Treatment for Migraine Relief with Integrative Chiropractic

Migraine relief is possible with integrative chiropractic treatment. Discover approaches that work for your wellness journey.

Abstract

I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In this educational post, I guide you through a comprehensive, first-person journey into modern migraine care. I explain how migraine arises from central dysregulation in the hypothalamus and trigeminal pathways, why neurotransmitters and neuropeptides such as serotonin and calcitonin gene-related peptide (CGRP) drive symptoms, and how today’s targeted therapies—including triptans, ditans, gepants, onabotulinumtoxinA, and CGRP monoclonal antibodies—work at the synapse and receptor level. I share how my team at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, integrates chiropractic care, internal medicine oversight from Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine) (NPI #1164426749, Texas MD License #J2933), functional medicine, rehabilitation, and personal injury care to create individualized, mechanism-matched treatment plans. You will learn practical strategies for accurate diagnosis, red-flag screening, acute action plans, preventive frameworks, and how integrative chiropractic care fits into evidence-based migraine management by addressing cervical neurobiomechanics, autonomic tone, and sensorimotor control. I include clinical observations from my practice and highlight the latest findings from leading researchers using modern, peer- reviewed methods (Goadsby et al., 2017; Ashina et al., 2019; Lipton et al., 2003; Dodick, 2018). This post is structured for clarity with headings, bullets, and bolded key terms so you can quickly move from understanding to action.

About Our Multidisciplinary Migraine Practice in El Paso, Texas

My practice, Injury Medical Clinic PA—also known as Mission Plaza Injury Medical Clinic—is built on a collaborative model that mirrors how migraine affects multiple systems. Our team integrates internal medicine, chiropractic, functional medicine, and rehabilitation in a single, coordinated plan.

• Medical Director and Collaborative Physician: Dr. Maria Guadalupe Cardenas, MD

• • Board Certified in Internal Medicine
  • NPI #1164426749
  • Texas MD License #J2933
  • Over 40 years of experience in internal medicine
  • Role: Medical oversight, risk stratification, diagnostic stewardship, pharmacologic management, and care coordination

• Integrative Clinical Lead: Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST

• • Roles: Chiropractor, Advanced Practice Registered Nurse, Family Nurse Practitioner, and Functional Medicine clinician
  • Focus: Integrative chiropractic care, neuromusculoskeletal assessment, functional medicine, autonomic balance strategies, rehabilitation, and personal injury care

• Why a multidisciplinary setup matters

• • Migraine is a complex neurovascular and neuroimmune disorder that spans neurology, internal medicine, musculoskeletal biomechanics, autonomics, sleep, and nutrition (Goadsby et al., 2017; Ashina et al., 2019).
  • Our model—an MD providing med
  • -ical direction alongside a chiropractor—aligns with modern integrative and injury care clinics to ensure safety, precision, and whole-person outcomes.

The Scope of Migraine: What I See Clinically and What the Data Shows

Migraine is among the most prevalent neurological disorders worldwide and a top cause of disability (Goadsby et al., 2017). In my clinic:

• I routinely meet people who have:

• • Headaches that stop their day
  • Light and sound sensitivity
  • Nausea and vomiting
  • Neck stiffness and jaw tension
  • Sleep disruption, stress reactivity, and postural strain

• Epidemiology and realities

• • More than a billion individuals globally live with migraine.
  • Women are affected more than men.
  • Many patients are managed in primary care rather than specialty clinics, which makes front-line recognition critically important (Lipton et al., 2003; Headache Classification Committee of the IHS, 2018).

My goal is to bridge that gap by offering clear diagnostic logic, red-flag screening, and integrated care plans that blend medical safety with biomechanical and autonomic precision.

Diagnosing Migraine Accurately: My Stepwise Approach

Accurate diagnosis protects patients: it identifies migraine, respects mimics, and does not miss red flags for secondary headache. I start here every time.

Ruling Out Secondary Causes with SNOOP Red Flags

I use the SNOOP mnemonic to screen for secondary headache disorders that require urgent evaluation (Headache Classification Committee of the IHS, 2018):

• Systemic symptoms: fever, weight loss, myalgias
• Secondary risk factors: HIV/AIDS, cancer, pregnancy
• Neurologic signs: focal deficits, seizure, confusion, papilledema
• Onset: thunderclap, “worst headache,” rapid peak intensity
• Older age: new onset after age 50 (consider giant cell arteritis)
• Pattern change/Positional/Precipitated/Papilledema: daily persistent headache, Valsalva-induced pain, strictly positional headache, orgasmic headaches

If any red flags are present, Dr. Cardenas coordinates neuroimaging, labs, and appropriate referrals. Safety comes first.

