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Introduction: Headache is one of the most frequent reported symptom after mild traumatic brain injury and it affects normal functioning and life as a whole. The goal: The goal is the evaluation of access, the quality and characteristics of the headache which occurs after the mild traumatic brain injury. Material and methods: The research has been done as a study section in the clinical center of Vojvodina, in the neurosurgery section. A survey questionnaire constructed for the purposes of this research was used as a research instrument. The survey questionnaire included twenty-one questions.. The norm for including respondents in the research was for them to be hospitalized patients with mild traumatic brain injury and the norm for determining how bad the injury was Glazgow's coma score was used. For determining the intensity of the headache the numeric pain rate scale from zero to ten was used. Results: The posttraumatic headache was present in all patients. Most of the respondents described the headache as dull pain of high intensity, 50% of them said that the headache is disturbing them while doing everyday activities and that the intensity of the pain is worst in the morning than at night. Also, some reported that bright light, thinking and talking increase the pain level. Conclusion: The data from this study indicate that headaches in patients after mild TBI can be a major problem in terms of their functional abilities. Thus, the primary focus of nurses should be on early detection and relief of these symptoms. We can also view this study as an initial step, which can affect nurses' practice, and thus the well-being of patients and society as a whole.

Posttraumatic headache (PTH) is a common debilitating condition arising from head injury and is highly prevalent among military service members and veterans with traumatic brain injury (TBI). Diagnosis and treatment for PTH is still evolving, and surprisingly little is known about the putative mechanisms that drive these headaches. This manuscript describes the design of a randomized clinical trial of two nonpharmacological (i.e., behavioral) interventions for posttraumatic headache. Design of this trial required careful consideration of PTH diagnosis and inclusion criteria, which was challenging due to the lack of standard clinical characteristics in PTH unique from other types of headaches. The treatments under study differed in clinical focus and dose (i.e., number of treatment sessions), but the trial was designed to balance the treatments as well as possible. Finally, while the primary endpoints for pain research can vary from assessments of pain intensity to objective and subjective functional measures, this trial of PTH interventions chose carefully to establish clinically relevant endpoints and to maximize the opportunity to detect significant differences between groups with two primary outcomes. All these issues are discussed in this manuscript.

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.

Background Post-traumatic headache (PTH) is one of the most common and long-lasting symptoms following mild traumatic brain injury (TBI). However, the pathological mechanisms underlying the development of persistent PTH remain poorly understood. The primary purpose of this prospective pilot study was to evaluate whether early pain modulatory profiles (sensitization and endogenous pain inhibitory capacity) and psychological factors after mild TBI predict the development of persistent PTH in mild TBI patients. Methods Adult mild TBI patients recruited from Level I Emergency Department Trauma Centers completed study sessions at 1–2 weeks, 1-month, and 4-months post mild TBI. Participants completed the following outcome measures during each session: conditioned pain modulation to measure endogenous pain inhibitory capacity, temporal summation of pain and pressure pain thresholds of the head to measure sensitization of the head, Pain Catastrophizing Scale, Center for Epidemiological Studies – Depression Scale, and a standardized headache survey. Participants were classified into persistent PTH (PPTH) and no-PPTH groups based on the 4-month data. Results The results revealed that mild TBI patients developing persistent PTH exhibited significantly diminished pain inhibitory capacity, and greater depression and pain catastrophizing following injury compared to those who do not develop persistent PTH. Furthermore, logistic regression indicated that headache pain intensity at 1–2 weeks and pain inhibitory capacity on the conditioned pain modulation test at 1–2 weeks predicted persistent PTH classification at 4 months post injury. Conclusions Overall, the results suggested that persistent PTH is characterized by dysfunctional alterations in endogenous pain modulatory function and psychological processes in the early stages following mild TBI, which likely exacerbate risk for the maintenance of PTH.

Background Mild 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. Methods Seventy-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. Results At 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. Conclusion The 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 registration ClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.

