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Purpose of review Medication overuse headache (MOH)is a disabling problem worldwide with areas of controversy regarding its cause. This article reviews the recent ideas regarding the development of this disorder and its effective management. Recent findings It has been proposed that all acute migraine medications can lead to MOH, with differences in the propensity of different agents to cause the problem. Early data suggests that gepants, which are small-molecule calcitonin gene-related peptide antagonists used for the acute treatment of migraine, may be an exception. Recent studies show that practitioners and the general public are still largely unaware of the problem of medication overuse and its damaging effects. Summary MOH is an accepted concept of an increase in headaches driven by the frequent administration of acute antimigraine drugs. The impressions of providers, and studies documenting the concept may be flawed. Although it is likely that MOH does occur, and restricting the amount of acute medications is necessary to prevent it, it is also possible that increasing amounts of acute medications are simply a reflection of poorly controlled headaches, rather than a cause. Objective markers need to be developed to identify those who have MOH, which does not include all with chronic migraine, and to use these markers in diagnosis and management, particularly in those patients where the frequent acute drugs might only be a reflection of frequent headaches, rather than a cause.

Introduction Tolosa-Hunt syndrome (THS), a condition characterized by painful ophthalmoplegia and accompanied by cranial nerve palsies, remains as a diagnosis of exclusion. Nevertheless, the 3rd Edition of the International Classification of Headache Disorders (ICHD) has refined its diagnostic criteria to require the demonstration of granulomatous inflammation on magnetic resonance imaging or biopsy. We sought to assess the effectiveness of the new criteria in arriving at accurate diagnoses. Methods We extracted all patient charts from our institution's electronic medical record associated with ICD-9 code 378.55 (external ophthalmoplegia). We then completed the retrospective diagnostic workups to determine if subjects met ICHD-3 criteria for THS and compared our findings with their final diagnoses. Results Of 62 patients associated with ICD-9 code 378.55, 10 (16%) was identified to have presenting symptoms concerning THS. The average age at the first onset of THS-like symptoms was 58 years. Five of the 10 (50%) met ICHD-3 criteria for THS. Two of the 5 (40%) meeting ICHD-3 criteria for THS were discovered to have other diagnoses. Two of the 5 (40%) patients not meeting ICHD-3 criteria for THS nevertheless received a final diagnosis of THS. Discussion Our false-negative rate of 40% is consistent with previous case series found in the literature. Our false-positive rate of 40% is, to our knowledge, a new contribution to the literature as no other case series includes more than a single false-positive. The false-positive rate is most concerning, as a preliminary misdiagnosis of THS can delay treatment tailored to the true etiology. Furthermore, infectious etiologies can be exacerbated with steroid treatment. Conclusion Our case series suggests that ICHD-3 criteria are suboptimal for the accurate diagnosis of THS. We recommend a close follow-up for all patients with symptoms concerning THS until a definitive responsible etiology is discovered and we encourage further studies assessing ICHD-3 guidelines to optimize their sensitivity and specificity in the diagnosis of THS.

Headache is one of the most common reasons for which people seek medical attention. Migraine, tension-type, and other primary headache disorders account for the majority of cases. Still, approximately 2–5% of patients presenting with headache will ultimately be diagnosed with secondary headache, many of which are serious and even life-threatening. This distinction between primary and secondary headache is the most important and often the most challenging step in the management of these patients. This chapter aims to review and clarify the worrisome headache “red flags” that can alert healthcare providers to a potential secondary etiology. The widely utilized mnemonic “SNOOP” was created over a decade ago to help providers remember these warning signs. As our knowledge base has increased, the mnemonic has gone through multiple iterations – most recently, “SNNOOP10” – but, for the sake of simplicity and clarity, we will use “SNOOPP” as our guide: systemic symptoms, neurologic signs and symptoms, onset, older age, pattern change, and positional quality. It is important to remember that when patients have a primary headache syndrome, most commonly migraine, they are more likely to develop a headache as a symptom of these new disorders. The headache they develop is often an amplification of the preexisting one.

