- Headache Medicine
Program Director, Headache Cooperative of the Pacific (2007 - 2011)
Vice President, Headache Cooperative of the Pacific (2007 - 2012)
Chair, Refractory Headache Special Interest Section, American Headache Society, American Headache Society (2012 - Present)
Director,Stanford Headache Program, Stanford University School of Medicine (2011 - Present)
President, Headache Cooperative of the Pacific (2012 - Present)
Honors & Awards
Magna Cum Laude, Clark University, Worcester, Massachusetts (1972)
Woodrow Wilson Scholar, Clark University, Worcester, Massachusetts (1972)
Chief Resident, LAC/USC, Los Angeles, California (1989)
Fellow, American Academy of Neurology (2006)
Fellow, American Headache Society (2010)
Boards, Advisory Committees, Professional Organizations
Member, Board of Directors, Alliance for Headache Disorders Advocacy (2009 - Present)
Member, Board of Directors, Headache Cooperative of the Pacific (2007 - Present)
Member, Advisory Committee, NCAA Select committee on headache in collegiate atheletes (2013 - Present)
Member,, American Headache Society (1995 - Present)
Member, American Academy of Neurology (1990 - Present)
Member, International Headache Society (2010 - Present)
Board Certification, Unified Council of Neurologic Subspecialties, Headache Medicine (2008)
Board Certification, American Academy of Pain Medicine (2000)
Residency:LAC and USC Medical Center (1990) CA
Internship:LAC and USC Medical Center (1987) CA
Medical Education:Keck School of Medicine University of Southern CA (1986) CA
Board Certification: Neurology, American Board of Psychiatry and Neurology (1994)
Community and International Work
Funding for Headache Research
Headache Researchers, Clinicians, and Patients
Opportunities for Student Involvement
American Headache Society
Patients with Headache
Opportunities for Student Involvement
Current Research and Scholarly Interests
Current interest focus on patient education technology and patient/physician communication with a particular emphasis on tools which increase encounter efficiency and improve outcomes. Basic research focuses on mechanisms of action in Chronic Daily Headache, with a particular emphasis on New Daily Persistent Headache. Techniques include fMRI, biomarker investigation and evoked potentials. Clinical research includes clinical trials of novel treatments for episodic and chronic headache forms.
Chronic Daily Headache Project, SunStar Foundation (8/15/2013)
Investigation into the basic mechanisms and biomarkers associated with various form of chronic daily headache. Resting state and structural imaging, analysis of blood and CSF for biomarker identification, and evoked action potentials are utilized to better characterize the pathophysiology of chronic headache.
Stanford University and other headache centers in U.S. and abroad.
Independent Studies (5)
- Directed Reading in Neurology and Neurological Science
NENS 299 (Aut, Win, Spr)
- Early Clinical Experience in Neurology and Neurological Sciences
NENS 280 (Aut, Win, Spr)
- Graduate Research
NENS 399 (Aut, Win, Spr)
- Medical Scholars Research
NENS 370 (Aut, Win, Spr)
- Undergraduate Research
NENS 199 (Aut, Win, Spr)
- Directed Reading in Neurology and Neurological Science
Comparison of parenteral treatments of acute primary headache in a large academic emergency department cohort
2015; 35 (9): 807-815
The objective of this article is to compare acute primary headache patient outcomes in those initially treated with parenteral opiates or non-opiate recommended headache medications in a large academic medical emergency department (ED).Many acute primary headache patients are not diagnosed with a specific headache type and are treated with opiates and nonspecific pain medications in the ED setting. This is inconsistent with multiple expert recommendations.Electronic charts were reviewed from 574 consecutive patients who visited the ED for acute primary headache (identified by chief complaint and ICD9 codes) and were treated with parenteral medications.Non-opiate recommended headache medications were given first line to 52.6% and opiates to 22.8% of all participants. Patients given opiates first had significantly longer length of stays (median 5.0 vs. 3.9 hours, p < 0.001) and higher rates of return ED visits within seven days (7.6% vs. 3.0%, p = 0.033) compared with those given non-opiate recommended medications in univariate analysis. Only the association with longer length of stay remained significant in multivariable regression including possible confounding variables.Initial opiate use is associated with longer length of stay compared with non-opiate first-line recommended medications for acute primary headache in the ED. This association remained strong and significant even after multivariable adjustment for headache diagnosis and other possible confounders.