Introduction Posttraumatic headache is one of the most common, debilitating, and difficult symptoms to manage after a traumatic head injury. The development of novel therapeutic approaches is nevertheless hampered by the paucity of preclinical models and poor understanding of the mechanisms underlying posttraumatic headache. To address these shortcomings, we previously characterized the development of posttraumatic headache-like pain behaviors in rats subjected to a single mild closed head injury using a 250 g weight drop. Here, we conducted a follow-up study to further extend the preclinical research toolbox for studying posttraumatic headache by exploring the development of headache-like pain behaviors in male rats subjected to a single, but more severe head trauma (450 g) as well as following repetitive, subconcussive head impacts (150 g). In addition, we tested whether these behaviors involve peripheral calcitonin gene-related peptide signaling by testing the effect of systemic treatment with an anti-calcitonin gene-related peptide monoclonal antibody (anti-calcitonin gene-related peptide mAb). Methods Adult male Sprague Dawley rats (total n = 138) were subjected to diffuse closed head injury using a weight-drop device, or a sham procedure. Three injury paradigms were employed: A single hit, using 450 g or 150 g weight drop, and three successive 150 g weight drop events conducted 72 hours apart. Changes in open field activity and development of cephalic and extracephalic tactile pain hypersensitivity were assessed up to 42 days post head trauma. Systemic administration of the anti-calcitonin gene-related peptide mAb or its control IgG (30 mg/kg) began immediately after the 450 g injury or the third 150 g weight drop with additional doses given every 6 days subsequently. Results Rats subjected to 450 g closed head injury displayed an acute decrease in rearing and increased thigmotaxis, together with cephalic tactile pain hypersensitivity that resolved by 6 weeks post-injury. Injured animals also displayed delayed and prolonged extracephalic tactile pain hypersensitivity that remained present at 6 weeks post-injury. Repetitive subconcussive head impacts using the 150 g weight drop, but not a single event, led to decreased vertical rearing as well as cephalic and extracephalic tactile pain hypersensitivity that resolved by 6 weeks post-injury. Early and prolonged anti-calcitonin gene-related peptide mAb treatment inhibited the development of the cephalic tactile pain hypersensitivity in both the severe and repetitive subconcussive head impact models. Conclusions Severe head injury gives rise to a prolonged state of cephalic and extracephalic tactile pain hypersensitivity. These pain behaviors also develop following repetitive, subconcussive head impacts. Extended cephalic tactile pain hypersensitivity following severe and repetitive mild closed head injury are ameliorated by early and prolonged anti-calcitonin gene-related peptide mAb treatment, suggesting a mechanism linked to calcitonin gene-related peptide signaling, potentially of trigeminal origin.

Background Most persistent posttraumatic headaches (PPTH) have a phenotype that meets diagnostic criteria for migraine or probable migraine. Although symptoms of autonomic dysfunction have been well described among those with migraine, the presence and relative severity of such symptoms among those with PPTH have yet to be reported. Objective The objective of this study was to assess and compare symptoms of autonomic dysfunction among those with PPTH attributed to mild traumatic brain injury (mTBI) vs migraine vs healthy controls using Composite Autonomic Symptom Score 31 (COMPASS-31) questionnaire scores. Methods Individuals with PPTH (n = 56) (87.5% of whom had a migraine/probable migraine phenotype), migraine (n = 30), and healthy controls (n = 36) were prospectively assessed in this cross-sectional cohort study using the COMPASS-31 questionnaire. Total COMPASS-31 scores and individual domain scores (bladder, gastrointestinal, orthostatic intolerance, pupillomotor, secretomotor, vasomotor) were compared between subject groups. Results COMPASS-31 mean total weighted score was 37.22 ± 15.44 in the PPTH group, 27.15 ± 14.37 in the migraine group, and 11.67 ± 8.98 for healthy controls. COMPASS-31 mean weighted total scores were significantly higher in those with PPTH vs migraine (P = .014), for PPTH vs healthy controls (P = .001), and for migraine vs healthy controls (P = .001). Those with PPTH had numerically higher scores for all COMPASS-31 domains compared to those with migraine, and the domain scores were significantly higher for orthostatic intolerance (PPTH = 4.80 ± 2.47 vs migraine = 3.33 ± 2.31, P = .027) and bladder (PPTH = 1.14 ± 1.45 vs migraine = 0.47 ± 0.73, P = .020). Among individuals with PPTH, post hoc correlations indicated a positive association between number of total lifetime TBIs with total weighted COMPASS-31 scores (rho = 0.32, P = .020), between years lived with headache and vasomotor domain subscores (rho = 0.27; P = .044), and between headache frequency with vasomotor domain subscores (rho = 0.27; P = .041). Conclusions Symptoms of autonomic dysfunction were greatest among those with PPTH compared to migraine and healthy controls. Among individuals with PPTH, number of lifetime TBIs was associated with greater symptoms of autonomic dysfunction, while greater headache burden was associated with higher vasomotor domain autonomic dysfunction subscores, potentially indicating that PPTH patients with higher disease burden have an increased risk for having autonomic dysfunction. Symptoms of autonomic dysfunction should be ascertained during the clinical management of patients with PPTH and might be a characteristic that helps differentiate PPTH from migraine.

