Abstracts and Citations
2007; Wiley; Volume: 47; Issue: 9 Linguagem: Inglês
10.1111/j.1526-4610.2007.00927.x
ISSN1526-4610
AutoresFrederick R. Taylor, Mark J. Stillman, Stewart J. Tepper,
ResumoThe objective of this study was to evaluate how the criteria of the second edition of the International Classification of Headache Disorders (ICHD-II) and the revised criteria fit a sample of patients with chronic daily headache (CDH). One hundred and five patients with CDH in a tertiary headache centre were included. Headache was assessed using a semi-structured interview. Patients were classified according to the ICHD-II and to the new appendix criteria of the ICHD. Using the ICHD-II, 91% of patients received a combination of diagnoses and 76% received only a probable diagnosis: 47% had probable chronic migraine (CM) with probable medication overuse headache (MOH), 28% had probable chronic tension-type headache (CTTH) with probable MOH, 20% had CTTH and 3.8% had CM. Using the new appendix criteria, 88.5% of patients required one diagnosis. Seventy-six percent of patients were classified as MOH, 17% had CTTH and 6.7% had CM. The classification of CDH remains controversial. Alternative criteria for CM with and without medication overuse are discussed. Comments: SJT is well published on this topic, and I know has thought about these issues much more than me. But this type of work always brings to mind the neurologic controversy over splitting versus lumping. I have always preferred lumping and in that regard both Bigal et al's1 report and this work particularly satisfy my needs. And I suspect most of yours, too. Bigal M, Rapoport A, Sheftell F, Tepper S, Lipton R. The International Classification of Headache Disorders revised criteria for chronic migraine-field testing in a headache specialty clinic. Cephalalgia. 2007;27:230-234. —Frederick R. Taylor, MD I agree with Fred; Stewart should be the one to practice his rhetorical skills on this topic. However, I would like to say that the use of operational criteria to classify disease states clinicians diagnose on the basis of subjective complaints will always be problematic. This issue has dogged the study of pain for centuries, and particularly since society started treating Medicine as a science and not necromancy. One does not have to look more than a few centimeters below the chin to find other examples of zebras being mistaken as horses. Not until we have a better understanding of the pathobiology of headaches, allowing us to rely less on semiology and reports of collections of headache symptoms, will the picture come into full focus. —Mark J. Stillman, MD Despite that cautionary admonition from MJS, let me list the new criteria for both primary Chronic Migraine (CM) and secondary Medication Overuse Headache (MOH). Both sets of proposed criteria work great in clinical practice and should be adopted by the IHS expeditiously, so that these diagnostic criteria do not languish in the Appendix. Revised Medication Overuse Headache criteria, A8.2 2006 A. Headache on ≥15 days/month B. Regular overuse for >3 months of ≥one acute/symptomatic treatment drugs: 1. Ergotamine, triptans, opioids, or combination analgesic medications on ≥10 days/month on a regular basis for > 3 months 2. Simple analgesics or any combination of ergotamine, triptans, analgesics opioids on ≥ 15 days/month on a regular basis for >3 months without overuse of any single class alone C. Headache has developed or markedly worsened during medication overuse1,2 Revised Chronic Migraine criteria, A8.2 2006 A. Headache (tension-type and/or migraine) on ≥15 days per month for ≥3 months B. Occurring in a patient who has a diagnosis of migraine without aura C. On ≥8 days per month for ≥ 3 months headache has fulfilled: Criteria for migraine without aura and/or Treated and relieved by triptan(s) or ergot No medication overuse or other cause2 Silberstein SD, Olesen J, Bousser MG, Diener HC, Dodick D, First M, Goadsby PJ, Göbel H, Lainez MJ, Lance JW, Lipton RB, Nappi G, Sakai F, Schoenen J, Steiner TJ; International Headache Society. The International Classification of Headache Disorders, 2nd Edition (ICHD-II)revision of criteria for 8.2 Medication-overuse headache. Cephalalgia. 2005;25:460-465. Headache Classification Committee: Olesen J, Bousser M-G, Diener H-C, Dodick D, First M, Goadsby PJ, Göbel H, Lainez MJA, Lance JW, Lipton RB, Nappi G, Sakai F, Schoenen J, Silberstein SD, Steiner TJ. New Appendix Criteria Open for a Broader Concept of Chronic Migraine. Cephalalgia 2006; 26:742-746. —Stewart J. Tepper, MD Migraine and obesity are associated in several ways. First, both are prevalent and disabling disorders influenced by genetic and environmental risk factors. Second, migraine with aura, as obesity, seems to be a risk factor for cardiovascular events. Finally, large population-based studies suggest that obesity is a risk factor for chronic migraine after adjusting for comorbidities. In this article, we discuss plausible mechanisms