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Migraine: The Painful Truth��by Dr. Gary Starkman

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What is a migraine?

Not just a headache
Greek origin: hemikranion, “half a head”
“The headache would get worse until it was a smashing weight, sending red pain through his head and neck with every pulse beat. Bright lights would make his eyes water helplessly and send darts of agony into the flesh just behind his eyes. Small noises magnified, ordinary noises insupportable. The headache would worsen until it felt as if his head were being crushed inside an inquisitor's lovecap…. He would be next to helpless.”

Stephen King, Firestarter�

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History

1500 BCE, ancient Egypt: Mentioned in the Ebers papyrus.
200 BCE, ancient Greece: The Hippocratic school of medicine described the visual aura that can precede the headache and a partial relief occurring through vomiting.
400 AD, Rome: Caelius Aurelianus, described hemicrania and "crotophon," referring to the pounding or hammering and was accompanied by vertigo with burning of the eyes, nausea or vomiting.
7th century AD, Greece: Paulus Aeginata of the Alexandrian school of Medicine recounted the factors which provoked migraine: "... Noises, cries, a brilliant light, drinking of wine and strong smelling things which fill the head. Some as if the whole head were struck, and some as if one half, in which case the complaint is called hemicrania.”

In De Capitis Passione, Caelius Aurelianus, born in A.D. 400 in Algeria, described hemicrania and "crotophon." This term meant a pounding or hammering and was accompanied by vertigo with burning of the eyes, nausea or vomiting. He described lachrymation, noises in the ears and deafness.

In the 7th century, a Greek physician Paulus Aeginata of the Alexandrian school of Medicine recounted the factors which provoked migraine: "... Noises, cries, a brilliant light, drinking of wine and strong smelling things which fill the head. Some as if the whole head were struck, and some as if one half, in which case the complaint is called hemicrania.”

https://jnnp.bmj.com/content/jnnp/49/10/1097.full.pdf

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An early description consistent with migraines is contained in the Ebers papyrus, written around 1500 BCE in ancient Egypt.^[18] In 200 BCE, writings from the Hippocratic school of medicine described the visual aura that can precede the headache and a partial relief occurring through vomiting.^[142]

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Statistics

3d most prevalent illness in the world
1 in 7 adults in the world are affected
6^th most disabling condition in the world
90% of sufferers unable to work or function normally
Women are 3 times more likely to suffer from migraines
10 % of school-age children get them
Increased risk for depression, anxiety, and sleep disturbances

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Migraine vs Headache

Migraine vs. Non-Migraine Headache

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Migraine

Primary headache
Headache on one side (50 % of the cases)
Can present without headache
Aura (15% of cases)
Visual disturbances (zigzagging lines, flashing lights, vision loss)
Numbness and tingling on the face, lips, tongue, or extremities
Nausea and vomiting
Light Sensitivity
Frequent and long lasting (3-72 hours)
Prodrome/Postdrome

Non-Migraine Headache

Other primary headaches

Tension Headaches
Cluster Headaches
SUNCT And Other TAC’s
Hemicrania
Nummular Headache
Primary Stabbing Headache
Exertional Headaches
Other types of primary headaches

Secondary headaches

Migraine vs. Non-Migraine Headache

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Comorbidities

Depression
Anxiety
Bipolar Disorder
Stroke
Epilepsy
IBS
Sleep Disorder
Chronic Pain
PFO
Coronary Heart Disease
Asthma

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What Causes Migraines?