Background Excessive daytime sleepiness (EDS, defined as Epworth sleepiness scale score > 10) is a common symptom, with a prevalence of 10–20% in the general population. It is associated with headache and other chronic pain disorders. However, little is known about the prevalence of EDS among people with secondary chronic headaches. Findings A total of 30,000 persons aged 30–44 from the general population was screened for headache by a questionnaire. The 633 eligible participants with self-reported chronic headache were interviewed and examined by a headache specialist who applied the International Classification of Headache Disorders with supplementary definitions for chronic rhinosinusitis and cervicogenic headache. A total of 93 participants had secondary chronic headache and completed the ESS. A total of 47 participants had chronic post-traumatic headache (CPTH) and/or cervicogenic headache (CEH), 39 participants had headache attributed to chronic rhinosinusitis (HACRS), while 7 had other secondary headaches. 23.3% of those with CPTH, CEH or HACRS reported EDS. In multivariable logistic regression analysis the odds ratios of EDS were not significantly different in people with CPTH/CEH or HACRS. Conclusion Almost one out of four subjects with secondary chronic headache reported EDS with no differences between the various secondary chronic headaches.

Objective:This review provides an in-depth overview of diagnostic schema and risk factors influencing recovery during the acute, subacute (operationally defined as up to 3 months postinjury), and chronic injury phases across the full spectrum of individuals (e.g., athletes to neurosurgery patients) with mild traumatic brain injury (mTBI). Particular emphasis is placed on the complex differential diagnoses for patients with prolonged postconcussive symptoms.Methods:Select literature review and synthesis.Results:In spite of an increase in public awareness surrounding the acute and potential long-term effects of mTBI, the medical field remains fragmented both in terms of the diagnostic (different criteria proffered by multiple medical organizations) and prognostic factors that influence patient care.Conclusions:Given the lack of objective biomarkers and the spectrum of different disorders that likely encompass mTBI, clinicians are encouraged to adopt a probabilistic, rather than definitive, diagnostic and prognostic framework. The relevance of accurately diagnosing and managing the different manifestations of mTBI becomes clear when one considers the overall incidence of the disorder (42 million people each year worldwide), and the different treatment implications for patients with a true neurodegenerative disorder (e.g., chronic traumatic encephalopathy; rare) vs potentially treatable conditions (e.g., depression or posttraumatic headache; frequent).

