Harness the power of integrative treatment to better manage severe headache conditions, such as migraines, with chiropractic care.

Unraveling the Complexity of Migraines: A Modern, Integrative Approach

Hello, I’m Dr. Alex Jimenez. With my extensive background as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), board-certified Family Nurse Practitioner (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), Applied Tonal Neurology (ATN), and Cranial Spinal Integration (CCST), my career has been dedicated to understanding and treating complex health conditions from a truly integrative perspective. At our practice, Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, we have cultivated a unique, multidisciplinary environment focused on comprehensive, patient-centered care.

This collaborative model is essential, especially when managing complex conditions like chronic migraines. A cornerstone of our clinic’s philosophy is my partnership with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a highly respected, board-certified Internist with over four decades of invaluable experience (NPI #1164426749, Texas MD License #J2933). She serves as our Medical Director and Collaborative Physician, providing the essential medical oversight that allows us to blend the best of medical and chiropractic care seamlessly. This structure, where an experienced MD provides medical direction alongside a chiropractor leading a team of diverse specialists, is common in progressive injury and integrative care settings. It ensures that our patients receive a full spectrum of care that is both safe and comprehensive.

Together, our team provides a comprehensive suite of services, including personal injury care, advanced rehabilitation, functional medicine, and integrative chiropractic care, all under one roof. This allows us to create highly individualized treatment plans that address migraines from every possible angle—structural, neurological, biochemical, and lifestyle-related.

Today, I want to guide you on an educational journey into one of the most common and debilitating neurological disorders: migraine. We will explore this condition through the lens of modern, evidence-based research, drawing upon the latest findings from leading experts in the field. Our goal is to demystify migraine, understand its underlying mechanisms, and explore the full spectrum of available treatments, from established protocols to groundbreaking new therapies. We will also discuss how our integrative chiropractic approach fits seamlessly into a comprehensive treatment plan for migraine sufferers, offering a path toward lasting relief and improved quality of life.

Abstract: A Deep Dive into Migraine Diagnosis and Treatment

Welcome to our educational journey into the intricate world of migraines. As a clinician and researcher dedicated to integrative and functional medicine, I am privileged to share insights that bridge cutting-edge neurological research and practical, patient-centered care. In this detailed discussion, we will explore the fundamental neurobiology of migraine, moving beyond outdated theories to embrace a modern understanding of this complex neurological disorder. We will begin by discussing migraine epidemiology, highlighting its widespread prevalence and the critical role of primary care providers in its management. We will then focus on the diagnostic process, using the SNOOP mnemonic to identify red flags that may indicate a more serious secondary headache disorder. We will compare migraine and tension-type headache in detail, along with practical screening tools like the ID Migraine screener to support accurate diagnosis. We will then journey through the distinct phases of a migraine attack—from the prodrome to the postdrome—to understand the full patient experience.

A central part of our discussion will be an in-depth look at migraine pathophysiology, exploring the central and peripheral nervous system mechanisms that drive this condition. We will focus on the interplay between the central nervous system, particularly the hypothalamus, and peripheral nerve inputs from the trigeminal system. I will explain the pivotal roles of key neurotransmitters, such as calcitonin gene-related peptide (CGRP) and serotonin, and how their delicate balance dictates the onset and severity of a migraine attack. We will also explore the clinical implications of this knowledge, including how it informs both acute and preventive treatment strategies. The post will cover the criteria for initiating preventive therapy and provide a detailed exploration of stratified care for acute migraine attacks, outlining a “toolkit” approach that matches treatment intensity to pain levels. We will deeply examine the mechanisms of action for drug classes like triptans, ditans, and gepants, and discuss the management of medication overuse headache (MOH).

The second half of the post shifts to preventive migraine therapy, highlighting the move toward migraine-specific treatments like CGRP-targeting therapies (gepants and monoclonal antibodies) and their growing acceptance as first-line options. We explain the mechanisms, efficacy, and side-effect profiles of these therapies, along with onabotulinumtoxinA (Botox). Throughout this exploration, we emphasize the critical role of our integrative care model at Injury Medical Clinic. We will illustrate how the medical oversight of Dr. Maria Cardenas, MD, and my expertise in integrative chiropractic care work in concert to provide a holistic and effective treatment strategy for patients suffering from migraines, addressing the underlying physiological dysfunctions that perpetuate this debilitating condition.

The Overlooked Epidemic: Understanding the True Scope of Migraine

When we consider common health issues, conditions like diabetes or heart disease often come to mind. However, migraine is a neurological disorder of epidemic proportions, and its prevalence is far greater than many people, including healthcare professionals, recognize. Let’s look at the staggering statistics that paint a clear picture of how widespread this condition is.

• Globally, more than a billion people suffer from migraine.
• In the United States, migraine affects one in five women and one in sixteen men.
• Even children are not spared; one in eleven children experiences migraine. Interestingly, before the onset of puberty, migraine affects boys and girls with roughly equal frequency.
• The impact extends to households, with studies showing that one in four households in the U.S. includes someone who suffers from migraine.

These numbers are not just abstract figures; they represent real people in our communities, workplaces, and even our own waiting rooms. If you were to look around a typical waiting room with about twenty people, it’s statistically likely that at least three or four of them are living with migraine.

The Front Lines of Migraine Care: The Role of Primary Providers

Given its high prevalence, a crucial question arises: who is caring for this vast population of migraine sufferers? The answer might surprise you. It’s not primarily neurologists or specialized headache centers. The front lines of migraine management are overwhelmingly in primary care. Epidemiological surveys reveal that approximately 70% of individuals with migraine are managed by primary care clinicians like family nurse practitioners, physician assistants, and general practitioners.

This reality places a significant responsibility on us as primary providers. We must be equipped with the knowledge to:

1. Accurately diagnose migraine and differentiate it from other headache types.
2. Identify red flags that could signal a more dangerous underlying condition.
3. Understand the pathophysiology—the “why”—behind the disorder.
4. Stay current with the full range of treatment options, from tried-and-true methods to the latest therapeutic advancements.

By arming ourselves with this knowledge, we can offer safe, effective, and compassionate care to the millions who rely on us for relief from this debilitating condition.

The Art and Science of Diagnosis: Identifying Migraine and Ruling Out Red Flags

One of the greatest challenges in managing headache disorders is achieving an accurate diagnosis. Migraine is a notorious chameleon; it doesn’t present with the same set of symptoms in every person or even in the same person during every attack. This variability often leads to misdiagnosis and, consequently, ineffective treatment.