The cause is not yet known
Originates in the brain, not with the blood vessels that surround it
Prevailing theory: migraines are caused by rapid waves of brain cell activity crossing the cortex, the thin outer layer of brain tissue, followed by periods of inactivity called cortical spreading depression (CSD)
CSD accounts for multiple migraine symptoms

Source: Harvard Health

The picture describes three theories of what causes migraines

https://www.health.harvard.edu/newsletter_article/understanding-migraine

For years, doctors believed that migraine headaches originated with the blood vessels, particularly those that supply the meninges, the thin membranes wrapped around the brain inside the skull (see illustration). It was thought that when those blood vessels widened — dilated is the medical term — they impinged on pain receptors on the lacy network of trigeminal nerves that service the meninges and other parts of the head. According to this vascular theory, aura was caused by low blood supply from the narrowing of those blood vessels before they rebounded and widened, causing pain. The vascular explanation had considerable intuitive appeal because of the pulsating quality of migraine headaches. Some doctors elaborated on the theory, assigning different sorts of pain to different blood vessels.

But now there is near-total agreement that migraines originate in the brain, not with the blood vessels that surround it. One prevailing theory is that migraines are caused by rapid waves of brain cell activity crossing the cortex, the thin outer layer of brain tissue, followed by periods of no activity. The unwieldy (and potentially confusing) name for this phenomenon is cortical spreading depression. A Brazilian researcher, Aristides Leo, first observed it in rat brains in 1944, but many studies since have confirmed it occurs in the human brain as well.

Cortical spreading depression makes sense as a cause of aura, but researchers have also linked it to headache. Proponents cite experimental evidence that suggests it sets off inflammatory and other processes that stimulate pain receptors on the trigeminal nerves. This "neurogenic" inflammation and the release of other factors make the receptors — and the parts of the brain that receive their signals — increasingly sensitive, so migraine becomes more likely.

Some leading researchers have expressed doubt about whether migraines start with cortical spreading depression. Experimental drugs that inhibit cortical spreading depression have been developed, but study results reported in 2009 for one of the most promising, a drug called tonabersat, showed a preventive effect on aura, but not on migraine headache.

So, say some researchers, migraines are best explained as beginning lower in the brain, in the brainstem. This "primitive" region of the brain controls basic functions, such as respiration and responses to pain, and modulates many others, including incoming sensory information. The theory is that if certain areas of the brainstem aren't working properly or are easily excited, they're capable of starting cascades of neurological events, including cortical spreading depression, that account for migraine's multiple symptoms.

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Triggers

Stress*
Anxiety
Hormonal changes in women
Bright or flashing lights
Loud noises
Strong smells
Medicines
Too much or not enough sleep
Sudden changes in weather or environment
Overexertion (too much physical activity)
Tobacco
Caffeine or caffeine withdrawal

Skipped meals
Medication overuse (taking medicine for migraines too often)
Certain foods and food additives:

Alcohol
Chocolate
Aged cheeses
MSG
Some fruits and nuts
Fermented or pickled goods
Yeast
Cured or processed meats
Etc.

*Interestingly, migraines tend to start not during moments of great stress but later on, as people wind down.

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Different Kinds

Migraine with Aura

Migraine with typical aura

Typical aura with headache
Typical aura without headache

Migraine with brainstem aura
Hemiplegic migraine (feels like a stroke)

Familial hemiplegic migraine type 1
Familial hemiplegic migraine type 2
Familial hemiplegic migraine type 3

Sporadic hemiplegic migraine
Ocular Migraine/Retinal Migraine

Migraine without Aura
Silent or Acephalgic Migraine (Migraine without head pain)
Episodic Migraine
Chronic Migraine (more than 15 days a month)

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Stages

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Migraine without aura (MO) diagnostic criteria

A. At least five headache attacks lasting 3 - 72 hours (untreated or unsuccessfully treated), which has at least two of the four following characteristics:

1. Unilateral location

2. Pulsating quality

3. Moderate or severe intensity (inhibits or prohibits daily activities)

4. Aggravated by walking stairs or similar routine physical activity

B. During headache at least following symptoms occur:

1. Phonophobia and photophobia

2. Nausea and/or vomiting

Migraine with aura (MA) diagnostic criteria

A. At least two attacks fulfilling with at least three of the following:

1. One or more fully reversible aura symptoms indicating focal cerebral cortical and/or brain stem functions

2. At least one aura symptom develops gradually over more than four minutes, or two or more symptoms occur in succession

3. No aura symptom lasts more than 60 minutes; if more than one aura symptom is present, accepted duration is proportionally increased