OBJECTIVES/GOALS: Military personnel are at significantly greater risk for developing tinnitus, due to increased exposure to acoustic trauma. Many psychiatric disorders are common among individuals with chronic tinnitus, including posttraumatic stress disorder (PTSD). Although tinnitus and PTSD are clearly different, research supports the notion of shared mechanisms between both disorders. First, there are overlapping symptoms between tinnitus-related distress and PTSD, including irritability, distorted cognitions, persistent negative emotional states, diminished interests in activities, exaggerated startle response, sleep disturbance, concentration problems, and hypervigilance. Second, tinnitus and PTSD are highly comorbid with one another, whereas 34% of veterans with tinnitus also carry a PTSD diagnosis. Third, those with both disorders are significantly more emotionally impaired compared to those with tinnitus and any other psychiatric disorder. Lastly, neuroimaging research has shown similar regions within the auditory vigilance network are implicated among those with tinnitus, and separately, among combat PTSD patients, suggesting shared neurobiological mechanisms between both disorders. Though we are aware that tinnitus and comorbid PTSD presents as a significantly greater clinical concern, the relationship between tinnitus-related distress and PTSD symptomotology it is still unknown. Canonical correlation analyses will be conducted to examine the relationship between tinnitus-related distress and PTSD among veterans as a part of a larger clinical trial for posttraumatic headache. Results of the study will shed light on the relationship between tinnitus-related distress and PTSD, and may suggest a different phenotype for those with both disorders. Researchers and clinicians will further understand and conceptualize the relationships among the cognitive, emotional, and behavioral symptoms associated with tinnitus and PTSD, both individually and conjointly. METHODS/STUDY POPULATION: Baseline data (N = 112) from a larger clinical trial examining the effectiveness of two different psychotherapies for the alleviation of posttraumatic headache was examined. The primary aim of this project was to evaluate the relationship between tinnitus-related distress and PTSD based on the eight subscale scores of the Tinnitus Functional Index (TFI) and the four scales of the Clinician Administered PTSD Scale for the DSM-5 (CAPS-5), respectively. To address this aim, canonical correlation analysis was used where the tinnitus-related symptom subscales made up one variable set and PTSD symptom subscales made up the second variable set. First, we evaluated the overall model fit based on Wilks Lambda to determine if the two variable sets were related at the p < .05 level. Next, we evaluated the canonical correlations (comparable to an eigenvalue) for each canonical dimension to determine the required number of significant canonical dimensions (or latent constructs) that were necessary to understand the association between the two variable sets. Finally, the standardized canonical coefficients, which are analogous to regression coefficients, evaluate the magnitude of variate relationships and determine which subscales best describe significant canonical dimensions. RESULTS/ANTICIPATED RESULTS: Prior to the canonical correlation analysis, total score descriptive statistics and subscale score zero-order correlations were carried out. The CAPS-5 total score was 33.24 (SD = 9.39) and the TFI total score was 50.81 (SD = 21.88) in this sample. Interpretation of the zero-order correlations indicated that TFI Relaxation subscale was the only tinnitus-related subscale moderately associated with a PTSD subscale (i.e., Reexperiencing, r = .35). Canonical correlation omnibus model fit analysis via the Wilks Lambda overall multivariate test indicated that the tinnitus variable set was significantly associated with the PTSD variable set, F = 1.55, p = .04. Evaluation of the canonical correlations indicated that one dimension was significant in explaining the relationship between the two variable sets and accounted for 25% of the overall variance, F = 1.55, p < .04, R2 = .249. Standardized canonical coefficients indicated that the PTSD subscales Reexperiencing (b = 0.64) and Negative Alterations in Cognition and Mood (b = 0.55) were the most representative of the identified canonical dimension. In terms of the TFI, the Relaxation (b = 1.28) and Sleep (b = 0.72) subscales appeared to be most related to the canonical dimension. The TFI subscales Auditory Difficulty (b = −0.30) and Quality of Life (b = 0.30) also appeared to be related the canonical dimension to a lesser degree. DISCUSSION/SIGNIFICANCE OF IMPACT: Findings support prior research suggesting particularly deleterious functional outcomes among individuals with comorbid tinnitus and PTSD. Results of this study suggest a latent variable that can explain the unique experience of individuals with both disorders. This latent variable consists of two PTSD constructs: Reexperiencing traumatic events (i.e., flashbacks, nightmares, intrusive memories), and Negative Alterations in Cognition and Mood (i.e., self- and other-blame, strong negative feelings, loss of interest, feeling distant). This latent variable also consists of two tinnitus-related constructs: Sleep (i.e., trouble falling and staying asleep, peaceful sleep) and Relaxation (i.e., ability to relax, enjoyment of peace and quiet). Auditory Difficulty (i.e., hear clearly, understand people) and Quality of Life (i.e., social activities, relationships, difficulty performing tasks) also contributed to the latent variable, but to a lesser degree. It is suggested that the constellation of symptoms related to the latent variable is a Dysphoric Factor, unique to individuals with PTSD, tinnitus, and posttraumatic headache. It may be necessary to incorporate different techniques into existing evidence-based treatments for both tinnitus and PTSD, for optimal symptom improvement.