that may account for this association. Several of the inflammatory mediators that are increased in obese individuals are important in migraine pathophysiology, including interleukins and calcitonin gene-related peptide (CGRP). These mediators may increase the frequency, severity, and duration of migraine attacks per se, which in turn would cause central sensitization. Repeated central sensitization may be associated with permanent neuronal damage close to the periaqueductal gray area, with poor modulation to pain. Obesity is also a state of sympathetic activation, which may contribute to increase in headache frequency. Furthermore, the levels of adiponectin are decreased in obesity. At low but not normal levels, adiponectin is nociceptive. Shared biologic predisposition may also play a major role. Orexins modulate both pain and metabolism. Dysfunction in the orexins pathways seems to be a risk factor for both conditions. Finally, conditions that are co-morbid to both states (eg, depression, sleep apnea) may also make the relationship between both diseases more complex. Comments: This is the only abstract from a commonly reviewed journal for this month. Furthermore, I have generally refrained from subject reviews unless they are systematic or meta-analytic reviews. But this is such a critical topic in headache medicine practice today that I just could not place it in my review section. So read and enjoy and contemplate the future and change in our practices. —Frederick R. Taylor, MD I agree that this review, though brief, should serve as an “appetizer” for the full course “meal” to come, when the pathobiologic mechanisms of migraine are further elucidated. It reemphasizes the critical importance of epidemiological study of a subject that had once only been the object of careful descriptive analysis. —Mark J. Stillman, MD Background: The vascular component of the migraine-specific physiologic profile and the observed adverse cardiovascular risk profile in migraineurs suggest an association between migraine and cardiovascular disease (CVD). In women, migraine has been associated with increased risk of CVD, including coronary events. Compatible data in men are lacking. Methods: Prospective cohort study of 20 084 men aged 40 to 84 years participating in the Physicians' Health Study. In yearly questionnaires, men were asked for information on migraine, risk factors, and the occurrence of study end points. We classified men as having migraine if they indicated migraine during the first 5 years, after which time follow-up began. Information on aura was not available. All the men were free of CVD at the start of follow-up. During a mean of 15.7 years, we followed up participants for the occurrence of a first major CVD event (nonfatal ischemic stroke, nonfatal myocardial infarction, or death from ischemic CVD). We also evaluated the individual end points, coronary revascularization, and angina. Results: A total of 1449 men (7.2%) reported migraine, and during follow-up, 2236 major CVD events occurred. Compared with nonmigraineurs, men who reported migraine had multivariable-adjusted hazard ratios (95% confidence intervals) of 1.24 (1.06–1.46; P = .008) for major CVD, 1.12 (0.84–1.50; P = .43) for ischemic stroke, 1.42 (1.15–1.77; P < .001) for myocardial infarction, 1.05 (0.89–1.24; P = .54) for coronary revascularization, 1.15 (0.99–1.33; P = .068) for angina, and 1.07 (0.80–1.43; P = .65) for ischemic cardiovascular death. Conclusion: In this large prospective cohort of apparently healthy men, migraine was associated with increased risk of major CVD, which was driven by increased risk of myocardial infarction. Comments: This report is a complement to the Women's Health Study (WHS), but uses prospective data on men from the Physicians Health Study (PHS).1 Differences between these studies include the lack of data on migraine with aura in the PHS compared to WHS and different study time periods. The lack of aura data limits the study greatly because the difference established in CVD risk for those with aura and those without in the WHS is simply not possible to establish here. So, in men, is this burden shared by all or by a more limited subset as in women? One methodologic limitation is that migraine was established as a self-diagnosis (and we know how error prone that can be). Data review indicates that 83.5% fulfilled all but 1 International Headache Society criterion (coded then as 1.7, migrainous disorder in ICHD-I, and what would now be 1.6 probable migraine in ICHD-II), and 46.6% fulfilled all International Headache Society criteria for migraine (code 1.1) Another limitation is the lack of information about drug use or type, especially migraine specific therapies. Compared with men who did not report migraine, the age-adjusted Hazards Ratio for ischemic stroke was 1.84 (95% CI, 1.10 to 3.08) for migraineurs younger than 55 years, whereas there was no significant association in the older age groups. Age did not significantly modify