Our societal archetype of a migraine sufferer is often a young woman, perhaps in her late twenties or early thirties, experiencing a severe, debilitating headache linked to her menstrual cycle. While this presentation is common, it is far from the only one. Men, older adults, and children all experience migraine, but their symptoms can look very different. For instance, men with migraine often endure their symptoms for years before seeking help, sometimes waiting until the condition becomes incredibly complex and difficult to manage. An image I’ve seen in a presentation, featuring an older man, serves as a powerful reminder to broaden our clinical perspective.

Therefore, our diagnostic process must be both systematic and nuanced. We need to understand the classic criteria for migraine while remaining alert to its many variations. Before we can confidently diagnose a primary headache disorder like migraine, our first and most critical responsibility is to rule out secondary causes—that is, headaches that are a symptom of another, potentially life-threatening, underlying condition.

The SNOOP Mnemonic: A Clinician’s Guide to Headache Red Flags

To systematically identify these “red flags,” we use the SNOOP mnemonic. Each letter represents a category of signs or symptoms that should prompt immediate and thorough investigation, often including neuroimaging and referral to a higher level of care. Let’s break down what each letter stands for.

·         S: Systemic Symptoms or Secondary Risk Factors

• • Systemic Symptoms: These are constitutional symptoms alongside the headache. If a patient presents with head pain accompanied by fever, myalgias (muscle aches), or unexplained weight loss, we must consider serious underlying conditions. For example, these symptoms could indicate a central nervous system infection, such as meningitis, or another inflammatory process affecting the meninges (the membranes surrounding the brain and spinal cord).
  • Secondary Risk Factors: This category involves the patient’s underlying health status. Individuals with compromised immune systems (HIV), a history of cancer (raising concerns for metastatic disease to the brain), or who are pregnant are at higher risk for secondary headaches. For example, a new-onset headache during pregnancy could be a sign of dangerously high intracranial pressure.

·         N: Neurologic Signs or Symptoms

• • This is perhaps the most critical red flag. If any focal neurologic findings accompany a patient’s headache, it demands immediate attention. These findings include:

• • Focal deficits: Weakness or numbness in one part of the body.
  • New-onset confusion or altered mental status.
  • New-onset seizure.
  • Papilledema: Swelling of the optic disc, visible on fundoscopic exam and a classic sign of increased intracranial pressure.

• • The presence of any of these signs warrants an urgent evaluation, typically in an emergency setting, to rule out conditions like a stroke, brain tumor, or hemorrhage.

·         O: Onset

• • The way a headache begins can provide crucial diagnostic clues. A headache with a sudden, explosive, or “thunderclap” onset is a medical emergency until proven otherwise. This type of onset, where the pain goes from zero to maximum intensity in a matter of seconds to minutes, is the hallmark of a subarachnoid hemorrhage (a bleed in the space surrounding the brain).
  • This is a key differentiator from migraine. While a migraine attack can sometimes awaken a person from sleep, its onset is typically more gradual. Migraine pain tends to wax and wane—it builds in intensity, may ease slightly, and then intensifies again. The unrelenting, instantaneous peak of a thunderclap headache is a distinctly different and far more ominous pattern.

·         O: Older Age of Onset

• • The typical age of onset for migraine is during adolescence or early adulthood. When an individual develops a new type of headache after the age of 50, our clinical suspicion for secondary causes should be high.
  • A primary concern in this age group is giant cell arteritis (GCA), also known as temporal arteritis. This vasculitis (inflammation of the blood vessels) can lead to blindness if not promptly diagnosed and treated with steroids. While GCA can sometimes mimic migraine, there are distinguishing features to look for, including:

• • • Jaw claudication: Pain or fatigue in the jaw muscles with chewing.
    • Scalp tenderness: Pain when touching the scalp or brushing hair.
    • Associated symptoms like weight loss and fatigue.

·         P: Pattern Change, Precipitating Factors, Positional Changes, Papilledema

• • Pattern Change: For patients with a long-standing history of headaches, any significant change in the headache’s frequency, severity, or characteristics is a red flag. For instance, if a 38-year-old woman who has had predictable menstrual migraines for years suddenly develops a new, persistent, daily headache, this warrants neuroimaging to investigate for any new intracranial pathology.
  • Precipitating Factors: If a headache is triggered exclusively by actions that increase intra-abdominal pressure, known as the Valsalva maneuver (e.g., coughing, sneezing, or bearing down), it raises concern for a space-occupying lesion (like a tumor or cyst) or a structural issue like a Chiari malformation.
  • Positional Changes: A headache that changes dramatically with body position is a classic sign of cerebrospinal fluid (CSF) pressure issues.

• Low-Pressure Headache (Spontaneous Intracranial Hypotension): The patient feels fine when lying down, but a severe headache develops upon sitting or standing up. The pain is completely relieved by lying flat again. A CSF leak often causes this.
• High-Pressure Headache: The pain is often worse when lying down and may be associated with papilledema.

• • Headache with Sexual Activity: This can manifest as an “orgasmic headache,” which is often related to the Valsalva effect. While sometimes benign, it always requires a thorough workup to rule out a more serious underlying cause, such as a vascular malformation or bleed.

By diligently applying the SNOOP mnemonic in every headache evaluation, we create a vital safety net and ensure we do not miss a dangerous secondary condition. At the same time, we work to diagnose and treat a primary headache disorder like migraine.

Decoding Migraine: The Official Diagnostic Criteria

Once we have carefully ruled out any red flags using the SNOOP criteria, we can proceed with diagnosing a primary headache disorder. The gold standard for this is the International Classification of Headache Disorders, 3rd edition (ICHD-3), published in the journal Cephalalgia (Headache Classification Committee of the International Headache Society, 2018). Let’s break down the specific criteria for the most common form of migraine: migraine without aura.

To meet the diagnosis, a patient must have had at least five headache attacks that fulfill the following characteristics. The criteria are specific and require a combination of features related to the pain itself and associated symptoms.