In 2010 onabotulinumtoxinA (OnabotA) was approved by the United States Food and Drug Administration for the treatment of chronic migraine (CM). Data supporting approval were derived primarily from two parallel placebo-controlled trials, the PREEMPT studies. Many clinicians and research investigators critical of those data have recommended that the dosing/injection paradigm for treating CM be "customized" to the needs of the individual patient rather than administered in a uniform fashion conforming to the methodology utilized in the PREEMPT studies. In this paper the authors debate the issue of whether treatment of CM with OnabotA should be standardized versus customized.

New daily persistent headache (NDPH) is a unique form of chronic daily headache. The distinguishing feature of NDPH is a headache that starts abruptly, and patients can often recall the exact day of headache onset. Clinically, NPDH lacks characteristic features and may resemble migraine or tension-type headache. Diagnosis relies on first eliminating secondary mimics. Several different classes of medications have been used for treatment of NDPH with varying results. In clinical practice, treatment is often chosen based on the headache phenotype. However, most therapies are ineffective or minimally effective thereby making NDPH one of the most refractory types of headache to treat.

Chronic daily headache (CDH) is a frequently used but nonspecific term that includes all the headaches which are experienced on more than 15 days per month for at least 3 months. There are numerous headache disorders, both primary and secondary, that behave like this. They represent a great challenge to medical professionals and a burden to the patient and society. The primary CDHs (for which no underlying cause is found) are the most common. Of those, chronic migraine is the leading problem encountered in specialized headache clinics, much more common than other primary CDHs of long duration (≥4 h/day). Most important primary CDHs of short duration (

Introduction The term Tolosa-Hunt Syndrome was first used more than half a century ago to describe painful ophthalmoplegia accompanied by cranial nerve palsies. In the decades since, its diagnostic criteria have evolved considerably. The beta version of the 3rd Edition of the International Classification of Headache Disorders narrows these criteria to require the demonstration of granulomatous inflammation on MRI or biopsy. We believe this may introduce challenges to accurate diagnosis. Discussion Requiring the demonstration of granulomatous inflammation for a diagnosis of Tolosa-Hunt Syndrome may introduce the potential for false negative and false positive diagnoses. Although the disorder presents secondary to granulomatous inflammation, MRI technology may not be able to identify it reliably, and biopsy is not always indicated for its symptomatology. Additionally, several cases have been reported of Tolosa-Hunt Syndrome diagnosed with MRI-confirmed granulomatous inflammation that later prove to be attributable to other pathologies. The emphasis on neuroimaging may therefore exclude some true Tolosa-Hunt Syndrome cases and include others resulting from other latent pathologies that are not visible on MRI. Conclusion We wish to offer several potential modifications to the International Classification of Headache Disorders guidelines for Tolosa-Hunt Syndrome, including making the demonstration of granulomatous inflammation on MRI or biopsy non-mandatory and lengthening patient follow-up to two years for cases in which MRI is unrevealing.

To assess the prevalence of headache in clinic and support group patients with celiac disease and inflammatory bowel disease (IBD) compared with a sample of healthy controls.European studies have demonstrated increased prevalence of headache of patients with celiac disease compared with controls.Subjects took a self-administered survey containing clinical, demographic, and dietary data, as well as questions about headache type and frequency. The ID-Migraine screening tool and the Headache Impact Test (HIT-6) were also used.Five hundred and two subjects who met exclusion criteria were analyzed - 188 with celiac disease, 111 with IBD, 25 with gluten sensitivity (GS), and 178 controls (C). Chronic headaches were reported by 30% of celiac disease, 56% of GS, 23% of IBD, and 14% of control subjects (P.0001). On multivariate logistic regression, celiac disease (odds ratio [OR] 3.79, 95% confidence interval [CI] 1.78-8.10), GS (OR 9.53, 95%CI 3.24-28.09), and IBD (OR 2.66, 95%CI 1.08-6.54) subjects all had significantly higher prevalence of migraine headaches compared with controls. Female sex (P=.01), depression, and anxiety (P=.0059) were independent predictors of migraine headaches, whereas age65 was protective (P=.0345). Seventy-two percent of celiac disease subjects graded their migraine as severe in impact, compared with 30% of IBD, 60% of GS, and 50% of C subjects (P=.0919). There was no correlation between years on gluten-free diet and migraine severity.Migraine was more prevalent in celiac disease and IBD subjects than in controls. Future studies should include screening migraine patients for celiac disease and assessing the effects of gluten-free diet on migraines in celiac disease.

