A Case‐Control Study on Cortical Thickness in Episodic Cluster Headache

Objective.— This study aims at investigating cortical thickness in cluster headache patients as compared with a healthy control group. Background.— The pathobiology of cluster headache is not yet fully understood, although a dysfunction of the hypothalamus has been suggested to be causal. Previous studies in migraine and trigeminal neuropathic pain have demonstrated changes in cortical thickness using cortex segmentation techniques, but no data have been published on cluster headache. Methods.— We investigated 12 men with episodic cluster headache during a phase without acute headache as well as age and sex‐matched healthy controls using high resolution T1‐weighted magnetic resonance imaging acquired at 3T and performed a categorical whole‐brain surface‐based comparison of cortical thickness between groups. Furthermore, a correlation analysis of disease duration and cortical thickness was conducted. Results.— In comparison with control subjects, we found a reduction of cortical thickness in the angular gyrus and the precentral gyrus in cluster headache patients contralaterally to the headache side. These reductions did not correlate with disease duration. The cortical thickness of an area within the primary sensory cortex correlated with disease duration. Conclusions.— This study demonstrates alterations in cortical thickness in cluster headache patients suggesting a potential role of cortical structures in cluster headache pathogenesis. However, it cannot be determined from this study whether the changes are cause or consequence of the disorder. The correlation of cortical thickness with disease duration in the somatosensory cortex may suggest disease‐related plasticity in the somatosensory system.     

Post‐Traumatic Headaches in Civilians and Military Personnel: A Comparative,Clinical Review

Post‐traumatic headache (PTH) is the most frequent symptom after traumatic brain injury (TBI). We review the epidemiology and characterization of PTH in military and civilian settings. PTH appears to be more likely to develop following mild TBI (concussion) compared with moderate or severe TBI. PTH often clinically resembles primary headache disorders, usually migraine. For migraine‐like PTH, individuals who had the most severe headache pain had the highest headache frequencies. Based on studies to date in both civilian and military settings, we recommend changes to the current definition of PTH. Anxiety disorders such as post‐traumatic stress disorder (PTSD) are frequently associated with TBI, especially in military populations and in combat settings. PTSD can complicate treatment of PTH as a comorbid condition of post‐concussion syndrome. PTH should not be treated as an isolated condition. Comorbid conditions such as PTSD and sleep disturbances also need to be treated. Double‐blind placebo‐controlled trials in PTH population are necessary to see whether similar phenotypes in the primary headache disorders and PTH will respond similarly to treatment. Until blinded treatment trials are completed, we suggest that, when possible, PTH be treated as one would treat the primary headache disorder(s) that the PTH most closely resembles.     

Management of post‐traumatic headaches in children and adolescents

Traumatic brain injuries (TBI) occur in an estimated 475,000 children aged 0–14 each year. Worldwide, mild traumatic brain injuries (mTBI) represent around 75–90% of all hospital admissions for TBI. mTBI are a common occurrence in children and adolescents, particularly in those involved in athletic activities. An estimated 1.6–3.8 million sports‐related TBIs occur each year, including those for which no medical care is sought. Headache is a common occurrence following TBI, reported in as many as 86% of high school and college athletes who have suffered from head trauma. As most clinicians who manage concussion and post‐traumatic headaches (PTHs) can attest, these headaches may be difficult to treat. There are currently no established guidelines for the treatment of PTHs, especially when persistent, and practices can vary widely from one clinician to the next. Making medical management more challenging, there are currently no randomized controlled trials evaluating the efficacy of therapies for PTHs in children and adolescents.     

Persistent Post‐Traumatic Headache,Postconcussion Syndrome,and Whiplash Injuries: The Evidence for a Non‐Traumatic Basis With an Historical Review

There has been intense controversy about postconcussion syndrome since Erichsen's publication in 1866 on railway brain and railway spine. The fascinating history of this debate will be reviewed and then the non‐organic explanations for postconcussion syndrome, headaches after head injury, and chronic whiplash injuries and headaches will be explored including the following: psychogenic, psychosocial, sociocultural, base rate misattribution, chronic pain, compensation and litigation, and malingering.     