The “Two-of-Four” Pain Characteristics

The diagnosis requires the presence of at least two of the following four pain features:

1. Unilateral Location: The pain is located on one side of the head. While this is a classic feature, it’s important to note that about 40% of migraines can be bilateral (on both sides), especially at the onset. The pain can also shift sides during an attack or from one attack to the next.
2. Pulsating or Throbbing Quality: The pain is often described as a rhythmic pounding or throbbing, in sync with the heartbeat. This quality is present in at least 50% of attacks.
3. Moderate to Severe Intensity: The pain is not a minor annoyance. It is intense enough to interfere with or prohibit daily activities. This key feature distinguishes it from a mild tension-type headache.
4. Aggravation by Routine Physical Activity: This is a highly specific and crucial criterion. The headache worsens with simple movements like walking up a flight of stairs, bending over, or even moving from sitting to standing. This forces the individual to seek rest and remain still.

The “One-of-Two” Associated Symptoms

In addition to the pain characteristics, the attack must be accompanied by at least one of the following two features:

1. Nausea and/or Vomiting: The gastrointestinal distress associated with migraine is a hallmark of the condition. Many patients experience profound nausea, and some will have episodes of vomiting.
2. Photophobia (Light Sensitivity) AND Phonophobia (Sound Sensitivity): During an attack, the patient experiences a heightened, often painful, sensitivity to both light and sound. This is why many migraine sufferers instinctively seek out a dark, quiet room.

Putting It All Together: The Diagnostic Puzzle

The flexibility of these criteria helps explain why migraine can present so differently. For example:

• A person with a unilateral, throbbing headache accompanied by light and sound sensitivity has migraine.
• Another person with a bilateral, pressure-like headache that is moderate in intensity and worsens with movement, and who is also nauseous, also has migraine.

This variability can be confusing. The pain doesn’t always have to be throbbing; it can feel like squeezing or pressure. The key is to listen carefully to the patient’s full story and see how the pieces fit the diagnostic puzzle. It’s also important to recognize that migraine exists on a spectrum. A single individual can have attacks that vary in intensity and symptomatology. They might describe their “bad headaches” as having all the classic features, while their “milder headaches” might only have a few. Understanding this continuum is vital for accurate diagnosis and effective management.

A Quick and Powerful Screening Tool: The ID Migraine™ Screener

In the busy environment of a primary care clinic or our own practice, we often need a quick, reliable way to screen for migraine. Dr. Richard Lipton, a leading neurologist and epidemiologist in the headache field, developed a simple yet remarkably effective tool called the ID Migraine™ screener (Lipton et al., 2003). It consists of just three “yes or no” questions that encapsulate the most disabling and specific features of migraine.

The screener uses the acronym PIN to make it easy to remember:

1. P – Photophobia: During your headache, does light bother you more than usual?
2. I – Impairment: Has a headache limited your ability to work, study, or do what you needed to do for at least one day in the last three months?
3. N – Nausea: Do you ever feel nauseous or sick to your stomach when you have a headache?

The diagnostic power of this simple tool is impressive. If a patient answers “yes” to two of these three questions, they have a 93% positive predictive value for migraine (assuming, of course, that red flags have been ruled out).

This screener is invaluable in a clinical setting. It allows us to quickly and efficiently identify patients who likely have migraine and need a more in-depth evaluation and treatment plan. It cuts through the complexity and focuses on the core symptoms that define the migraine experience: sensory hypersensitivity (photophobia), disability (impairment), and autonomic dysfunction (nausea).

Migraine vs. Tension-Type Headache: A Critical Distinction

One of the most common diagnostic pitfalls is confusing migraine with a severe tension-type headache. Many patients come to our clinic believing they have “sinus headaches” or “tension headaches” when they are, in fact, experiencing migraine. Making the correct distinction is absolutely critical because the treatment approaches for these two conditions are fundamentally different.

Let’s compare and contrast the key features of migraine and tension-type headache, based on data published in the journal Cephalalgia.

Feature	Migraine	Tension-Type Headache
Duration	4 to 72 hours in adults (can be as short as 2 hours in children)	30 minutes to 7 days
Location	Unilateral (one-sided) in ~60% of cases; bilateral in ~40%	Always bilateral (both sides)
Pain Quality	Throbbing or pulsating in >50% of cases	Non-pulsating; described as pressing, tightening, or squeezing
Pain Intensity	Moderate to severe	Mild to moderate
Aggravation by Activity	Yes, worsened by routine physical activity	No, not worsened by routine physical activity
Associated Symptoms	Nausea and/or vomiting and/or photophobia AND phonophobia	No nausea or vomiting; may have either photophobia OR phonophobia, but not both

The Single Most Important Question

If you could ask only one question to differentiate migraine from tension-type headache, it would be: “Does routine physical activity make your headache worse?”

• If a patient says, “Yes, if I walk up the stairs or even get up from a chair, the pain gets worse,” it strongly suggests migraine. A migraineur’s defining behavior is wanting to lie still in a dark, quiet room.
• If the patient says, “No, in fact, I often feel a bit better if I get up, stretch my neck, and move around,” this points toward tension-type headache.

This difference in response to activity reflects the underlying pathophysiology. Migraine is a state of central nervous system hypersensitivity, where any sensory input, including movement, can amplify the pain. Tension-type headache is more often linked to musculoskeletal factors, where gentle movement and stretching can actually provide relief.

Most patients who seek medical care for a headache are experiencing migraine. People with tension-type headaches can typically manage them at home with over-the-counter medication or simple physical measures. So, as a clinician, it’s wise to think migraine first when a patient presents with a significant headache complaint, provided there are no neurologic red flags.

Beyond the Pain: The Four Phases of a Migraine Attack

Many people think of migraine as simply a bad headache. However, the headache phase is just one part of a complex neurological event that can unfold over several days. A complete migraine attack consists of four distinct phases. Understanding these phases is crucial for diagnosis and for helping patients recognize triggers and start early treatment.

As a clinician, asking patients about their experiences before and after the headache can provide valuable diagnostic information and reveal the true burden of the disorder. Let’s walk through the entire continuum of a migraine attack.

1. The Interictal Phase

This is the period between migraine attacks. For some, this phase is completely symptom-free. However, for those with frequent or chronic migraine, this “pain-free” window can be very short or even non-existent. One goal of preventive therapy is to lengthen this interictal phase, giving patients more days of clarity and freedom from symptoms.

2. The Prodrome Phase (The Warning Stage)

This phase can begin hours or even a day or two before the headache pain starts. It is experienced by up to 70% of people with migraine and serves as a kind of “warning sign” that an attack is imminent. The prodrome is driven by dysfunction in the hypothalamus, a deep brain structure that regulates many of our body’s essential functions.

