic brain injuries (mTBI) is becoming more apparent. Concussive head trauma results in a constellation of cognitive and somatic symptoms of which post-traumatic headache is the most common. Our understanding of post-traumatic headache is limited by the paucity of well validated, characterized, and clinically relevant animal models with strong predictive validity. In this review, we aim to summarize and discuss current animal models of concussion/mTBI and related data that start to shed light on the pathophysiology of post-traumatic headache. Each of the models will be discussed in terms of their face, construct, and predictive validity as well as overall translational relevance to concussion, mTBI, and post-traumatic headache. Significant contributions to the pathophysiology of PTH garnered from these models are discussed as well as potential contributors to the development of chronic post-traumatic headache. Although post-traumatic headache is one of the most common symptoms following mild head trauma, there remains a disconnect between the study of mild traumatic brain injury and headache in the pre-clinical literature. A greater understanding of the relationship between these phenomena is currently needed to provide more insight into the increasing frequency of this debilitating condition in both military and civilian populations.