Traumatic Brain Injury,Neuroinflammation, and Post‐Traumatic Headaches

Concussions following head and/or neck injury are common, and although most people with mild injuries recover uneventfully, a subset of individuals develop persistent post‐concussive symptoms that often include headaches. Post‐traumatic headaches vary in presentation and may progress to become chronic and in some cases debilitating. Little is known about the pathogenesis of post‐traumatic headaches, although shared pathophysiology with that of the brain injury is suspected. Following primary injury to brain tissues, inflammation rapidly ensues; while this inflammatory response initially provides a defensive/reparative function, it can persist beyond its beneficial effect, potentially leading to secondary injuries because of alterations in neuronal excitability, axonal integrity, central processing, and other changes. These changes may account for the neurological symptoms often observed after traumatic brain injury, including headaches. This review considers selected aspects of the inflammatory response following traumatic brain injury, with an emphasis on the role of glial cells as mediators of maladaptive post‐traumatic inflammation.     

Proton Spectroscopy in Patients With Post-Traumatic Headache Attributed to Mild Head Injury

Background.— Post traumatic headaches (PTH) following mild head injury (MHI) impose important diagnostic challenges to clinicians, and are often the scope of litigation.
Objective.— To investigate whether spectroscopy magnetic resonance imaging (MRS) demonstrates markers of PTH following MHI.
Methods.— We imaged individuals with PTH following MHI (n = 17), as well as controls (n = 12), using Proton MRS (1-HS MRI). We estimated the metabolic ratios of N-acetylaspartate (NAA) and choline (Cho), relative to creatine (Cr). Compared with controls, individuals with PTH following MHI had reduced values of NAA in the right (1.64 ppm vs 2.05 ppm, P  = .012) and left anterior regions of the frontal lobe white matter (1.52 ppm vs 2.10 ppm; P  = .024); anterior (1.52 ppm vs 1.78 ppm; P  = .0155) and posterior medial region of the frontal lobes (1.6 ppm vs 2.07 ppm; P  = .0045), and medial region of parietal lobes (1.76 ppm vs 2.23 ppm; P  = .0065). Contrasted to controls, Cho measures were statistically increased in the posterior region of the white matter of the right side fontal lobe (1.18 ppm vs 0.99 ppm; P  = .0095), anterior medial region of the frontal lobe (1.20 ppm; vs 1.07 ppm; P  = .0265), and medial region of the parietal lobes (0.92 ppm vs 0.65 ppm; P  = .0005).
Conclusions.— Proton MRS may be useful as an imaging marker for PTH following mild injury. Future studies should contrast PTH following mild vs severe trauma, as well as PTH with other forms of headache, to clarify if the findings are specific of the disease, may be correlated with disease severity, or if they are unspecific headache markers.     

Frequency of Magnetic Resonance Imaging Abnormalities in Patients With Migraine

Background.-The frequency of magnetic resonance imaging (MRI) abnormalities in patients with migraine has been reported at 12% to 46%. We examined a series of patients to determine the frequency of MRI abnormalities, and any relationship of frequency with patient age, sex, migraine type, duration of symptoms, and other medical conditions.
Methods.-Magnetic resonance imaging findings were reviewed retrospectively with respect to presence of focal white matter hyperintensities in 185 consecutive patients. Patients had been diagnosed with migraine by a neurologist. All images had been interpreted by a neuroradiologist. Clinical information was obtained by chart review.
Results.-Sixteen percent had focal white matter abnormalities. Among patients less than 50 years old, and without other medical problems such as hypertension, atherosclerotic heart disease, diabetes mellitus, autoimmune disorder or demyelinating disease, only 6% had white matter abnormalities. Increased frequency of white matter abnormalities was associated with age and medical risk factors, but not with sex, migraine subtype, or duration of migraine symptoms.
Conclusion.-The observed frequency of MRI abnormalities in our series is lower than has been previously reported. In many cases, these abnormalities may be unrelated to migraine. When such changes are discovered in a patient with migraine, other etiologies should be considered.