Common symptoms of the prodrome include:

• Sensory Hypersensitivity: Increased sensitivity to light, sound, or smells.
• Cognitive Changes: Difficulty concentrating, trouble finding words (“anomia”), or a feeling of being in a “fog.”
• Mood Changes: Irritability, depression, or sometimes euphoria.
• Fatigue and Yawning: Overwhelming tiredness and excessive yawning.
• Neck Stiffness: Many people experience a stiff, sore neck. It is crucial to understand that neck stiffness is often a symptom of the impending migraine, not the cause of it. Patients frequently misinterpret this as a “tension headache” that is causing the migraine, when in reality, it’s the brain signaling the start of the attack.
• Dizziness or Vertigo: A feeling of being off-balance or that the room is spinning.

Recognizing these prodromal symptoms is a powerful tool. It gives the patient a window of opportunity to take acute medication, avoid known triggers, and prepare for the potential onset of a full-blown attack.

3. The Aura Phase

The aura phase is experienced by about 30% of migraine sufferers. An aura consists of fully reversible neurological symptoms that typically precede, or sometimes accompany, the headache. These symptoms usually develop over 5 to 20 minutes and last for less than 60 minutes.

• Visual Aura (Most Common): This is the most frequent type of aura. Unlike the visual loss associated with a transient ischemic attack (TIA), a migraine aura is typically a positive phenomenon, meaning the brain is creating a visual stimulus. Patients may see:

• • Bright, shimmering, or jagged lines (fortification spectra).
  • Spots of light or geometric shapes.
  • A visual phenomenon that starts in the center of the visual field and slowly expands outward.

• Sensory Aura: This can involve tingling or numbness that often starts in the fingertips, marches up the arm, and may spread to the face and tongue.
• Language Aura (Aphasia): Temporary difficulty with speech or word-finding.

Differentiating a migraine aura from a TIA is critical. A TIA typically involves negative phenomena, such as sudden vision loss (like a curtain coming down over an eye) or a distinct visual field cut. A migraine aura, in contrast, is an active, evolving visual disturbance.

4. The Headache Phase

This is the most recognized phase of the attack, characterized by the pain and associated symptoms we discussed in the diagnostic criteria. It typically lasts from 4 to 72 hours if untreated or ineffectively treated. The pain is often throbbing, moderate to severe, and disabling. It is accompanied by nausea, vomiting, and extreme sensitivity to light and sound.

5. The Postdrome Phase (The Migraine “Hangover”)

After the headache pain finally subsides, the migraine attack is not necessarily over. The postdrome phase can last for another 24 to 48 hours. During this time, patients often feel completely drained, exhausted, and “hungover.”

Common symptoms of the postdrome include:

• Extreme fatigue and weariness.
• Difficulty concentrating.
• Muscle aches and scalp tenderness. The muscles of the head, neck, and shoulders can be very sore to the touch.
• Lingering mood changes.

When we add up all the phases—prodrome, aura (if present), headache, and postdrome—a single migraine “event” can disable a person for several days. This highlights migraine’s profound impact on an individual’s quality of life and underscores the importance of effective, comprehensive treatment.

The Engine of Pain: Unraveling the Pathophysiology of Migraine

To treat migraine effectively, we must first understand what is happening inside the brain and nervous system that causes it. For many years, the prevailing belief was that migraines were simply a vascular problem—a painful headache caused by the swelling and shrinking of blood vessels in the brain. While vascular changes do occur, modern research has revealed a more sophisticated, nuanced reality. Migraine is now understood as a primary neurological disorder with a strong genetic basis, originating from a state of hyperexcitability within the central nervous system. Let’s journey into the brain to understand what this truly means. We will explore the key players in this process, dividing them into two main categories: central mechanisms (originating in the brain) and peripheral mechanisms (involving nerves outside the brain).

Central Innervation: The Brain’s Role in Migraine

The evidence strongly suggests that migraine begins deep within the brain.

• A Strong Genetic Component: Genetics is the first clue. In about 70% of people with migraine, we can identify at least one other first-degree relative who also has the disorder. This indicates a powerful inherited predisposition. The genes involved seem to control neuronal excitability and ion-channel function, essentially setting the brain’s “volume” for processing sensory information too high.
• The Hypothalamus: The Migraine Generator?

• Increasingly, research from pioneers in the field points to the hypothalamus as a key “generator” or initiator of migraine attacks (Schulte & May, 2016). This small but mighty structure, located in the diencephalon at the base of the brain, acts as a master regulator for many of the body’s vital functions.
• Think of the hypothalamus as an orchestra conductor, keeping different sections of the body in harmony. It maintains homeostasis—regulating sleep-wake cycles (circadian rhythms), appetite, thirst, body temperature, and hormone release. It is also deeply intertwined with the limbic system, the brain’s emotional hub, and plays a crucial role in processing and modulating sensory information.
• In individuals who experience migraines, this critical region is in a state of dysmodulation or dysfunction. It’s as if the conductor is a bit “wonky” or overly sensitive. The hypothalamus in a migraineur’s brain appears to be chronically overstimulated or hyperexcitable. This inherent sensitivity means it’s predisposed to overreact to various internal and external triggers.
• This explains why so many pre-migraine symptoms, known as the prodrome phase—fatigue, yawning, food cravings, mood swings, or fatigue—are linked to hypothalamic functions. These aren’t random occurrences; they are direct signs that the hypothalamus is beginning to misfire. This central dysfunction, however, doesn’t exist in a vacuum. It requires a spark to ignite the full-blown migraine cascade. That spark often comes from the periphery.

The Trigeminal Nerve: The Peripheral Trigger for a Central Storm

While the hypothalamus sets the stage for a migraine, the trigeminal nerve is often the primary actor that initiates the performance. The largest and most complex of the twelve cranial nerves, it primarily provides sensation to the face and head. Crucially, it also innervates the pain-sensitive structures within the cranium, such as the meninges (the protective layers surrounding the brain) and the cerebral blood vessels.

To visualize this, imagine the trigeminal nerve as a vast network of sensory wires spread throughout your head. Our clinical understanding, supported by extensive research (Goadsby et al., 2017), points specifically to the ophthalmic division (V1) of this nerve as a major contributor. It gathers sensory information from the forehead, scalp, and the structures inside the skull.