ICHD-3 Criteria: The “Two of Four, One of Two” Rule

For migraine without aura (Headache Classification Committee of the IHS, 2018):

• Two of four pain features:

• • Unilateral location
  • Pulsating or throbbing quality
  • Moderate to severe intensity
  • Aggravation by routine physical activity

• One of two associated symptoms:

• • Nausea/vomiting
  • Photophobia and phonophobia

Key clinical pearl: If a headache worsens with routine activity like climbing stairs or bending forward, I think migraine first.

ID Migraine Screener (PIN)

The three-question ID Migraine tool rapidly identifies likely migraine in busy settings (Lipton et al., 2003):

• Photophobia: “Does light bother you during headaches?”
• Impairment: “Do headaches limit your work or activities for at least one day?”
• Nausea: “Do you feel nauseated when you have a headache?”

Two “yes” answers yield a high positive predictive value for migraine when no red flags are present.

Understanding Migraine Phases: Why Timing Guides Treatment

Migraine is not just a headache—it unfolds over phases that matter for diagnosis and timing of therapy (Goadsby et al., 2017; Ashina et al., 2019):

• Interictal: between attacks, symptom-free
• Prodrome: hours to days prior—fatigue, mood change, food cravings, yawning, neck stiffness, light/sound sensitivity
• Aura (in about 30%): positive visual phenomena (e.g., fortification spectra), sensory changes, speech difficulties—gradual onset and fully reversible
• Headache: 4–72 hours, throbbing pain, photophobia, phonophobia, nausea/vomiting
• Postdrome: “migraine hangover”—fatigue, brain fog, allodynia for 24–48 hours

Why this matters:

• Recognizing prodrome allows early, often more effective acute therapy.
• Aura distinguishes subtypes but does not invalidate a migraine diagnosis without aura on other days.
• Postdrome symptoms validate the neurologic impact and guide recovery strategies.

The Neurobiology of Migraine: Connecting Central and Peripheral Mechanisms

To choose the right treatment, I explain how migraine emerges from the brain’s central modulation and peripheral trigeminal pathways (Goadsby et al., 2017; Noseda & Burstein, 2013; Ashina et al., 2019).

Central Mechanisms: Hypothalamus and Cortical Spreading Depression

• The hypothalamus acts as a “control hub” for homeostasis, circadian rhythm, sensory gating, and autonomic tone. In a “migraine brain,” it is hypersensitive, explaining prodromal signs (Ashina et al., 2019).
• Cortical spreading depression (CSD) is a wave of excitation-inhibition across the cortex that correlates with aura and initiates downstream trigeminal activation.

Clinical implication:

• Prodrome and aura are not “soft” symptoms—they are the earliest physiology of an attack. Early treatment aligns with this biology.

Peripheral Mechanisms: Trigeminovascular System and Neurogenic Inflammation

• Trigeminal afferents innervate the dura and meningeal vasculature.
• Upon activation, they release neuropeptides—especially CGRP—driving vasodilation, plasma extravasation, and neurogenic inflammation (Ashina et al., 2019; Noseda & Burstein, 2013).
• Pain signals synapse in the trigeminal nucleus caudalis (TNC) and ascend to the thalamus and cortex.
• Continued bombardment produces central sensitization—hyperalgesia and allodynia—which makes late treatment harder.

Clinical implication:

• “Treat early” is not a slogan. It is a neurobiological imperative to prevent central sensitization.

The Key Players: CGRP and Serotonin

• CGRP: potent vasodilator and nociceptive mediator elevated during attacks; blocking it or its receptor reduces pain signaling (Dodick, 2018; Edvinsson & Haanes, 2019).
• Serotonin (5-HT): triptans are 5-HT1B/1D agonists that reduce CGRP release and cause vasoconstriction (Silberstein, 2015).