4. Headache follows aura with free interval of at least 60 minutes (it may also simultaneously begin with the aura

B. At least one of the following aura features establishes a diagnosis of migraine with typical aura:

1. Homonymous visual disturbance

2. Unilateral paresthesia and/or numbness

3. Unilateral weakness

4. Aphasia or unclassifiable speech difficulty

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Diagnostic Criteria

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Diagnostic Techniques

Medical history
Symptoms
Physical and neurological examination

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Treatment Options

I. Medication

Abortive/ Acute Treatment (oral vs. intranasal)

Steroidal and nonsteroidal anti-inflammatory
Triptans
DHE
Anti-nausea medications
Nerve blocks

Preventive Treatment (oral, intranasal, injection)

Anticonvulsants/neuronal membrane stabilizers (TPX, VPA,GBP)
Beta blockers
Tricyclics
Magnesium
Riboflavin
Herbal supplements (feverfew, butterbur, etc.)
Botox
CGRP blockers

II. Electronic Devices (various stimulators including VNS)

III. Treating Underlying and Comorbid Conditions

IV. Lifestyle Changes

Internal factors (diet, medication, sleep hygiene, exercise, etc.)
Environmental factors (pollution, noise, smell, light, temperature, etc.)

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Neurotoxin Treatment

Botulinum neurotoxin (BoNT) is a protein complex produced by the Gram-positive, anaerobic bacterium Clostridium botulinum. In small doses this toxin temporarily inhibits muscle contractions in the muscle in which it is injected and overall affects pain for approximately 3 months.

Botox injections for migraine can help to reduce frequency and severity by blocking the transfer of information from the motor nerve to the muscle.

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After intramuscular or subcutaneous injection BoNT is internalized into peripheral motor neurons via SV2 binding protein [Mahrhold et al . 2006]. Once translocated into the cytosol, BoNT enzymatically cleaves the 25 kDa synaptosomal-associated protein (SNAP-25), a protein, which mediates the fusion of neurotransmitter-containing vesicles with the cell membrane. Through this mechanism, BoNT inhibits the release of neurotransmitters from presynaptic nerve endings [Rummel, 2015]. This effect has been best studied for the suppression of acetylcholine release at the neuromuscular junction. However, more recent studies show that BoNT also modifies the release of neurotransmitters, which are relevant in the transduction of pain such as substance P [Purkiss et al . 2000; Welch et al . 2000] or calcitonin gene-related peptide (GCRP) [Durham et al . 2004]. It is supposed that the inhibition of peripheral sensitization leads to an indirect inhibition of central sensitization and thus is a possible mechanism for the efficacy of BoNT in chronic pain [Aoki, 2003]

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In other words, Botox works for migraine headaches because it blocks chemicals called neurotransmitters that carry pain signals from your brain.

Botox is like a roadblock in that pathway. It stops the chemicals before they get to the nerve endings around your head and neck.

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Migraine: Frequently Asked Questions

Q: Do migraines cause stroke?

A: People with migraine, particularly women who have migraine with aura, have an increased risk of a type of stroke that is caused by a lack of blood flow to the brain (ischemic stroke), but this is a rare occurrence.

Q: Do genetics matter?

A: Migraine is a disorder that almost certainly has a genetic basis. An older theory on the causation of migraine included that migraine is primarily a disease of the blood vessels. It is now accepted that migraine is not related to any vascular pathology and brain mechanisms are more likely involved in the development of migraine attacks.

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Famous Migraineurs �

Julius Caesar
Napoleon
Thomas Jefferson
Van Gogh
JFK
Sigmund Freud
Princes Margaret
Elizabeth Taylor
Janet Jackson
Kanye West
Serena Williams
Many more

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Q & A

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CAYMAN NEUROLOGY�& PAIN MANAGEMENT�☎️ + 1 345-943-6900 �🖥️ caymanneurologist.com