Tracing the Pain Pathway: From Periphery to Perception

Let’s follow the journey of a pain signal as it travels through this system, ultimately culminating in the debilitating pain of a migraine. This model is often called trigeminovascular system activation.

1. Peripheral Activation: The process begins with input or irritation at the peripheral endings of the trigeminal nerve. This could be triggered by stress, certain foods, bright lights, hormonal shifts, or even physical tension in the neck and jaw.
2. Convergence at the Trigeminal Nucleus Caudalis (TNC): All these disparate sensory impulses from the head and upper neck don’t travel in isolation. They bundle together and converge at a critical processing center at the top of the spinal cord called the trigeminal nucleus caudalis (TNC). Think of the TNC as a central relay station or a switchboard that collects all incoming calls from the head and face region. This anatomical convergence is profoundly important, as we will discuss in the context of chiropractic care.
3. Ascension to Higher Brain Centers: From the TNC, specialized nerve cells called second-order neurons take this bundled information and transmit it upward, directly into the hypothalamic region we discussed earlier, and onward to the thalamus, the brain’s main sensory processing center.
4. Central Amplification and Perception: Here is where the central dysfunction becomes critical. When these signals reach the already hyperexcitable hypothalamus and thalamus, they overreact. Instead of filtering the signals appropriately, these centers amplify them and send an excessive barrage of impulses onward to the cerebral cortex—the part of the brain where we consciously perceive sensations. At this final step, the individual “feels” the intense, throbbing pain of a migraine (Noseda & Burstein, 2013).

This is not just a simple linear pathway; it’s a cascade, a chain reaction. The initial peripheral signal ignites a central firestorm in a brain that is already primed for it. This model elegantly explains how diverse triggers can all lead to the same endpoint: a migraine attack.

The Chemical Messengers of Migraine: CGRP and Serotonin

To understand and treat migraines effectively, we must look deeper than anatomical pathways to the neurotransmitters—the chemical messengers that let nerve cells communicate. Two players have taken center stage in modern migraine research: Calcitonin Gene-Related Peptide (CGRP) and Serotonin.

Calcitonin Gene-Related Peptide (CGRP): The “Migraine Molecule”

If a single molecule could be named the “villain” in the migraine story, it would be CGRP. This peptide is found throughout the body, but it is particularly abundant in the trigeminal nervous system. Research has illuminated its multifaceted and crucial role in generating migraine pain (Edvinsson et al., 2018).

• A Powerful Vasodilator: CGRP is one of the most potent vasodilators known in the human body. When released, it causes blood vessels to expand or dilate. This action contributes to the throbbing sensation many migraine sufferers experience.
• Pain Transmission: Beyond its vascular effects, CGRP is fundamentally involved in transmitting pain signals. It acts like a volume knob for pain, turning up the intensity of the signals traveling through the trigeminal system.
• Widespread Expression: CGRP is incredibly abundant within the trigeminal system. It is expressed in approximately 35% to 50% of the neurons in the trigeminal ganglia. This high concentration underscores its importance. It’s found predominantly in C-fibers, which transmit pain signals more slowly, leading to the dull, aching, persistent quality of migraine pain, and in A-delta fibers, which transmit pain more rapidly. This dual action helps explain the complex nature of migraine pain.

The evidence for CGRP’s central role is compelling and directly observable. Researchers have conducted studies in which they draw blood from patients during a migraine attack. The findings are consistent and revolutionary: CGRP levels are significantly elevated during a migraine and return to normal between attacks. Furthermore, infusing CGRP into individuals prone to migraines can reliably trigger a migraine attack (Ashina et al., 2019). This isn’t just a correlation; it’s a causal link.

• Neurogenic Inflammation: When released from trigeminal nerve endings, CGRP also orchestrates an inflammatory response. It triggers the degranulation of mast cells, immune cells that, when activated, release a cocktail of inflammatory substances (like histamine) into the surrounding tissue. This process, known as neurogenic inflammation, creates an “inflammatory soup” around the nerves and blood vessels of the meninges, making them even more sensitive and perpetuating the pain cycle.
• Central Sensitization: CGRP propagates pain signals forward, activating central structures like the TNC and thalamus. This leads to central sensitization, a phenomenon in which the central nervous system becomes so wound up and hypersensitive that it starts to interpret normal, non-painful stimuli as painful (a condition called allodynia). This is why, during a migraine, a person’s scalp can become tender to the touch, or the light pressure of glasses can feel unbearable. The nervous system is on high alert, and CGRP is a key driver of this state (Burstein et al., 2015).

Serotonin: The Counterbalancing Force

On the other side of this neurochemical equation is serotonin (5-HT), a neurotransmitter known for its role in mood but also vital to the trigeminal system. For decades, long before we fully understood CGRP, we knew that manipulating serotonin could stop a migraine. The key lies in the inverse relationship between serotonin and CGRP at the synapse:

When serotonin levels at the synapse are high, CGRP release is suppressed.

This single biological fact was the foundation for an entire class of migraine medications: the triptans (e.g., sumatriptan). Triptans are serotonin agonists. They work by mimicking serotonin, binding to its receptors on the presynaptic nerve terminal. By increasing the serotonin-like activity at the synapse, they effectively put the brakes on CGRP release. This reduces neurogenic inflammation, reverses vasodilation, and blocks pain signal transmission, thereby aborting a migraine attack.

The Fundamental Goals of Migraine Treatment and Initiating Prevention

When a patient comes to our clinic seeking help for migraines, our primary objectives are clear and shared: to achieve pain freedom, if possible, and to facilitate a full return to normal function. These two goals are inextricably linked. A life punctuated by debilitating head pain is a life diminished.

But when do we move from treating individual attacks to implementing a long-term preventive strategy? This crucial question requires a collaborative decision between the clinician and the patient. Clear guidelines help us navigate this.

• For Highly Disabling Attacks: Even if a person experiences just one migraine attack per month, if that single attack is incredibly disabling—perhaps it completely incapacitates them—it is essential to offer and initiate preventive therapy. Severity and impact on quality of life, not just frequency, are paramount.
• For Moderate Frequency and Intensity: According to the American Headache Society, if an individual has two to four migraine attacks per month, depending on intensity, they are a strong candidate for preventive treatment.
• For Higher Frequency: If attacks occur four to six times a month, regardless of pain intensity, it becomes essential to offer a preventive therapy plan.