View details for DOI 10.1177/0333102414557703
View details for Web of Science ID 000357953100009
View details for PubMedID 25366551
Prevalence of migraine headache and its weight on neurological burden in Africa: a 43-year systematic review and meta-analysis of community-based studies.
Journal of the neurological sciences
2014; 342 (1-2): 1-15
Headache burden is not adequately explored in Africa. Here, we measured weighted migraine prevalence from community-based studies in Africa.PubMed search was employed using terms 'headache in Africa' AND/OR 'migraine in Africa' for published literature from 1970 until January 31, 2014. PRISMA was applied for systematic review. Forest-plot meta-analysis, inter-study heterogeneity, and odds ratio were used to measure weighted prevalence, inter-gender, and urban-rural differences. Disability adjusted life years (DALYs) for migraine and other neurologic disorders in Africa were extracted from Global Burden of Diseases (GBD) 2000-2030.Among 21 community-based studies included (n=137,277), pooled migraine prevalence was 5.61% (95% CI 4.61, 6.70; random effects) among general population; while 14.89% (14.06, 15.74; fixed effects) among student cohorts. Female students had weighted OR of 2.13 (1.34, 3.37; p=0.0013). Prevalence of migraine was higher among urban population compared to rural settings. Migraine burden is bound to increase by more than 10% DALYs within the next decade.Africa has a crude estimate of 56 million people suffering from migraine. By virtue of mainly afflicting the younger working-age group, migraine disability has wider socioeconomic implications. Improving early headache management access points at community-level, training and research at facility-level, and healthy lifestyle modification among urban residents can help reduce this costly and disabling chronic progressive health problem.
View details for DOI 10.1016/j.jns.2014.04.019
View details for PubMedID 24814950
- Prevalence of migraine headache and its weight on neurological burden in Africa: A 43-year systematic review and Meta-analysis of community-based studies JOURNAL OF THE NEUROLOGICAL SCIENCES 2014; 342 (1-2): 1-15
CAM in the Real World: You May Practice Evidence-Based Medicine, But Your Patients Don't
2014; 54 (6): 1097-1102
Complementary and Alternative Medicine (CAM) approaches are widely used among individuals suffering from headache. The medical literature has focused on the evidence base for such use and has largely ignored the fact that these approaches are in wide use despite that evidence base.This article focuses on the uses of CAM by patients and suggests strategies for understanding and addressing this use without referring back to the evidence base. The rationale for this discussion pivots on the observation that patients are already using these approaches, and for many there are anecdotal and historical bases for use which patients find persuasive in the absence of scientific evidence.Until such time as the body of scientific literature adequately addresses non-conventional approaches, physicians must acknowledge and understand, as best as possible, CAM approaches which are in common use by patients. This is illustrated with a case study and examples from practice. This article does not review the evidence base for various CAM practices as this has been done well elsewhere.
View details for DOI 10.1111/head.12364
View details for Web of Science ID 000337640200019
View details for PubMedID 24766436
Does exercise make migraines worse and tension type headaches better?
Current pain and headache reports
2013; 17 (12): 380-?
Many non-pharmacological treatments have been implicated in the treatment of primary headache, with exercise being a common recommendation. In this review we first provide an overview of the relationship between exercise and primary headaches. We then review the physiology of pain modulation, with focus on the endogenous opioids, endocannabinoids, and neuropeptides calcitonin gene-related peptide (CGRP) and brain-derived neurotrophic factor (BDNF), and their associations with primary headache and exercise. Finally, we summarize current literature evaluating effects of exercise on primary headache in an effort to understand the benefits and disadvantages of exercise in primary headaches.