Purpose of review This article provides an overview of the differences in epidemiology, presentation, and treatment of pediatric headache compared to adult headache. New findings New proposals are presented regarding the classification of pediatric migraine and ophthalmoplegic migraine. The distinction between basilar migraine and migraine with aura is reconsidered. Summary Pediatric headache is a common but underdiagnosed condition. Primary headache syndromes, in particular migraine, can present differently in children than in adults. Diagnosis can be problematic, especially in young children, because standard criteria used for classification are often incomplete. Treatment focuses on biobehavioral modification and adapted use of standard adult medication management.

Objective: To update the 2008 American Academy of Neurology (AAN) guidelines regarding botulinum neurotoxin for blepharospasm, cervical dystonia (CD), headache, and adult spasticity. Methods: We searched the literature for relevant articles and classified them using 2004 AAN criteria. Results and recommendations: Blepharospasm: OnabotulinumtoxinA (onaBoNT-A) and incobotulinumtoxinA (incoBoNT-A) are probably effective and should be considered (Level B). AbobotulinumtoxinA (aboBoNT-A) is possibly effective and may be considered (Level C). CD: AboBoNT-A and rimabotulinumtoxinB (rimaBoNT-B) are established as effective and should be offered (Level A), and onaBoNT-A and incoBoNT-A are probably effective and should be considered (Level B). Adult spasticity: AboBoNT-A, incoBoNT-A, and onaBoNT-A are established as effective and should be offered (Level A), and rimaBoNT-B is probably effective and should be considered (Level B), for upper limb spasticity. AboBoNT-A and onaBoNT-A are established as effective and should be offered (Level A) for lower-limb spasticity. Headache: OnaBoNT-A is established as effective and should be offered to increase headache-free days (Level A) and is probably effective and should be considered to improve health-related quality of life (Level B) in chronic migraine. OnaBoNT-A is established as ineffective and should not be offered for episodic migraine (Level A) and is probably ineffective for chronic tension-type headaches (Level B).

The extent to which patients take chronic pain medications as prescribed is not well studied, and there are no generally agreed-upon measures. The Quantitative Analgesic Questionnaire (QAQ) is a new instrument designed to comprehensively document patient-reported medication use, generate scores to quantify it (by individual drug, class, and/or overall), and compare it (qualitatively and/or quantitatively) to the regimen as prescribed.The aim of this study was to describe the development and preliminary validation of the QAQ.The QAQ was studied in a convenience sample of 149 HIV-infected participants.We found that the QAQ scores computed for participants' chronic pain medication regimens were valid based on their correlation with 1) patient-reported pain intensity (r = 0.38; P 0.001) and 2) experienced pain management physicians' independent quantification of the regimens (r = 0.89; P 0.001). The QAQ also demonstrated high interrater reliability (r = 0.957; P 0.001). Detailed examination of the QAQ data in a subset of 34 participants demonstrated that the QAQ revealed suboptimal adherence in 44% of participants and contained information that would not have been gleaned from review of the medical record alone in 94%, including use of over-the-counter medications and quantification of "as needed" dosing. The QAQ also was found to be useful in quantifying change in the medication regimen over time, capturing a change in 50% of the participants from baseline to eight week follow-up.The QAQ is a simple tool that can facilitate understanding of patient-reported chronic pain medication regimens, including calculation of percent adherence and generation of quantitative scores suitable for estimating and tracking change in medication use over time.

Migraine affects 12% of the population with recurrent attacks, and the features of these vary widely. This condition is likely due to a variety of genetic predilections, which lower the threshold for activating the trigeminovascular system in the brain. Migraine is also an inflammatory disorder. Failure to treat an attack rapidly reduces the chance of rendering the sufferer pain free. There is evidence that migraine can be progressive, is adversely influenced by the burden of migraine, and that aggressive management may be disease modifying.