the association between migraine and major CVD and MI. While the age for men is older than women, an age relationship is known for women and therefore familiar to us. Generalizability may be limited given a white physician population. If this CVD burden is due to multiple migraine-related vascular risk factors, should we be surprised that men with migraine also share an increased burden of CVD risk? I do not think so. But overall this additional data require all headache medicine specialists to become familiar with CVD risk factor analysis and incorporate CVD risk factor reduction into our office visits. Kurth T, Gaziano JM, Cook NR, Logroscino G, Diener HC, Buring JE. Migraine and risk of cardiovascular disease in women. JAMA. 2006;296:283-291. —Frederick R. Taylor, MD I agree with all that Fred writes. This detailed, 16-year prospective cohort study highlights the difficulties entailed in the construction of epidemiological studies. Pitfalls in design include, among other things, changing definitions of the target endpoint diseases or entry criteria, correctly choosing a representative study population, and the accumulation of new information on risk factors during the performance of the study. Still the positive association of migraine headaches with myocardial infarction in middle aged male physicians supports the belief that migraine headaches are associated with a yet to be characterized vasculopathy. —Mark J. Stillman, MD I am still wrestling with the fascinating work of Dr. Tobias Kurth and colleagues. If I understand both studies, the increased cardiac risk in migraine may, in fact, be due to migraineurs having more cardiac risk factors, rather than to an intrinsic property of migraine itself. In women, this seemed more apparent in aura patients, and as FRT noted, we cannot tell in men from the PHS. Other potential causes of vascular events in aura patients include toxicity of the aura itself, via matrix metalloproteinase activation, or emboli via shunts, but in the above study, sadly, we cannot distinguish differences in risks for migraine subtypes. —Stewart J. Tepper, MD Background: The aim of this study was to ascertain whether oxidative stress is a causative factor of migraine attacks for Helicobacter pylori-infected migraineurs. Materials and Methods: A total of 35 consecutive migraine patients without aura who came to gastroenterology polyclinic with various complaints and diagnosed H. pylori infection were included in the study group and compared with a group of 29 patients (control group) without migraine and H. infection. H. pylori infection was diagnosed by histopathological biopsies, which were taken by endoscopy (Olympus-GIFXQ240 endoscope). Both the diagnosis and the classification of migraine were made according to the International Headache Society criteria. Blood samples for nitric oxide were taken from patients with migraine during headache-free period as well as the control group. The interaction of nitric oxide was measured by the determination of both nitrite and nitrate concentrations in the sample. Results: The study group included 31 women and 4 men (mean age 49 ± 8 years) and the control group included 25 women and 4 men (mean age 52.6 ± 11 years). The mean frequency of migraine attacks was 2.94 ± 1.58 days/month and the mean duration of attacks was 21.2 ± 3 hours. It was found that the study group has lower nitrate levels than the control group. Conclusions: Our results do not support the role of oxidative stress in patients suffering from H. pylori infection and migraine. Comments: Imagine my surprise to learn of a Journal dedicated solely to a specific bacterium. This organism, Helicobacter pylori, probably does deserve its own “followers.” I state this based on the number of headache patients in my office asking me to address H. pylori and their headache. It is not uncommon in my clinics to either have patients ask questions about definitive testing or to inform me of their own prior treatment for H. Pylori and its outcome. Sometimes it is reported in quite positive terms! I have therefore found myself needing more information and at the same time becoming more confused as to whether H. pylori deserves any attention whatsoever in the field of headache medicine. I admit, I am skeptical of a cause-and-effect relationship and conform to the belief that “in the absence of any specific link between H. pylori and migraine, the association, when present, must be considered as merely casual.” But I consider the issue as not yet resolved. This is the second study I am aware of which fails to define a relationship between H. pylori and oxidative stress in migraineurs, for what that is worth!1 For a different viewpoint see reference 2 by the same authors. Ciancarelli I, Di Massimo C, Tozzi-Ciancarelli MG, De Matteis G, Marini C, Carolei A. Helicobacter pylori infection and migraine. Cephalalgia. 