The overarching goal of any preventive therapy is threefold:

1. Reduce the frequency of migraine attacks.
2. Reduce the intensity of the attacks that do occur.
3. Reduce the duration of those attacks.

With a vast and ever-expanding arsenal of treatments available, a common question arises: “How do I choose the right one?” This is where the art and science of medicine converge, requiring a personalized, stratified approach to care.

Stratified Care for Acute Attacks: The Migraine Treatment Toolkit

At Injury Medical Clinic, we empower patients by developing a personalized “toolkit” for their headaches. This involves a deep dialogue to understand the unique character of their attacks. A one-size-fits-all approach is doomed to fail.

A patient might tell me, “Dr. Jimenez, if a headache starts on both sides of my head, I know it’s probably not going to be a full-blown migraine. I can usually manage it with an over-the-counter anti-inflammatory.” This suggests that for mild-to-moderate headaches, a simple intervention works. However, the same patient might continue, “But if the pain begins behind my left eye, a sharp, throbbing pain, that’s when I know I’m in trouble.” This is the essence of stratified care. We categorize the headache’s intensity and tailor the treatment accordingly.

For Mild Pain

For headaches that the patient identifies as mild, we might begin with a simple analgesic.

• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Medications like ibuprofen or naproxen are often effective.
• Acetaminophen: This can also be an option.

Of course, a thorough review of the patient’s health history is non-negotiable to screen for risks such as peptic ulcer disease or renal disease. This is where the collaboration with Dr. Cardenas is invaluable. Her internal medicine expertise ensures we choose the safest possible option.

For Moderate Pain

When the pain escalates to a moderate level, it’s time to deploy a migraine-specific agent.

• Triptans: (e.g., sumatriptan, rizatriptan)
• Ergotamines: (e.g., dihydroergotamine or DHE 45)
• Ditans: (lasmiditan)
• Gepants: (e.g., ubrogepant, rimegepant)

When considering these options, a comprehensive review of the patient’s vascular health is critical. Many of my patients are now in their fifties and sixties. They may have developed conditions like hypertension or are on medications that could interact, particularly those metabolized by the cytochrome P450 3A4 (CYP3A4) enzyme system.

For Severe Pain

For severe, incapacitating migraine attacks, we need our most powerful tools.

• A Migraine-Specific Agent: We would start with a triptan, ditan, gepant, or DHE 45.
• A Dopamine Antagonist: To enhance the treatment, we often add a dopamine antagonist like metoclopramide or prochlorperazine. These agents are potent antiemetics that directly combat severe nausea and vomiting. They may also boost the pain-fighting power of migraine-specific agents by modulating central pain pathways.

A universal principle of acute migraine treatment is to treat early. Intervening at the first sign of pain, before central sensitization fully takes hold, dramatically increases the likelihood that the medication will work.

A Closer Look at Acute Migraine Medications and Their Mechanisms

The landscape of acute migraine therapy is constantly evolving. To use these medications effectively, we need to look under the hood at their mechanisms of action.

The Triptans: Presynaptic Serotonin Agonists

As we discussed, triptans are serotonin (5-HT) 1 B/1D receptor agonists. They act on the presynaptic neuron to activate specific serotonin receptors, which act like a brake by inhibiting CGRP release. However, the 5-HT1B receptor is also found on blood vessels, and its activation causes vasoconstriction. This is why triptans are generally contraindicated in individuals with uncontrolled hypertension or significant vascular disease.

New formulations offer benefits:

• Low-Dose Subcutaneous Sumatriptan: A 3 mg option is now available, offering better tolerability for sensitive patients.
• Enhanced Nasal Formulations: A nasal spray with a permeation enhancer and a breath-activated nasal powder improve absorption.
• Triptan-NSAID Combination: A new combination tablet pairing rizatriptan with meloxicam (an NSAID) attacks the migraine through two different mechanisms simultaneously.

DHE 45 (Dihydroergotamine): An Old Ally in a New Device

Dihydroergotamine, or DHE 45, is a venerable but highly effective medication for severe migraines. A major barrier to its use was its cumbersome delivery method. In recent months, this has changed dramatically with the introduction of a DHE 45 auto-injector, making this potent therapy accessible and easy to use.

The Ditans (Lasmiditan): A Selective Serotonin Modulator

For patients who cannot take triptans due to vascular risks, we now have a revolutionary alternative: the ditans. The only ditan currently on the market is lasmiditan. It selectively targets the serotonin 5-HT1F receptor, which is not located on blood vessels. Therefore, lasmiditan can inhibit CGRP release without causing vasoconstriction (Goadsby et al., 2019).

However, it comes with a distinct set of disadvantages. Lasmiditan can cause significant central nervous system (CNS) side effects, including dizziness and somnolence (drowsiness). Due to these CNS effects, there is a strict restriction: patients must not drive or operate heavy machinery for at least eight hours after taking a dose. I often prescribe lasmiditan for patients with very severe attacks in the evening, instructing them to take it and go to bed, using the somnolence as a therapeutic tool to facilitate restorative sleep.

The Gepants: Post-Synaptic CGRP Blockers

The third major category of acute migraine-specific drugs is the gepants, or CGRP receptor antagonists. The currently available acute gepants include ubrogepant, rimegepant, and a nasal spray called zavegepant. Instead of preventing CGRP release, gepants work post-synaptically. They bind to the receiving neuron and physically block the CGRP receptor site, acting as a shield (Dodick et al., 2019).

Gepants offer several key advantages:

• No Vasoconstriction: Safe for patients with cardiovascular risk factors.
• No Risk of Medication Overuse Headache (MOH): This is a massive advantage. Medication Overuse Headache (MOH) is a paradoxical condition where the frequent use of acute medication (triptans, ergots, or combination analgesics on 10+ days/month; simple analgesics on 15+ days/month) causes more headaches. Gepants have been shown not to cause MOH, making them excellent for high-frequency patients.
• Metabolism via CYP3A4: Gepants are metabolized by the CYP3A4 enzyme system in the liver. This requires careful screening of a patient’s other medications. Drugs that induce this enzyme (like topiramate) may require a higher gepant dose, while inhibitors (like verapamil) may require a lower dose.