Objective To report the observed effect of erenumab in mild posttraumatic headache migraine phenotype with and without aura. Background There is no clinical algorithm of pharmacotherapy for migraine following posttraumatic headache. Most migraine preventatives that are typically used are either ineffective or not tolerated. Methods Seven patients who met the clinical criteria for migraine with or without aura following posttraumatic headache who failed or were intolerant of conventional migraine preventatives were treated with erenumab 140 mg subcutaneously. Most had no history of migraine. In those patients with a history of migraine, the posttraumatic headache migraine headaches were different than the past migraine experience. Descriptive headache intensity or disability using the Head Impact Test-6 and monthly headache days were recorded before and after treatment. All patients were debilitated on presentation and demonstrated no signs of spontaneous resolution. Results Patients responded with a 95% (SD 1.22, p Conclusions Erenumab is effective in the treatment of posttraumatic headache with migraine phenotype in this small cohort. Large-scale studies are urgently required for this highly prevalent, disabling, condition which has no effective established treatment.

BackgroundLight sensitivity can be a disabling symptom in posttraumatic headache (PTH). The objective of this pilot study was to characterize photophobia symptoms and visual pain thresholds in PTH compared to healthy controls (HC).MethodsIndividuals with PTH attributed to mild traumatic brain injury (mTBI) (N = 18) and HC (N = 20), aged 18–65, were prospectively assessed using the Photosensitivity Assessment Questionnaire (PAQ), State Trait Anxiety Inventory (STAI), and Beck Depression Inventory (BDI). A progressive light stimulation device was used to quantify visual pain thresholds. Visual pain thresholds were determined by the intensity of light at which subjects first noted pain. The mean of 3 trials was considered the visual pain threshold. Two sample t-test, Wilcoxon rank sum test, χ2 test and Fisher exact test was used to compare the 2 groups for their demographics, clinical characteristics, and outcomes measures.ResultsThere were no differences in demographics including age, gender, or race. The average time since onset of PTH was 50.7 (73.6) months. Those with PTH had 15.8 (9.2) headache days per month. BDI and STAI scores were significantly higher in PTH compared to HC. Photophobia was higher in PTH compared to HC, 0.64 (0.25) vs 0.24 (0.24), p < 0.0001. Visual pain thresholds were lower in PTH (median 50.1 lux; quartiles 15.3 to 300.0) compared to HC (median 863.5 lux; quartiles 519.9 to 4,906.5; p = 0.0002).ConclusionPhotophobia symptoms are higher and visual pain thresholds are lower in PTH compared to HC. Light sensitivity is a well-known disabling symptom in PTH and this pilot study provides objective data through a validated photophobia scale and visual pain thresholds to characterize light sensitivity. Additional studies are needed to confirm this data, to compare acute to persistent PTH, to compare PTH to other headache disorders, and to determine if photophobia and visual pain thresholds will improve with intervention.

Repeat CT or MRI of the brain should be considered in posttraumatic headache. We describe two patients with posttraumatic headache who had negative CT scans on initial presentation. One patient later had bilateral subdural hematomas on CT, and the other had temporal lobe hemorrhage on MRI. We recommend considering repeat CT or MRI for persisting posttraumatic headache and mental status change.