2002;22:222-225. Tunca A, Türkay C, Tekin O, Kargili A, Erbayrak MI. Helicobacter pylori infection a risk factor for migraine? A case-control study. Acta Neurol Belg. 2004;104:161-164. —Frederick R. Taylor, MD As a Neurology resident in the 1980s, I suffered from a bout of the flu, which was then complicated by an exacerbation of my migraines. In my ignorance, I started ingesting large amounts of a combination tablet containing caffeine, acetaminophen, and ASA (the name of which I'd better not mention). After I suffered an UGI bleed I tried to blame it on one particular attending physician who was always trying to sneak in his private admissions when I was not looking. But my mother had her own ideas and pointed to the spicy, ethnic foods I liked to eat. Unbeknownst to me, she convinced my landlord to let her into my apartment, and she threw everything in my refrigerator away! Now, years later, unlike other aging, balding neurologists who suffer nightly attacks of heartburn (GERD), I suffer from recurrent nightmares (PTSD) related to that sneak attack on my refrigerator! So, migraineurs (and neurologists), listen to your mother! Watch what you eat (and what you read)! —Mark J. Stillman, MD As a Neurology resident, I personally had to cover for MJS when he was hospitalized at the House of God in Boston for his sanguinous analgesic-induced enteropathy. Unlike FRT, I am not very open-minded about an H. Pylori- migraine link. I think analgesic overuse usually explains both the transformation into worsening and then daily headache, as well as the GI toxicity often clinging to MOH and CDH, and MJS was my first experience with a patient in this arena. —Stewart J. Tepper, MD In this randomized, double-blind, crossover clinical trial, adult patients treated two migraine attacks: one with almotriptan 12.5 mg and the other with ergotamine 2 mg plus caffeine 200 mg. Treatment with almotriptan was associated with a significantly greater proportion of patients achieving 2-h pain free (20.9% vs. 13.7%; P < 0.05) and 2-h pain relief (57.7% vs. 44.5%; P < 0.01) compared with ergotamine plus caffeine therapy; significant differences were not seen at 1 h. Rates for sustained pain free and sustained pain free plus no adverse events (AEs) also were significantly greater after almotriptan treatment than after the use of ergotamine plus caffeine (P < 0.05). Almotriptan was associated with a significantly lower rate of photophobia at 90 min (P < 0.05), phonophobia at 60, 90, and 120 min (P < 0.05 to <0.01), and nausea and vomiting at 90 and 120 min (P < 0.01) compared with ergotamine plus caffeine. A significantly greater proportion of patients were more satisfied with almotriptan than with ergotamine plus caffeine (P < 0.05). Sixteen patients reported adverse events during almotriptan treatment and 27 patients reported AEs during the ergotamine plus caffeine therapy. Most AEs were mild-to-moderate and did not result in treatment-related discontinuations. In conclusion, almotriptan was associated with significantly greater efficacy for treating migraine compared with ergotamine plus caffeine, was generally well tolerated and was associated with greater rate of treatment satisfaction. Comments: Contact your Abstract Editors! Do you as a reader still want to read these studies? I apparently felt compelled to beat another dead horse to death! Since reading the 2000 Brain article on use of ergots, I have felt that insufficient rationale exists to use oral ergots in any routine clinical setting.1 So are any of us really surprised by this study's outcome? Two earlier comparisons between second generation triptans and an ergot yielded very similar results.2,3 And if that is not enough, add increased CVD risks to ergotamine over triptans in overuse.4 Tfelt-Hansen P, Saxena PR, Dahlöf C, Pascual J, Láinez M, Henry P, Diener H, Schoenen J, Ferrari MD, Goadsby PJ. Ergotamine in the acute treatment of migraine: A review and European consensus. Brain 2000;123:9-18. Christie S, Göbel H, Mateos V, Allen C, Vrijens F, Shivaprakash M; Rizatriptan-Ergotamine/Caffeine Preference Study Group. Crossover comparison of efficacy and preference for rizatriptan 10 mg versus ergotamine/caffeine in migraine. Eur Neurol. 2003;49:20-29. Diener HC, Jansen JP, Reches A, Pascual J, Pitei D, Steiner TJ; Eletriptan and Cafergot Comparative Study Group. Efficacy, tolerability and safety of oral eletriptan and ergotamine plus caffeine (Cafergot) in the acute treatment of migraine: A multicentre, randomised, double-blind, placebo-controlled comparison. Eur Neurol. 