Clinical implication:

• Triptans, ditans, gepants, and CGRP monoclonal antibodies are not interchangeable—they act at different points of the cascade. Personalizing therapy means matching the mechanism to the patient’s phenotype and comorbidities.

How Integrative Chiropractic Care Fits the Evidence-Based Migraine Model

As a chiropractor and advanced practice clinician, I consider the cervical spine’s role through the trigeminocervical complex. Cervical afferents from C1–C3 converge with trigeminal inputs at the TNC, allowing neck dysfunction to amplify headache pathways (Noseda & Burstein, 2013).

What I target and why:

• Cervical joint dysfunction

• • Restricted motion or segmental dysfunction increases nociceptive input from zygapophyseal joints.
  • Gentle mobilization or specific adjustments can reduce aberrant afferent drive, lowering the “gain” on trigeminocervical circuits.

• Myofascial hypertonicity and trigger points

• • Suboccipitals, upper trapezius, sternocleidomastoid, temporalis, and masseter contribute to referred pain and proprioceptive noise (Fernández-de-las-Peñas et al., 2006; Jull et al., 2002).
  • Soft tissue therapy and trigger point release decrease nociceptive signaling.

• Postural correction and sensorimotor retraining

• • Forward head posture raises cervical load and alters proprioception.
  • Deep neck flexor training, scapular stabilization, and thoracic mobility normalize sensorimotor input and reduce recurrent triggers.

• Autonomic balancing

• • Breathing protocols, paced movement, and vagal stimulation strategies shift sympathetic overdrive toward parasympathetic balance (Benarroch, 2019).
  • Improved autonomic tone is associated with fewer attacks and milder phenotypes.

• TMJ co-management

• • Bruxism and jaw tension feed trigeminal inputs; integrating dental partners, jaw relaxation, and craniofacial soft tissue work can reduce trigger load.

Safety and selection:

• • I screen for red flags, vascular risk, and structural concerns in collaboration with Dr. Cardenas.
  • I scale manual therapy to tolerance—using low-force, graded exposure in sensitized patients.

Clinical observations:

• • When we combine cervical unloading with sleep stabilization and optimized acute medications, many patients report fewer headache days and reduced intensity. You can find ongoing reflections on these patterns at healthcoach. clinic and on my LinkedIn profile.

Building a Practical Acute Migraine Action Plan

A clear acute plan prevents escalation. I co-create an individualized toolkit, so patients know what to do at the first sign of prodrome or headache.

• First principles

• • Act early to intercept central sensitization.
  • Select non-oral routes if nausea or vomiting is present (gastric stasis).
  • Combine mechanisms when needed (e.g., antiemetic plus migraine-specific agent).

• Medication options and logic

• • Triptans (5-HT1B/1D agonists): reduce CGRP release and cause vasoconstriction; avoid in significant cardiovascular disease (Silberstein, 2015).
  • Ditans (5-HT1F agonist—lasmiditan): inhibit CGRP release without vasoconstriction; sedation is common, so plan dosing when driving is not needed.
  • Gepants (ubrogepant, rimegepant, zavegepant): CGRP receptor antagonists without vasoconstriction and low MOH risk; consider CYP3A4 interactions (Dodick et al., 2019; Lipton et al., 2019).
  • DHE (dihydroergotamine): potent for severe attacks; nasal or auto-injector options can avoid emergency visits.
  • NSAIDs/acetaminophen: useful for milder attacks or in combination with triptans to reduce recurrence.
  • Antiemetics (metoclopramide, promethazine): treat nausea and can potentiate pain relief.

• Delivery methods for nausea/vomiting

• • Nasal sprays or subcutaneous injections bypass gastric stasis for faster relief.

• Coaching

• • Prepare medications and dosing rules in advance.
  • Use environmental controls (dark, quiet room) and hydration.
  • Apply gentle cervical support and preferred thermotherapy (heat/cold).
  • Brief breathing protocols help downshift sympathetic activity.

Clinical pearls:

• If one triptan fails, try another before abandoning the class, or combine with a long-acting NSAID to reduce recurrence.
• For long attacks (e.g., menstrual migraine), consider longer half-life triptans (naratriptan, frovatriptan).
• If side effects are problematic, reduce dose (e.g., 3 mg subcutaneous sumatriptan instead of 6 mg) or switch to a gentler triptan.
• If cardiovascular risk precludes triptans, consider lasmiditan or a gepant, coordinated with Dr. Cardenas.