Kopfschmerzen nach Schädel-Hirn-Traumen sind in der ärztlichen Begutachtung eine häufige Beschwerde. Die Genese ist umstritten und die diesbezügliche Evidenzlage unzureichend. In einer prospektiven Studie wurden 124 Patienten nach einem Schädel-Hirn-Trauma während der frührehabilitativen Phase B (im Mittelwert 42 Jahre alt, 27% weiblichen Geschlechts) untersucht und die Häufigkeit, die Art, der Verlauf sowie die Behandlungsergebnisse von Kopfschmerzsyndromen erfasst. Entsprechend den Kriterien des National Institute of Health Traumatic Coma Data Bank erfolgte die Einteilung des Schädel-Hirn-Traumas in leichtgradig (3%), mittelgradig (9%) und schwergradig (88%). Das mittlere Zeitintervall zwischen dem Schädel-Hirn-Trauma-Ereignis und dem Studieneinschluss betrug 28 Tage (Range 3-103 Tage). In 61% der Fälle waren Verkehrsunfälle, in 36% der Fälle Stürze im Arbeits- und Freizeitbereich und in 3% der Fälle andere Ursachen für das Trauma verantwortlich. Die Einteilung der Kopfschmerzen erfolgte nach den Kriterien des Headache Classification Committee of the International Headache Society. Die Kopfschmerzen wurden in migränös, Kopfschmerzen vom Spannungstyp, Kopfschmerz infolge Infekt oder neurochirurgischer Intervention und in nicht klassifizierbare Kopfschmerzen unterteilt. Des Weiteren wurden die Dauer des Kopfschmerzes, mit einer Einteilung in episodisch und chronisch, sowie die Häufigkeit des Auftretens, als einmalige oder wiederkehrende Episoden, untersucht. Insgesamt berichteten 18% (n=22) der Patienten [95% CI: 10%-24%] über Kopfschmerzen. Diese standen im Zusammenhang mit Infektionen (n=11), neurochirurgischen Interventionen (n=6) sowie Stürzen während der Rehabilitations-phase (n=4) und zeigten sich zügig regredient. Lediglich ein Patient (1%) beklagte einen kontinuierlichen, kaum veränderlichen Kalottenklopfschmerz nach einer lokalen Gewalteinwirkung auf den Schädel mit einer Skalpverletzung und Einzelnervläsion. Dieser Kopfschmerz wurde als neuropathischer Schmerz gewertet. Während einer mittleren Beobachtungszeit von 68 Tagen (Range 2-247 Tage) berichtete kein Patient über einen chronischen oder episodischen Kopfschmerz vom migränösen Typ, vom Spannungstyp oder einem nicht klassifizierten Kopfschmerz. Weder in den Schweregraden des Schädel- Hirn-Traumas noch im Verletzungsmuster des Gehirns oder innerhalb der verschiedenen Schädel-Hirn-Trauma-Ursachen fanden sich Unterschiede in der Häufigkeit von Kopfschmerzsyndromen oder in der Analyse der Kopfschmerzformen. Auch wurden Kopfschmerzsyndrome bei den in der Studie eingeschlossenen Patienten mit einem leichtgradigen Schädel-Hirn-Trauma (3%) nicht beobachtet. Schlussfolgerung: 1.In der Phase der Frührehabilitation nach einem Schädel- Hirn-Trauma besteht eine niedrige Inzidenz und geringe klinische Wertigkeit von Kopfschmerzsyndromen. 2.In dieser Krankheitsphase ergibt sich kein Hinweis für das Auftreten eines sogenannten posttraumatischen Kopfschmerzes. Vielmehr waren die beobachteten Kopfschmerzen mit anderen Kausalitäten, wie Infekten, neurochirurgischen Interventionen oder Stürzen assoziiert und reversibel. Ein pathophysiologischer Zusammenhang für das Auftreten eines posttraumatischen Kopfschmerzes nach einem Schädel-Hirn-Trauma konnte nicht abgeleitet werden., Headache is a frequent complaint in the medio-legal evaluation of brain trauma victims. However, the etiology of posttraumatic headache remains controversial, and data from systematic prospective assessments of headache syndromes following brain trauma is scarce. In a prospective study, 124 patients after traumatic brain injury during the early brain trauma rehabilitation (age 42 years, 27% female) were studied, and the frequency, type, course, and treatment response of headache syndromes was recorded. The classification of brain trauma based on the criteria of the National Institute of Health Traumatic Coma Data Bank in mild (3%), moderate (9%) and severe (88%). The mean time interval between brain trauma and study inclusion was 28 days (range 3-103 days). Causes of brain trauma were motor vehicle (61%), work-place and home accidents (36%), and other trauma events (3%). Headache was classified by criteria of the Headache Classification Committee of the International Headache Society in migrainous, tension type, unclassified, and headache associated with infections and surgical procedures. Duration (episodic, chronic) and frequency (single versus recurrent episodes) of headaches were recorded. A total of 22 patients (18%, CI 10% to 24%) reported headaches associated with infections (n=11), neurosurgical interventions (n=6), and falls with head trauma during rehabilitation (n=4) and were rapidly reversible. One additional patient (1%) persistently complained of a circumscribed local pain on scalp palpation. This headache was considered as neuropathic pain. During a mean observation period of 68 days (range 2-247days) no patient (0%, CI 0% to 3%) revealed chronic or recurrent episodic headaches of migrainous, tension or unclassified type. The frequency of headache syndromes neither differed significantly in strata of mild to moderate versus severe brain trauma nor by brain lesion pattern or clinical outcome. Analyses by headache subtypes, by different causes of brain trauma revealed similar results. Also were no headache syndromes in those included in the study, patients with mild brain trauma (3%). Conclusion: 1.In the setting of early brain trauma rehabilitation, our findings suggest a low incidence and minor clinical importance of headache syndromes following brain trauma. 2.In this phase of the disease is no evidence for the occurrence of a so-called post-traumatic headache. The observed headaches were other causalities, such as infections, associated with neurosurgical interventions or falls, and reversible. A pathophysiological context for the appearance of posttraumatic headache after a brain trauma could not be established.