2002;47:99-107. E.A. Wammes-van der Heijden, PharmD; H. Rahimtoola, PharmD, PhD; H.G.M. Leufkens, PharmD, PhD; C.C. Tijssen, MD, PhD; and A.C.G. Egberts, PharmD, PhD. Risk of ischemic complications related to the intensity of triptan and ergotamine use. Neurology 2006;67:1128-1134. —Frederick R. Taylor, MD Ditto. — Mark J. Stillman, MD The three co-Abstracts editors are all old enough to have significant clinical experience with ergotamine. The Brain article led to the removal of ergotamine from availability in Germany through Dr. Diener's auspices. Dr. Marcelo Bigal and I summarized our views on ergotamine, also unfavorable, in a review several years ago.1 Bigal ME, Tepper SJ. Ergotamine and Dihydroergotamine: A Review. Curr Pain Headache Reports 2003;7:55-62. —Stewart J. Tepper, MD Objective: To test treatment combining a beta-blocker plus topiramate in migraine patients previously resistant to the two medications in monotherapy. Patients and Methods: Those patients who had not responded to a beta-blocker and topiramate received combined treatment. Results: Fifty-eight patients (47 women, age 25–76 years) received the combined treatment. Thirty-three (57%) met criteria for chronic migraine/medication overuse headache, 18 (31%) for migraine without aura and seven (12%) with aura. Ten (17%) discontinued due to adverse events. Among the 48 patients who tolerated the combination, 36 (75%, 62% of the total series) showed response (>50% reduction in frequency), while 12 (25%) did not. The number of days with headache/month decreased from 15.1 to 6.5 (57%). Sixteen (44% of responders) showed an excellent (>75%) response. Eighteen patients (38%) experienced a total of 26 adverse events (mild-moderate). Conclusions: The combination of beta-blocker plus topiramate showed a benefit in around 60% of patients who had not previously responded to monotherapy. Adverse events led to discontinuation in one out of six patients. From these open results, it seems reasonable to recommend this combination, complementary in terms of mechanism of action, as a potential strategy in patients with refractory migraine. In this small, but short and sweet, open label study the authors replicate a previous study combining β-blockers with valproate as prophylaxis for migraineurs resistant to both agents individually. Nearly 60% of patients met ICHD-II criteria for chronic migraine or medication overuse headaches, and the rest were episodic migraine sufferers. Nadolol and propranolol were used as the β-blockers and the authors assumed them to be equipotent mg for mg. Sixty-two percent of the total (75% of those completing the 3 month study; 36/48) had a response, defined as a greater than 50% reduction in the number of headache days during month 3. Even more encouraging was the 50% proportion of the patients who lost weight, with the mean weight loss being 5.3 kg. The study needs confirmation in a larger, multi-center setting, but it intuitively makes sense. Polypharmacy is the lord of the battlefield in the war against refractory pain, for obvious reasons. If this study were repeated, I would expect inclusion criteria to include a trial of the individual agents longer than 1.5 months before calling it treatment failure. —Mark J. Stillman, MD Headache is a health problem with considerable impact at personal, social, and financial levels in terms of distress, disability, and cost. In the past, many studies have investigated the use of various behavioural treatment modalities for headache. Literature reviews consistently support the effectiveness of behavioural therapeutic approaches for the treatment of the most common primary headaches, namely migraine and tension-type headache. This article recommends that behavioural headache therapies should be developed, tested, and integrated into primary care practice, where most patients with headache are seen and treated. The large population seen in general practice, most of whom have uncomplicated primary headaches, could represent the ideal target for testing behavioural therapies. Ridsdale L, Clark LV, Dowson AJ, Goldstein LH, Jenkins L, McCrone P, Morgan M, Seed PT. How do patients referred to neurologists for headache differ from those managed in primary care?Br J Gen Pract. 2007;57:388-395. Background: Headache is the neurological symptom most frequently presented to GPs and referred to neurologists, but little is known about how referred patients differ from patients managed by GPs. Aim: To describe and compare headache patients managed in primary care with those referred to neurologists. Design of Study: Prospective study. Setting: Eighteen general practices in south-east England. Method: This study examined 488 eligible patients consulting GPs with primary headache over 7 weeks and 81 patients referred to neurologists over 1 year. Headache disability was measured by the Migraine Disability Assessment Score, headache impact by the Headache Impact Test, emotional distress by the Hospital Anxiety and Depression Scale and illness perception was assessed using the Illness Perception Questionnaire. Results: Participants were 303 patients who agreed to participate. Both groups reported severe disability and very severe impact on functioning. Referred patients consulted more frequently than those not referred in the 3 months before referral (P = 0.003). There was no significant difference between GP-managed and referred groups in mean headache disability, impact, anxiety, depression, or satisfaction with care. The referred group were more likely