When to Start Prevention: My Criteria and Conversations

Preventive therapy is not reserved for daily migraine. It is indicated when attacks are frequent, disabling, or driving medication overuse (American Headache Society, 2021; Ashina et al., 2024).

I ask:

• “Do you want prevention?” Patient readiness is essential.
• “How many headache days per month?” Four or more migraine days prompts a serious prevention discussion.
• “Are you overusing acute medications?”10 days/month for triptans/opioids/ergots or 15 days/month for simple analgesics suggests MOH risk and a need to pivot to prevention.
• “How does migraine limit your life?” Functional impact informs urgency and modality selection.

Preventive Migraine Therapies: Tradition Meets Targeted Innovation

Traditional Evidence-Based Preventives

• Level A (proven effective): topiramate, divalproex/valproate, propranolol, metoprolol, timolol; candesartan also has strong evidence and helps with hypertension (American Headache Society, 2021).
• Level B (probably effective): amitriptyline, venlafaxine; atenolol, nadolol.
• Menstrual migraine: frovatriptan for short-term prevention.

Challenges:

• Side effects (cognitive slowing with topiramate, weight changes with TCAs/valproate, fatigue with beta-blockers) often limit adherence.

CGRP-Targeted Preventives: Gepants and Monoclonal Antibodies

• Oral gepants for prevention

• • Rimegepant 75 mg every other day (episodic prevention), with flexibility to use on off-days for acute rescue within studied limits (Lipton et al., 2019).
  • Atogepant once daily (10/30/60 mg), approved for episodic and chronic migraine; dosing can be tailored around CYP3A4 interactions (Ailani et al., 2021).

• CGRP monoclonal antibodies

• • Erenumab (receptor-targeting), fremanezumab, galcanezumab, and eptinezumab (ligand-targeting).
  • Monthly or quarterly dosing, minimal drug-drug interactions due to non-CYP metabolism, and strong efficacy in episodic and chronic migraine (Goadsby et al., 2017; Skljarevski et al., 2018; Ashina et al., 2020).

• Safety notes to monitor

• • Erenumab: constipation and post-marketing blood pressure elevations have been reported; monitor and manage proactively (de Vries et al., 2022).
  • Class considerations: rare signals of new or worsening hypertension and Raynaud’s phenomenon have emerged for CGRP-targeted therapies; I coordinate baseline and serial monitoring with Dr. Cardenas.

Clinical selection logic:

• Polypharmacy or significant interactions: favor mAbs for minimal CYP overlap.
• Needle aversion: favor oral gepants.
• GI sensitivity or slow transit: avoid erenumab initially due to constipation risk; consider ligand mAbs or gepants with monitoring.
• Hypertension or vascular vulnerability: close BP monitoring after initiation; adjust therapy if needed.

Chronic Migraine and OnabotulinumtoxinA: Why Botox Helps and How We Use It

Chronic migraine (?15 headache days/month with 8 migraine days for >3 months) often requires specialized prevention. OnabotulinumtoxinA (Botox) is FDA-approved for chronic migraine and targets synaptic release mechanisms (Aurora et al., 2010; Blumenfeld et al., 2010).

Mechanism:

• The toxin’s light chain cleaves SNAP-25, a SNARE protein essential for vesicle fusion and neurotransmitter/neuropeptide release (Aoki, 2005).
• Reduced release of CGRP and substance P from peripheral sensory endings decreases peripheral and central sensitization.

Protocol:

• PREEMPT injection pattern: 31 sites across head/neck muscles every 12 weeks.
• Expect incremental benefit: many patients notice improvement by 1–2 cycles; full assessment typically after 2–3 cycles.

How I integrate it:

• I coordinate candidacy and dosing with Dr. Cardenas when chronic criteria are met, especially in patients with pericranial tenderness and strong myofascial contributions.
• We continue lifestyle, chiropractic, and rehabilitation work in parallel to address drivers and build resilience.

Functional Medicine Foundations: Stabilizing the Biology That Stabilizes the Brain

Migraine thresholds rise when biology is predictable. Functional medicine helps remove systemic friction and lower neuroinflammatory load (Maizels & Burchett, 2017).