The Intricate Dance of Neurotransmission and the SNARE Complex

To understand how some of the most advanced preventive therapies work, we must journey back into the microscopic world of our nervous system. For neurotransmitters like CGRP to be released, the vesicle containing them must fuse with the presynaptic nerve membrane. This requires a sophisticated “docking” mechanism involving a group of proteins known as the SNARE complex. A key protein in this complex is SNAP-25 (Synaptosomal-Associated Protein 25). It works with other proteins to form the complete SNARE complex, which acts like a zipper, pulling the vesicle and the nerve membrane together to facilitate neurotransmitter release.

The Changing Landscape of Migraine Prevention

For individuals who experience frequent or debilitating migraines, acute treatment alone is not enough. The focus must shift to preventive therapy. The world of standard-of-care therapy for migraine prevention is undergoing a seismic shift. For decades, our options were borrowed from other conditions (beta-blockers, antidepressants, anticonvulsants). In the last several years, we have witnessed the introduction of the first-ever migraine-specific preventive therapies.

A physician statement in 2024 advocated for these new CGRP-targeted therapies as first-line treatment options, rather than requiring patients to fail multiple older medications first (Ashina et al., 2024). While we still often fight with insurance carriers, a 2022 position statement from the National Headache Foundation reinforces that preventive therapy should be a collaborative decision between clinician and patient, not dictated by rigid algorithms (National Headache Foundation, 2022).

OnabotulinumtoxinA (Botox): Disrupting the Signal at its Source

One of the established treatments for chronic migraine is OnabotulinumtoxinA, approved for chronic migraine in 2010. This neurotoxin works by directly interfering with the SNARE complex. Its light chain component specifically targets and cleaves the SNAP-25 protein. By breaking this essential protein, the toxin effectively sabotages the docking platform. The vesicle can no longer dock and fuse, blocking CGRP release.

The PREEMPT (Phase 3 REsearch Evaluating Migraine Prophylaxis Therapy) clinical trials (Blumenfeld et al., 2018) established the efficacy of onabotulinumtoxinA for chronic migraine. This led to a standardized injection protocol involving 31 injections across seven specific head-and-neck muscle groups, administered every 12 weeks. By blocking neurotransmitter release at these key locations, we can effectively create a “firewall” that prevents the initiation and propagation of migraine pain signals.

CGRP Monoclonal Antibodies: A New Era of Targeted Prevention

CGRP monoclonal antibodies have been a game-changer for many of my patients. These large-molecule biologic drugs are designed to block the CGRP pathway specifically.

Medication	Route of Administration	Dosing Frequency	Site of Action	Key Distinguishing Features
Eptinezumab	Intravenous (IV)	Every 3 months	Ligand	The only IV formulation; rapid onset of action.
Fremanezumab	Subcutaneous (SQ)	Monthly or every 3 months	Ligand	Offers flexible dosing with monthly or quarterly options.
Galcanezumab	Subcutaneous (SQ)	Monthly	Ligand	Administered monthly after an initial loading dose.
Erenumab	Subcutaneous (SQ)	Monthly	Receptor	The only antibody that targets the CGRP receptor directly.

One of their most significant advantages is their metabolism. Unlike oral preventives processed by the liver’s cytochrome P450 system, these antibodies are metabolized at a cellular level, meaning they have very few, if any, significant drug-drug interactions (Sacco et al., 2019). This is a massive clinical advantage for medically complex patients.

• Side Effects: While well-tolerated, injection site reactions are common. Erenumab, the receptor blocker, is associated with constipation, so I tend to avoid it in patients with a history of GI issues.
• New Safety Information on CGRP Antagonists: The FDA has released important new safety information concerning CGRP antagonists as a class (both antibodies and gepants). There have been infrequent reports of new onset or worsening of hypertension and new onset or worsening of Raynaud’s phenomenon (U.S. Food and Drug Administration, 2023). This reinforces the importance of monitoring blood pressure and discussing Raynaud’s symptoms with all patients starting these therapies.

Gepants for Migraine Prevention

The same small-molecule CGRP receptor antagonists used for acute treatment are also approved for prevention.

• Rimegepant (Nurtec ODT): Dosed at 75 mg every other day for episodic migraine prevention. It has a unique dual role: a patient on the preventive schedule can take an extra tablet as an acute treatment for a breakthrough migraine.
• Atogepant (Qulipta): A once-daily pill approved for both episodic and chronic migraine. Common side effects include nausea and constipation. A small percentage of people may experience modest weight loss, which can be a welcome side effect for patients who have gained weight on other preventives.

Clinical Pearls for Selecting Preventive Migraine Therapy

The expanded toolkit allows for a personalized, “two-for-one” approach.

• Migraine and Hypertension: A beta-blocker (propranolol) or ARB (candesartan) is a logical first step.
• Migraine and Depression/Anxiety: An antidepressant like venlafaxine or amitriptyline can be an excellent choice.
• Migraine and Obesity: Topiramate can be a strategic choice, as weight loss is a common side effect.
• Migraine in Women of Childbearing Age: I am extremely cautious and generally avoid valproic acid and topiramate due to their known teratogenic effects (risk of congenital disabilities).

The Integrative Care Model: Where Chiropractic and Medical Management Converge

This brings us back to the core philosophy of our practice at Injury Medical Clinic. Managing a complex condition like chronic migraine rarely succeeds with a single-modality approach. This is where our multidisciplinary team, under the collaborative guidance of Dr. Maria Cardenas and me, truly shines. While the pharmacologic treatments address the biochemical aspects of migraine, they do not address the significant biomechanical and musculoskeletal components. This is where integrative chiropractic care becomes indispensable.

The Cervicogenic Connection and the Trigeminal Nucleus Caudalis (TNC)

One of the most critical connections between chiropractic care and migraine is the anatomical and functional link between the upper cervical spine and the trigeminal nucleus caudalis (TNC). As we discussed, the TNC is the central hub where sensory information from the head (via the trigeminal nerve) converges with sensory information from the neck (via the upper cervical nerve roots C1, C2, and C3). This is not a theoretical connection; it is hard-wired into our neuroanatomy (Chaibi & Russell, 2014).

• Biomechanical Stress as a Trigger: Poor posture, joint restrictions (vertebral subluxations), and muscle tension in the upper neck can generate a constant stream of aberrant or “noisy” sensory signals.
• Sensitizing the TNC: This barrage of nociceptive (pain-related) input from the neck can lower the activation threshold of the neurons within the TNC, making them more excitable and lowering the migraine threshold. The neck essentially becomes a primary contributor to the overall “allostatic load” on the nervous system.