to link an increased number of symptoms to their headaches (P = 0.01), to have stronger emotional representations of their headaches (P = 0.006), to worry more (P = 0.001), and were made anxious by their headache symptoms (P = 0.044). Conclusion: Patients who consult for headache experience severe disability and impact, and up to a third report anxiety and/or depression. Referral is not related to clinical severity of headaches, but is associated with higher consultation frequency and patients' anxiety and concern about their headache symptoms. In this article, we meta-analytically examined the efficacy of biofeedback (BFB) in treating migraine. A computerized literature search of the databases Medline, PsycInfo, Psyndex and the Cochrane library, enhanced by a hand search, identified 86 outcome studies. A total of 55 studies, including randomized controlled trials as well as pre–post trials, met our inclusion criteria and were integrated. A medium effect size (d = 0.58, 95% CI = 0.52, 0.64) resulted for all BFB interventions and proved stable over an average follow-up phase of 17 months. Also, BFB was more effective than control conditions. Frequency of migraine attacks and perceived self-efficacy demonstrated the strongest improvements. Blood-volume-pulse feedback yielded higher effect sizes than peripheral skin temperature feedback and electromyography feedback. Moderator analyses revealed BFB in combination with home training to be more effective than therapies without home training. The influence of the meta-analytical methods on the effect sizes was systematically explored and the results proved to be robust across different methods of effect size calculation. Furthermore, there was no substantial relation between the validity of the integrated studies and the direct treatment effects. Finally, an intention-to-treat analysis showed that the treatment effects remained stable, even when drop-outs were considered as nonresponders. The 12-member National Institute of Health Technology Assessment Panel on Integration of Behavioral and Relaxation Approaches into the Treatment of Chronic Pain and Insomnia (1996) reviewed outcome studies on hypnosis with cancer pain and concluded that research evidence was strong and that other evidence suggested hypnosis may be effective with some chronic pain, including tension headaches. This paper provides an updated review of the literature on the effectiveness of hypnosis in the treatment of headaches and migraines, concluding that it meets the clinical psychology research criteria for being a well-established and efficacious treatment and is virtually free of the side effects, risks of adverse reactions, and ongoing expense associated with medication treatments. Comments: I admit it. I loved discovering and reading this particular set of 4 articles. I had to reference 2 additional pertinent articles.1,2 In the Reviews Section, please see the Henningsen et al article and see Sierpina et al in the section called Papers Not Abstracted But Worth Reading. This series of articles provides further background and evidence base for the practice of Behavioral Headache Management. In fact, they support the necessity of good behavioral practice for success with our patients. As delineated by Risdale et al, the difference in the patients who remain in primary care from the ones seen in Specialty Care is not related to the severity of headache, but to the number of symptoms of their headaches, the stronger emotional representations of their headaches, and the worry, and anxiety produced by their headache symptoms. These characteristics are not appropriately or adequately addressed by acute or preventive drug therapy, but by relationship-centered physician-patient care with behavioral therapies. Finally, perhaps someday Behavioral Headache Management will be more user-friendly as we master the use of the internet for medical care.2 Juhasz G, Zsombok T, Gonda X, Nagyne N, Modosne E, Bagdy G. Effects of autogenic training on nitroglycerin-induced headaches. Headache. 2007;47:371-383. Devineni T, Blanchard EB. A randomized controlled trial of an internet-based treatment for chronic headache. Behav Res Ther. 2005;43:277-292. —Frederick R. Taylor, MD These articles emphasize the myopia of the current health care system, which is all too happy to reward procedural medicine and ignore anything to do with mental health. Sadly, it is hard to imagine improvement in future coverage for biobehavioral medicine with the record U.S. deficits and the approaching insolvency of Medicare. —Mark Stillman, MD I have practiced Headache Medicine first without and then with psychology back up, and I have the extreme good fortune to practice currently with 2 outstanding, well published headache psychologists, Drs. Steve Baskin and Randy Weeks. To list the many ways they help patient care would take the rest of the journal, but the bottom line is dramatically improved patient o
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