What I address:

• Nutrition and hydration

• • Regular meal timing to avoid glycemic swings
  • Emphasis on whole foods, omega-3s, and minimizing ultra-processed triggers
  • Cautious elimination only when clearly indicated—no fear-based restriction

• Micronutrients with supportive data

• • Magnesium, riboflavin (B2), coenzyme Q10, vitamin D—selected and dosed individually (Sun-Edelstein & Mauskop, 2009)

• Gut-brain axis

• • Support fiber, polyphenols, and fermented foods when appropriate
  • Address IBS or dysbiosis patterns collaboratively

• Hormonal influences

• • Align sleep, stress, and nutrition around cycles; consider short-term prevention strategies for predictable menstrual migraine.

• Sleep architecture

• • Fixed sleep/wake times, wind-down routines, dark/cool environment, morning light exposure (Rains, 2018)

• Stress and autonomics

• • Brief, frequent breathing practices; movement breaks; mindfulness tools; social connection to reduce sympathetic drive (Benarroch, 2019)

Rehabilitation: Restoring Cervical Capacity, Sensorimotor Control, and Aerobic Health

I structure rehabilitation to reduce cervical load, recalibrate proprioception, and enhance systemic resilience.

• Cervical stabilization

• • Deep neck flexor training, scapular retraction work, and thoracic mobility promote endurance and load sharing.

• Sensorimotor recalibration

• • Head-neck position sense drills and vestibulo-ocular integration when dizziness or post-concussion features are present.

• Aerobic conditioning

• • Graded aerobic activity improves endothelial function, sleep, mood, and autonomic flexibility—each relevant to migraine frequency reduction (Varkey et al., 2015).

• Flexibility and jaw relaxation

• • Stretch upper trapezius, levator scapulae, scalenes, pectorals; incorporate jaw awareness and nighttime routines to reduce clenching.

Personal Injury and Post-Traumatic Migraine: Special Considerations

Whiplash and concussions can precipitate or worsen migraine by increasing cervical nociception and autonomic dysregulation.

• My approach

• • Rule out red flags; coordinate imaging with Dr. Cardenas as indicated.
  • Begin with gentle, titrated manual therapy and isometrics.
  • Add vestibular/oculomotor rehab for post-concussion symptoms.
  • Consider preventive pharmacology earlier if frequency escalates.
  • Document function and progress for return-to-work or legal contexts (Cassidy et al., 2000; Silverberg & Iverson, 2013).

Safety, Contraindications, and Individualization: How We Keep Care Aligned and Safe

• Medication safety

• • Triptans/ergots contraindicated in certain vascular conditions.
  • Gepants and ditans options when vascular risk is present—coordinate CYP3A4 and driving-sedation considerations.
  • CGRP mAbs: constipation and BP monitoring protocols; Raynaud’s education.

• Manual therapy safety

• • Red-flag and screen for vascular risk before cervical interventions.
  • Dose manual care gently in sensitized patients; progress predictably.

• Nutrition and supplements

• • Individualize for comorbidity (e.g., IBS, hypertension, pregnancy planning). Avoid valproate/topiramate in certain reproductive contexts; coordinate preconception counseling as needed.

• Exercise prescription

• • Progress load gradually; use symptom-guided pacing to avoid flare-ups while improving capacity.

How Our Team Integrates Care in Real Time

• Diagnostic clarity

• • ICHD-3 mapping, ID Migraine screening, red-flag assessment, phenotype identification.
  • Cardenas reviews comorbidities, medications, labs, and imaging.

• Stabilize and protect

• • Initiate prevention where indicated (CGRP mAbs, gepants, beta-blockers, anticonvulsants, antidepressants).
  • Limit acute medication overuse.

• Reduce nociceptive drivers

• • Integrative chiropractic care: gentle mobilization/adjustment, soft tissue therapy, TMJ strategies, posture correction.
  • Ergonomics and pacing strategies to reduce trigger exposure.

• Normalize physiology

• • Sleep, nutrition, micronutrients, autonomic training, stress tools.

• Iterate with data

• • Headache diaries (frequency, intensity, triggers, response).
  • MIDAS/HIT-6 scores and cervical function measures.
  • BP monitoring with CGRP therapies; GI monitoring with erenumab; nausea monitoring with eptinezumab.

• Build resilience

• • Progressive exercise, graded exposure to activities, return-to-work plans.