Concussive head injury opens a temporary window of brain vulnerability due to the impairment of cellular energetic metabolism. As experimentally demonstrated, a second mild injury occurring during this period can lead to severe brain damage, a condition clinically described as the second impact syndrome. To corroborate the validity of proton magnetic resonance spectroscopy in monitoring cerebral metabolic changes following mild traumatic brain injury, apart from the magnetic field strength (1.5 or 3.0 T) and mode of acquisition, we undertook a multicentre prospective study in which a cohort of 40 athletes suffering from concussion and a group of 30 control healthy subjects were admitted. Athletes (aged 16-35 years) were recruited and examined at three different institutions between September 2007 and June 2009. They underwent assessment of brain metabolism at 3, 15, 22 and 30 days post-injury through proton magnetic resonance spectroscopy for the determination of N-acetylaspartate, creatine and choline-containing compounds. Values of these representative brain metabolites were compared with those observed in the group of non-injured controls. Comparison of spectroscopic data, obtained in controls using different field strength and/or mode of acquisition, did not show any difference in the brain metabolite ratios. Athletes with concussion exhibited the most significant alteration of metabolite ratios at Day 3 post-injury (N-acetylaspartate/creatine: -17.6%, N-acetylaspartate/choline: -21.4%; P

We investigated 112 patients [mean age 39.5 +/- 10.5 years, 59% women (n=66)] with chronic posttraumatic headache following cranio-cervical acceleration/deceleration trauma after an average time interval of 2.5 +/- 1.9 years from trauma. Headache following minor head injury or whiplash is one of the most prominent problems in neurotraumatology. Previous research is inconclusive regarding the symptomatic approach of this type of headache. Details of the phenomenology of posttraumatic headache in the previous literature are inconclusive. This may lead to inappropriate treatment strategies, because recent advances in therapy of different headache types may be neglected. Patients were investigated at the outpatient service of the Department of Psychiatry. Headache was analyzed according to its principal location, laterality, projection, quality, precipitation or aggravation and possible additional symptoms. For this analysis, headache was diagnosed according to the classification of the International Headache Society. The results showed that 42 patients (37%) had tension-type headache, 30 (27%) were identified as suffering from migraine, whereas 20 patients (18%) had cervicogenic headache. An additional 18% of patients suffered from headache that did not fulfill criteria of a particular category. In 104 patients (93%), neck pain was associated in time with headache. Each of the diagnosed headache types in this study may require specific treatment strategies based upon empirical studies of non-traumatic headache types. For these reasons a detailed analysis of headache following cranio-cervical acceleration/deceleration trauma is necessary.