Chiropractic adjustments (spinal manipulative therapy) are specifically designed to address these biomechanical issues. By restoring proper motion to the joints of the cervical spine, reducing nerve irritation, and decreasing surrounding muscle tension, we can:

• Reduce Nociceptive Input: Turn down the volume of aberrant signals flowing from the neck to the TNC.
• Desensitize the TNC: Help “reset” the sensitivity of the TNC, raising the threshold for a migraine attack.
• Improve Cerebrospinal Fluid (CSF) and Blood Flow: Proper spinal mechanics are also believed to influence the flow of CSF and blood to and from the brain, helping reduce congestion and inflammation.

From my clinical observations, documented on platforms like my LinkedIn profile and in our PUSHASRX functional fitness programs, patients who receive targeted cervical chiropractic care often report a significant reduction in the frequency, intensity, and duration of their migraines. This is no coincidence; it is a direct result of addressing a key, often overlooked, contributor to their condition.

Myofascial Trigger Points and Postural Rehabilitation

Chronic postural strain can lead to taut bands of muscle known as myofascial trigger points in the neck and shoulder muscles. These can refer pain directly to the head, triggering attacks. I utilize a variety of manual therapies, including trigger point therapy and myofascial release, to deactivate these points. A key part of my treatment also involves prescribing specific therapeutic exercises to correct poor posture, especially “forward head posture,” reducing chronic mechanical stress.

Functional Medicine and Nutritional Counseling

My training in Functional Medicine (CFMP, IFMCP) allows us to look even deeper for root causes. We can explore dietary triggers, nutrient deficiencies (e.g., magnesium, riboflavin, CoQ10), and gut health issues that contribute to systemic inflammation and lower the migraine threshold. We work with patients to implement anti-inflammatory diets and targeted supplementation protocols that support neurological health from the inside out.

The Collaborative Power of MD and DC

This is where the collaboration between Dr. Cardenas and me creates a uniquely powerful therapeutic model.

• A patient with chronic migraines might see Dr. Cardenas, who will conduct a thorough medical evaluation, manage comorbidities, and prescribe and manage advanced pharmacologic treatments, such as a CGRP monoclonal antibody.
• At the same time, that same patient will see me for a comprehensive biomechanical and functional assessment. I will identify and treat the cervical spine dysfunction, myofascial restrictions, and postural imbalances contributing to their condition.
• We communicate constantly. This integrated approach ensures we treat the whole person—the biochemistry and the biomechanics. By attacking the problem from multiple angles at once, we can often achieve results far superior to what either discipline could accomplish alone.

We are not just chasing the pain with pills; we are rebuilding the patient’s health from the ground up, reducing their reliance on medication, and empowering them to reclaim their lives from migraine. This, in its truest sense, is the future of healthcare. Thank you very much for your time and attention.

References

• Ailani, J., Burch, R. C., & Robbins, M. S. (2021). The American Headache Society Consensus Statement: Update on integrating new migraine treatments into clinical practice. Headache: The Journal of Head and Face Pain, 61(7), 1021–1039.
• Ashina, M., Buse, D. C., Ashina, H., Pozo-Rosich, P., Dumkrieger, G., Tassorelli, C., … & Lipton, R. B. (2024). First-line therapies for migraine prevention: Is it time to rethink the current treatment paradigm?. The Journal of Headache and Pain, 25(1), 1-13.
• Ashina, M., Hansen, J. M., Do, T. P., & Olesen, J. (2019). Migraine and the trigeminovascular system—40 years and onwards. The Lancet Neurology, 18(8), 785–794.
• Blumenfeld, A. M., Stark, R. J., Freeman, M. C., Orejudos, A., & Manack Adams, A. (2018). Long-term study of the efficacy and safety of OnabotulinumtoxinA for the prevention of chronic migraine: COMPEL study. The Journal of Headache and Pain, 19(1), 1-12.
• Burstein, R., Noseda, R., & Borsook, D. (2015). Migraine: Multiple processes, complex pathophysiology. The Journal of Neuroscience, 35(17), 6619–6629.
• Chaibi, A., & Russell, M. B. (2014). Manual therapies for cervicogenic headache: a systematic review. The Journal of Headache and Pain, 15(1), 67.
• Dodick, D. W., Lipton, R. B., Ailani, J., Lu, K., Finnegan, M., Trugman, J. M., & Szegedi, A. (2019). Ubrogepant for the treatment of migraine. New England Journal of Medicine, 381(23), 2230-2241.
• Edvinsson, L., Haanes, K. A., Warfvinge, K., & Krause, D. N. (2018). CGRP and the trigeminal system: Mechanisms and role in migraine. Nature Reviews Neurology, 14(6), 338–350.
• Goadsby, P. J., Holland, P. R., Martins-Oliveira, M., Hoffmann, J., Schankin, C., & Akerman, S. (2017). Pathophysiology of migraine: A disease of the brain. Physiological Reviews, 97(2), 553–622.
• Goadsby, P. J., Wietecha, L. A., Dennehy, E. B., Kuca, B., & Case, M. G. (2019). Phase 3, randomized, double-masked, placebo-controlled study to evaluate the efficacy and safety of lasmiditan for acute treatment of migraine. Cephalalgia, 39(12), 1497-1508.
• Headache Classification Committee of the International Headache Society (IHS). (2018). The International Classification of Headache Disorders, 3rd edition. Cephalalgia, 38(1), 1–211.
• 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.
• National Headache Foundation. (2022). National Headache Foundation Position Statement on Preventive Treatment of Migraine.
• 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.
• Sacco, S., Bendtsen, L., Ashina, M., Reuter, U., Terwindt, G., Mitsikostas, D. D., & Martelletti, P. (2019). European Headache Federation guideline on the use of monoclonal antibodies acting on the calcitonin gene-related peptide or its receptor for migraine prevention. The Journal of Headache and Pain, 20(1), 6.
• Schulte, L. H., & May, A. (2016). The migraine generator revisited: Continuous scanning of the migraine cycle over 30 days and three spontaneous attacks. Brain, 139(7), 1987–1993.
• S. Food and Drug Administration. (2023). FDA Drug Safety Communication: FDA warns about new or worsening hypertension and Raynaud’s phenomenon with CGRP antagonists for migraine prevention. FDA.gov.

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