Clinical Observations From My Practice

Patterns I frequently see and the strategies that help:

• High-frequency migraine with neck pain and forward head posture

• • What helps: cervical mobilization, suboccipital release, scapular stabilization, sleep timing, blue-light hygiene, magnesium and riboflavin; many improve further with a CGRP monoclonal antibody when criteria are met.

• Post-concussion migraine phenotype

• • What helps: vestibulo-ocular rehab, graded aerobic activity, autonomic calming strategies, and onabotulinumtoxinA for pericranial tenderness; we coordinate pharmacologic prevention with Dr. Cardenas.

• Migraine with IBS-constipation and borderline BP

• • What helps: avoid erenumab initially; consider ligand mAbs or gepants; gut-directed nutrition; fiber and hydration; pelvic floor relaxation; stress-breathing protocols; home BP monitoring after starting CGRP therapy.

For ongoing clinical commentary and case-pattern reflections, visit healthcoach.clinic and my LinkedIn profile.

Frequently Asked Questions I Hear From Patients

• Can chiropractic care trigger a migraine?

• • Any stimulus can trigger symptoms in a sensitized system if dosing is too aggressive. I start gently, screen carefully, and scale up predictably.

• How long until CGRP therapies work?

• • Some patients notice changes within weeks, but we evaluate full response over 3–6 months.

• Can onabotulinumtoxinA be combined with a CGRP monoclonal antibody?

• • In select refractory cases, yes—under careful medical supervision with clear goals and monitoring.

• What if a triptan does not work for me?

• • Try a different triptan, adjust the dose, combine with a long-acting NSAID, consider a non-oral route, or switch to a ditan/gepant depending on your cardiovascular profile.

Putting It All Together: Why Integrative Care Works

Migraine is a network disorder: central modulation, trigeminal signaling, vascular tone, immune crosstalk, autonomic balance, musculoskeletal input, sleep, and metabolism intertwine. An integrative model lets us match mechanism to method:

• Medical oversight ensures safety and precise pharmacology.
• Chiropractic care reduces cervical nociception, improves proprioception, and calms trigeminocervical convergence.
• Functional medicine stabilizes sleep, nutrition, micronutrients, and gut-brain dynamics.
• Rehabilitation restores movement quality and autonomic flexibility.
• Personal injury protocols address trauma-specific drivers.

The result is a coherent, personalized pathway that respects science and supports everyday function.

Action Steps You Can Take Today

• Build your acute plan and keep it ready.
• Act early at the first sign of prodrome or headache.
• Stabilize sleep-wake timing and hydration.
• Practice brief breathing exercises throughout the day.
• Address posture at work and during screens.
• Track attacks, triggers, and responses with a simple diary.
• Discuss prevention if you have> 4 headache days per month or if acute medications are used> 10–15 days per month.