Patients with chronic posttraumatic headache (CPTH) after mild traumatic brain injury may develop multiple emotional, cognitive and somatic symptoms but these symptoms are often unspecific and reported among other headache patients, too. The aim is to investigate whether CPTH patients report more symptoms in general and with a higher severity of these symptoms than other headache patients.

Little is known about chronic posttraumatic headache (PTH) in children and adolescents. In this study we report on symptoms, clinical findings, and management of all children seen in our headache clinic who presented with recurrent headache following head injuries. A total of 23 children were identified over a period of 4 years. Twenty-one children (13 male, eight female; mean age 11.2 years, age range 3.3 to 14.9 years, median 12.1 years) fulfilled the International Headache Society's clinical criteria for the diagnosis of chronic PTH. Mean duration of headache was 13.3 months (range 2 to 60 months, median 7 months). Children were followed up for a period of 5 to 29 months (mean 12.5 months, median 9 months). Head injuries were classified as serious in four patients and minor in 17. Clinical variables were compared between children with PTH and those without a history of head injury. The headaches were migraine in five patients, tension type in 13, and mixed in three patients. Tension-type headache was significantly more common in children with chronic PTH than in those with no history of head injury, but the clinical course was comparable in the two groups.

Background Chronic headache following traumatic brain injury (TBI) sustained in military service, while common, is highly challenging to treat with existing pharmacologic and non-pharmacologic interventions and may be complicated by co-morbid posttraumatic stress. Recently, a novel form of brainwave-based intervention known as the Flexyx Neurotherapy System (FNS) that involves minute pulses of electromagnetic energy stimulation of brainwave activity has been suggested as a means to address symptoms of TBI. This study reports on a clinical series of patients with chronic headache following service-connected TBI treated with FNS. Methods Nine veterans of the wars in Afghanistan and Iraq with moderate to severe chronic headaches following service-connected TBI and complicated by posttraumatic stress symptoms were treated in 20 individual FNS sessions at the Brain Wellness and Biofeedback Center of Washington (in Bethesda, Maryland, USA). They periodically completed measures including the Brief Pain Inventory-Headache (BPI-HA) past week worst and average pain ratings, the Posttraumatic Stress Disorder Checklist-Military version (PCL-M), and individual treatment session numerical rating scale (NRS) for degree of cognitive dysfunction. Data analyses included beginning to end of treatment t-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS. Results All beginning to end of treatment t-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS indicated statistically significant decreases. All but one participant experienced reduction in headaches along with reductions in posttraumatic stress and perceived cognitive dysfunction, with a subset experiencing virtual elimination of headaches. One participant obtained modest headache relief but no improvement in posttraumatic stress or cognitive dysfunction. Conclusions FNS may be a potentially efficacious treatment for chronic posttraumatic headache sustained in military service. Further research is needed to investigate the efficacy of FNS within a randomized, controlled clinical trial, to identify characteristics of those most likely to respond, and to explore underlying mechanisms that may contribute to improvement.

BACKGROUND Posttraumatic headache (PTH) occurs in up to 82% of patients with traumatic brain injury (TBI). Posttraumatic stress disorder (PTSD) occurs in 39% of those with PTH. This study evaluates whether PTSD affects PTH disability. METHODS Eighty-six patients with TBI were prospectively evaluated in a secondary care trauma center. Headache disability was assessed using the Headache Impact Test version 6 and signs indicative of PTSD using the PTSD Check List Civilian version. RESULTS Increased PTSD-type symptoms were significantly associated with increased headache disability (p