The term “complicated migraine” (CM) is often applied to unexplained transient neurological symptoms by clinicians. CM is a diagnosis requiring an exclusion of other pathologies using rigorous criteria. The varied symptoms and presentations of complex aura are a fascinating window into the pathophysiology of migraine. Unilateral, bilateral, positive, and negative phenomena all occur, and are transient, reversible, and generally without permanent neurological sequelae. CM requires prompt medical attention to rule out other neurological disorders that may be amenable to treatment. In a presentation in which cerebral infarction is a likely differential diagnosis, triptans are avoided. Connecting its multiple presentations is a common denominator: the difficulty in diagnosis and lack of data to support preventive and acute therapies. This can be frustrating for the patient and clinician. There is need for further research and discovery in this field.

Objective.—To examine the metabolic effects of three divalproex dosing regimens in patients with migraine. Background.—Epidemiological and clinical studies have demonstrated a strong association between serum lipid levels and the development of coronary artery disease. Thus, it is important to understand the impact of chronically administered medications on serum lipids. Metabolic properties of divalproex, an approved and commonly used treatment for migraine prophylaxis, have not been systematically studied in patients with migraine. Methods.—Adult patients with migraine were randomized to receive one of three daily doses of divalproex (500 mg [n = 45], 1000 mg [n = 43], or 1500 mg [n = 44]) or placebo (n = 44) for 12 weeks. Post hoc analyses were performed to determine the effects of divalproex on total cholesterol, glucose, weight, and body mass index (BMI). Results.—The treatment groups were similar at baseline based on demographic and clinical characteristics and the use of concomitant medications. Divalproex resulted in a dose-related mean decrease from baseline in total cholesterol: −5.7 mg/dL or 3% reduction with 500 mg/day; −8.4 mg/dL or 4% reduction with 1000 mg/day; and −12.8 mg/dL or 7% reduction with 1500 mg/day (P < .05 for 1500 mg/day vs. placebo). There were no differences between any divalproex dose group and placebo for mean change from baseline in glucose, weight, or BMI. Conclusions.—Divalproex results in a dose-dependent reduction in serum cholesterol within the first 3 months of therapy, with no significant change in serum glucose or BMI.

Sufferers of severe headaches present for emergent treatment when attacks are unusually severe or refractory to therapy. Secondary headaches must always be considered.Most severe attacks are due to migraine, but cluster headaches may present for emergent treatment as well. It is unusual for a tension-type headache to be severe, unless it is associated with migraine. Options for emergent treatment of migraine depend upon which treatments have been recently utilized and what associated symptoms are present.Options include neuroleptics, triptans, nonsteroidal antiinflammatory agents, ergots, and intravenous valproic acid. Cluster headaches are best managed with oxygen inhalation, injectable sumatriptan, or dihydroergotamine.

This article identifies the pertinent historical issues that lead to the identification of those headaches needing additional testing to exclude a serious underlying cause.Recurrences of giant cell arteritis, even after presumed successful treatment, are common. Postural orthostatic tachycardia syndrome is an often unrecognized cause of headache.Patients with a primary headache disorder are more susceptible to the development of headache when a secondary cause occurs. Their headaches may be phenotypically similar to their primary headache disorder. Therefore, a secondary cause should be considered in patients with preexisting headache disorders who develop a significant increase in the number and severity of those attacks.

For years in Navy system/equipment acquisitions, a program requirement that has been particularly troublesome to program managers (PMs), integrated logistic support managers (ILSMs), and logistic element managers (LEMs) is logistic support analysis (LSA). Performance of the tasks to satisfy this LSA requirement has dismayed many logistics engineers and analysts as well. Unfortunately, what has caused such consternation in the past is still present and shall negatively impact LSA requirements in the future unless some reformation occurs. A few of the main problems encountered when involved with an LSA are: the analysis is started too late; the effort is complex and diverse; the LSA military standards contain ambiguities, vague descriptions, and other deficiencies; and the LSA process allows many possible approaches leading to results with numerous possible interpretations. In many cases, expensive LSA processes produce data that is neither timely nor of great use. The result of an inefficient LSA is usually a bandaided end item in the field, one without adequate and cost-effective support. This paper addresses LSA-related problems, evidenced through research and personal experience, and recommends solutions to enhance the LSA process. This paper also stresses conducting the appropriate amount of analysis (through tailoring) to derive the ideal supportability system—one of sufficient performance that maximizes life cycle affordability.