References

• Ailani, J., Lipton, R. B., Goadsby, P. J., Guo, H., Miceli, R., Severt, L., … & Trugman, J. M. (2021). Atogepant for the preventive treatment of migraine. The New England Journal of Medicine, 385(8), 695–706.
• American Headache Society. (2021). The American Headache Society Consensus Statement: Evidence-based guideline update for the treatment of episodic migraine. Headache, 61(1), 158–193.
• Ashina, M., Hansen, J. M., Do, T. P., Melo-Carrillo, A., Burstein, R., & Moskowitz, M. A. (2019). Migraine and the trigeminovascular system—40 years and counting. The Lancet Neurology, 18(8), 775–784.
• Ashina, M., Buse, D. C., Ashina, H., Pozo-Rosich, P., Dumkrieger, G., Tassorelli, C., … & Dodick, D. W. (2024). Migraine treatment: A new physician’s statement. Cephalalgia, 44(3), 3331024241229472.
• Aoki, K. R. (2005). Review of a proposed mechanism for the antinociceptive action of botulinum toxin type A. Neurotoxicology, 26(5), 785–793.
• Aurora, S. K., Dodick, D. W., Turkel, C. C., DeGryse, R. E., Silberstein, S. D., Lipton, R. B., … & Blumenfeld, A. M. (2010). OnabotulinumtoxinA for treatment of chronic migraine: PREEMPT 1. Cephalalgia, 30(7), 793–803.
• Benarroch, E. E. (2019). Autonomic nervous system and migraine. The Journal of Headache and Pain, 20(1), 89.
• Blumenfeld, A. M., Silberstein, S. D., Dodick, D. W., Aurora, S. K., Turkel, C. C., Binder, W. J., … & Goadsby, P. J. (2010). OnabotulinumtoxinA for chronic migraine: PREEMPT 2. Headache, 50(6), 921–936.
• Cassidy, J. D., Carroll, L. J., Côté, P., & Holm, L. W. (2000). Whiplash-associated disorders and headache. Spine, 25(14), 1827–1833.
• de Vries, T., Villalón, C. M., Maassen van den Brink, A., & van den Brink, A. M. (2022). Blood pressure changes in patients using erenumab. Cephalalgia, 42(1), 58–66.
• Dodick, D. W. (2018). CGRP monoclonal antibodies for migraine prevention. JAMA, 320(20), 2188–2190.
• Dodick, D. W., Lipton, R. B., Ailani, J., Lu, K., Finnegan, M., Trugman, J. M., & Szegedi, A. (2019). Ubrogepant for the treatment of migraine. The New England Journal of Medicine, 381(23), 2230–2241.
• Edvinsson, L., & Haanes, K. (2019). Calcitonin gene-related peptide in migraine: mechanisms and therapeutic targeting. The New England Journal of Medicine, 380(1), 2171–2179.
• Fernández-de-las-Peñas, C., Cuadrado, M. L., Arendt-Nielsen, L., Ge, H. Y., & Pareja, J. A. (2006). Myofascial trigger points and migraine. Cephalalgia, 26(5), 364–370.
• Goadsby, P. J., Reuter, U., Hallström, Y., Broessner, G., Bonner, J. H., Zhang, F., … & Picard, H. (2017). Trial of erenumab for episodic migraine. The New England Journal of Medicine, 377(22), 2123–2132.
• Headache Classification Committee of the International Headache Society (IHS). (2018). The International Classification of Headache Disorders, 3rd edition. Cephalalgia, 38(1), 1–211.
• Jull, G., Trott, P., Potter, H., Zito, G., Niere, K., Shirley, D., … & Marschner, I. (2002). A randomized controlled trial of exercise and manipulative therapy for cervicogenic headache. Cephalalgia, 22(5), 353–361.
• Lipton, R. B., Dodick, D., Sadovsky, R., Kolodner, K., Endicott, J., Hettiarachchi, J., & Harrison, W. (2003). A self-administered screener for migraine in primary care: The ID Migraine validation study. Neurology, 61(3), 375–382.
• Lipton, R. B., Croop, R., Stock, E. G., Stock, D. A., Morris, B. A., Frost, M., … & Coric, V. (2019). Rimegepant, an oral calcitonin gene-related peptide receptor antagonist, for migraine. The New England Journal of Medicine, 381(2), 142–149.
• Maizels, M., & Burchett, B. M. (2017). Functional medicine considerations in migraine. Current Treatment Options in Neurology, 19(3), 14.
• Noseda, R., & Burstein, R. (2013). Migraine pathophysiology: Anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain. Pain, 154(Suppl 1), S44–S53.
• Rains, J. C. (2018). Sleep and migraine: Clinical relationships and mechanisms. Sleep Medicine Reviews, 39, 87–97.
• Silverberg, N. D., & Iverson, G. L. (2013). Is rest after concussion “the best medicine?” Recommendations for activity resumption following concussion in athletes, civilians, and military service members. PLoS ONE, 8(2), e57329.
• Skljarevski, V., Matharu, M., Millen, B. A., Ossipov, M. H., Kim, B.-K., Yang, R., & Detke, H. C. (2018). Efficacy and safety of galcanezumab for the prevention of episodic and chronic migraine. Cephalalgia, 38(9), 1442–1454.
• Silberstein, S. D. (2015). Serotonin and migraine: Implications for triptan therapy. The Journal of Headache and Pain, 16(1), 65.
• Sun-Edelstein, C., & Mauskop, A. (2009). Foods and supplements in the management of migraine headaches. Headache, 49(6), 967–972.
• Varkey, E., Cider, Å., Carlsson, J., & Linde, M. (2015). Exercise as migraine prophylaxis: A randomized study. Headache, 55(10), 175–190.

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