View details for DOI 10.1007/s11916-013-0380-5
View details for PubMedID 24234818
Executive Function Changes before Memory in Preclinical Alzheimer's Pathology: A Prospective, Cross-Sectional, Case Control Study
2013; 8 (11)
Early treatment of Alzheimer's disease may reduce its devastating effects. By focusing research on asymptomatic individuals with Alzheimer's disease pathology (the preclinical stage), earlier indicators of disease may be discovered. Decreasing cerebrospinal fluid beta-amyloid42 is the first indicator of preclinical disorder, but it is not known which pathology causes the first clinical effects. Our hypothesis is that neuropsychological changes within the normal range will help to predict preclinical disease and locate early pathology.We recruited adults with probable Alzheimer's disease or asymptomatic cognitively healthy adults, classified after medical and neuropsychological examination. By logistic regression, we derived a cutoff for the cerebrospinal fluid beta amyloid42/tau ratios that correctly classified 85% of those with Alzheimer's disease. We separated the asymptomatic group into those with (n = 34; preclinical Alzheimer's disease) and without (n = 36; controls) abnormal beta amyloid42/tau ratios; these subgroups had similar distributions of age, gender, education, medications, apolipoprotein-ε genotype, vascular risk factors, and magnetic resonance imaging features of small vessel disease. Multivariable analysis of neuropsychological data revealed that only Stroop Interference (response inhibition) independently predicted preclinical pathology (OR = 0.13, 95% CI = 0.04-0.42). Lack of longitudinal and post-mortem data, older age, and small population size are limitations of this study.Our data suggest that clinical effects from early amyloid pathophysiology precede those from hippocampal intraneuronal neurofibrillary pathology. Altered cerebrospinal fluid beta amyloid42 with decreased executive performance before memory impairment matches the deposits of extracellular amyloid that appear in the basal isocortex first, and only later involve the hippocampus. We propose that Stroop Interference may be an additional important screen for early pathology and useful to monitor treatment of preclinical Alzheimer's disease; measures of executive and memory functions in a longitudinal design will be necessary to more fully evaluate this approach.
View details for DOI 10.1371/journal.pone.0079378
View details for Web of Science ID 000327308500055
View details for PubMedID 24260210
- Does Exercise Make Migraines Worse and Tension Type Headaches Better? CURRENT PAIN AND HEADACHE REPORTS 2013; 17 (12)
Phospholipase C activity increases in cerebrospinal fluid from migraineurs in proportion to the number of comorbid conditions: a case-control study
JOURNAL OF HEADACHE AND PAIN
Migraineurs are more often afflicted by comorbid conditions than those without primary headache disorders, though the linking pathophysiological mechanism(s) is not known. We previously reported that phosphatidylcholine-specific phospholipase C (PC-PLC) activity in cerebrospinal fluid (CSF) increased during migraine compared to the same individual's well state. Here, we examined whether PC-PLC activity from a larger group of well-state migraineurs is related to the number of their migraine comorbidities.In a case-control study, migraineurs were diagnosed using International Headache Society criteria, and controls had no primary headache disorder or family history of migraine. Medication use, migraine frequency, and physician-diagnosed comorbidities were recorded for all participants. Lumbar CSF was collected between the hours of 1 and 5 pm, examined immediately for cells and total protein, and stored at -80°C. PC-PLC activity in thawed CSF was measured using a fluorometric enzyme assay. Multivariable logistic regression was used to evaluate age, gender, medication use, migraine frequency, personality scores, and comorbidities as potential predictors of PC-PLC activity in CSF.A total of 18 migraineurs-without-aura and 17 controls participated. In a multivariable analysis, only the number of comorbidities was related to PC-PLC activity in CSF, and only in migraineurs [parameter estimate (standard error) = 1.77, p = 0.009].PC-PLC activity in CSF increases with increasing number of comorbidities in migraine-without-aura. These data support involvement of a common lipid signaling pathway in migraine and in the comorbid conditions.
View details for DOI 10.1186/1129-2377-14-60
View details for Web of Science ID 000321647800001
View details for PubMedID 23826990
- Cerebrospinal fluid phosopholipase C activity increases in migraine. Cephalalgia 2011; 31 (4): 456-462
- Capillary Endothelial Na+, K+, ATPase Transporter Homeostasis and a New Theory for Migraine Pathophysiology. Headache 2010; 50 (3): 459-78
- The morphology and biochemistry of nanostructures provide evidence for synthesis and signaling functions in human cerebrospinal fluid. Cerebrospinal Fluid Res. 2009: 6:10
- Prostaglandin D Synthase Isoforms from Cerebrospinal Fluid Vary with Brain Physiology. Disease Markers 2006; 22 (1-2): 73-81
- Cerebrospinal Fluid Sodium Increases in Migraine Headache 2006; 46 (7): 1128-1135