Headache, and in particular, migraine, is often associated with comorbid psychiatric illness. The complex relationships between these disorders are slowly becoming understood. Successful management requires an integrated approach of neurologic and psychiatric management.

Trigeminal neuralgia results from disturbances in the trigeminal root entry zone which generate repetitive action potentials. Drugs which relieve the pain of trigeminal neuralgia depressed these potentials. Anticonvulsants which exert this or related effects, and which have been demonstrated to be efficacious in trigeminal neuralgia, include carbamazepine, phenytoin, clonazepam, and valproic acid. Baclofen may act by facilitating segmental inhibition of the trigeminal complex. The mechanism of action of pimozide for treating trigeminal neuralgia is not known. Carbamazepine is suggested as the drug of first choice; baclofen or clonazepam could be added if carbamazepine monotherapy is ineffective. When these fail, monotherapy with phenytoin, pimozide, or valproic acid would be a reasonable next step.

Your initial visit with the doctor represents a crucial step towards securing effective control over your headaches. Even though your headaches may have driven you to the depths of desperation, despair, and neediness, never forget that the management process involves a transaction between two parties that will require your active participation. The physician is not your savior; ideally he or she will serve as a compassionate, informed consultant who will advise you how best to direct your own ongoing headache management. Get this process off on the right foot. In this chapter we will offer suggestions as to how to maximize the benefits obtained from your initial visit. Although headache is endemic in our society and headache sufferers fill the waiting rooms of our clinics and EDs, surprisingly few healthcare providers are proficient in the diagnosis and treatment of headache, and many have a distinct aversion to dealing with headache patients. Your initial visit to the doctor will be far more productive if you arrive for that visit adequately prepared.

While most head pain results from a primary headache disorder such as migraine, at times headache may be a symptom of a more serious, underlying disease. In this chapter, we will explore these “secondary” headaches in some detail, identifying their most common causes and the characteristics of the symptomatology that should compel one to seek immediate or elective medical attention.

That so many theories to explain the origins of headache have been advanced and rejected over the centuries indicates both its long enduring impact on society’s health and wellbeing and man’s determination to understand the condition and so rid himself of its burden. Happily, we no longer bore holes into the skulls of headache sufferers so as to release the evil spirits, humors, or vapors accumulated within, and our therapies today are considerably more effective as well as less invasive. The path from “there to here” is a fascinating one; the personalities of the individuals who have shaped headache theory often have been as brilliantly compelling as their theories have been wrong-headed. In this chapter we will trace that path.

The primary headache disorders account for the vast majority of the episodic and chronic head pain that is so pervasive in our society. Unlike the secondary headaches described in the last chapter, these primary headaches do not point towards the presence of serious, underlying disease. Even so, the financial, physical and emotional cost imposed by these disorders is staggering, and it is no exaggeration to state that migraine in particular has been and remains a chronic public health care emergency. In this chapter, we will begin our effort to provide the reader with the education and tools he or she requires to cope more effectively with migraine, the intimate enemy.

That the mind influences disease prevention and healing is inarguable, and for those skeptics who continue to resist this association there exists abundant “hard science” in its support. If one’s emotional state can influence the ability of individual white blood cells to combat infection, it requires no great leap of faith to perceive that chronic headache and psychological health inextricably are wedded. In this chapter, we will discuss common migraine triggers, the utility of migraine diets, other lifestyle modifications as therapy for migraine, and the use of various other “alternative” therapies for migraine suppression. In addition, we will discuss disorders that are comorbid with migraine, disorders whose existence may influence the clinical expression of migraine and whose successful treatment may improve that expression.

Many headache clinics are affiliated with hospitals. These facilities were often started before the era of managed care. The new incentives and disincentives of managed care will force these programs to change their structures. Only those which document value are likely to survive.