Migraine

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The key takeaways are that migraine is a neurovascular disorder characterized by prolonged headaches, nausea, sensitivity to light and sound, and can be accompanied by aura. It is one of the most common diseases worldwide.

Common symptoms of migraine include prolonged headache, nausea, decreased ability to function, headache worsening with activity, sensitivity to light, sensitivity to noise, aura, and vomiting.

Migraine is defined by the International Headache Society as a recurrent headache that occurs with or without aura and lasts 2 to 48 hours. It is usually unilateral in nature, of gradual onset, pulsating in quality, of moderate or severe intensity, and is aggravated by routine physical activity.

MIGRAINE

PREPARED BY: MOHAMMED PHARAON R1


• Prolonged headache
• Nausea
• Decreased ability to function
• Headache worse with activity
• Sensitivity to light
Key Features • Sensitivity to noise
• Aura
• Vomiting
• Unilateral
• Throbbing
Definition
Migraine is defined by the International Headache Society
as a recurrent headache that occurs with or without aura
and lasts 2 to 48 hours. It is usually unilateral in nature, of
gradual onset (15 to 30 minutes), pulsating in quality, of
moderate or severe intensity, and is aggravated by routine
physical activity. Nausea, vomiting, photophobia, and
phonophobia are common accompanying symptoms.
Epidemiology
Migraine is reported to be the third most common disease worldwide,
with an estimated global prevalence of approximately 15%. It is
ranked globally as the seventh most disabling disease, accounting for
approximately 3% of all years of life lost to disability, and it is the
leading cause of disability among neurologic disorders. Historically,
migraine was believed to preferentially affect people living in high-
income countries, but this is no longer thought to be accurate. Before
puberty, migraine prevalence is higher in boys than in girls, but
following adolescence it becomes more common in women of all ages.
Prevalence declines with age in both sexes.
US government health survey data suggest that migraine affects
around 1 in 6 people (15.3% total prevalence; 20.7% female, 9.7%
male) over a 3-month period. Prevalence has been stable over a 19-
year period. Summary data from the 2015 National Health Interview
Study indicate that the prevalence of migraine or severe headache was
higher in Native Hawaiians or other Pacific Islanders (20.3%) than in
American-Indians and Alaska Natives (18.4%), black and African
American people (16.2%), and white people (15.4%), with the lowest
prevalence in Asian-Americans (11.3%). A higher migraine burden
was reported in people ages 18-44 years, those who are unemployed or
with a family income <$35,000 USD per year, as well as older and
disabled people.
•Migraine is a neurovascular disorder, in which neurologic events precede and initiate
headache.
•The headache of migraine results from neurogenic inflammation of first-division
trigeminal sensory neurons that innervate the large vessels and meninges of the brain.
This causes a change in the way that pain is processed by the brain. Increased neuronal
activity can be demonstrated in areas of the brainstem during migraine, and this persists
even when the headache is relieved by triptans. It is not known whether this brainstem
activation reflects the cause of migraine (the so-called brainstem generator) or instead
signifies activation of endogenous pain-control systems.
•When activated, the trigeminal neurons release substances that cause dilation of
meningeal blood vessels, leakage of plasma proteins into surrounding tissue, and platelet

Pathophysiology
activation. This sensitizes nerve fibers so that previously ignored stimuli, such as the
normal pulsations of meningeal vessels, are interpreted as painful (peripheral
sensitization).  This probably accounts for the pulsating, throbbing character of migraine
pain. If the headache continues, second- and third-order neurons are sensitized (central
sensitization) and cutaneous stimuli, such as light touch, are interpreted as painful.
•Aura is caused by neuronal dysfunction. A wave of neuronal excitation spreads anteriorly
in the cortex, at a rate of 3-5 mm/minute (which correlates temporally with the reported
rate of change in visual symptoms). This is followed by a prolonged period of decreased
neuronal activity, and finally neuronal recovery. Cortical depression causes release of
excitatory amino acids and other mediators of excitation, resulting in activation of
nociceptors in adjacent dura and blood vessels, leading to activation of the trigeminal
sensory nucleus. How these neurons are triggered in migraine without aura is unknown,
but one hypothesis is that cortical spreading depression in migraine without aura occurs
in "silent" areas of the brain that do not produce recognizable symptoms of aura.
• 1st Tests to Order
• clinical diagnosis
• Other Tests to consider
• erythrocyte sedimentation rate (ESR)
Diagnostics • lumbar puncture (LP)

Tests •
cerebrospinal fluid (CSF) culture
MRI brain
• CT head
•International classification of headache disorders, 3rd edition (ICHD-3)
•1.1 Migraine without aura: recurrent headache disorder manifesting in
attacks lasting 4 to 72 hours. Typical characteristics of the headache are
unilateral location, pulsating quality, moderate or severe intensity,
aggravation by routine physical activity, and association with nausea and/or
photophobia and phonophobia.
•1.2 Migraine with aura: recurrent attacks, lasting minutes, of unilateral fully
reversible visual, sensory, or other central nervous system symptoms that
usually develop gradually and are usually followed by headache and
Classification associated migraine symptoms
•1.2.1 Migraine with typical aura: migraine with aura, in which aura consists
s of visual and/or sensory and/or speech/language symptoms, but no motor
weakness, and is characterized by gradual development, duration of each
symptom no longer than 1 hour, a mix of positive and negative features, and
complete reversibility
•1.2.2 Migraine with brainstem aura: migraine with aura symptoms clearly
originating from the brainstem, but no motor weakness
•1.2.3 Hemiplegic migraine: migraine with aura including motor weakness
•1.2.3.1 Familial hemiplegic migraine (FHM)
•1.2.3.1.1 Familial hemiplegic migraine type 1 (FHM1)
•1.2.3.1.2 Familial hemiplegic migraine type 2 (FHM2)
•1.2.3.1.3 Familial hemiplegic migraine type 3 (FHM3)
•1.2.3.1.4 Familial hemiplegic migraine, other loci
•1.2.3.2 Sporadic hemiplegic migraine (SHM)

Classification •1.2.4 Retinal migraine: repeated attacks of monocular


visual disturbance, including scintillations, scotomata, or
s blindness, associated with migraine headache.
•1.3 Chronic migraine: headache occurring on 15 or more
days/month for more than 3 months, which, on at least 8
days/month, has the features of migraine headache.
•1.4.1 Status Migrainosus: a debilitating migraine attack
lasting for more than 72 hours
•Menstrual Migraine
Vignettes
Common Vignette 1
A 32-year-old woman presents with a 13-year history of 1-3 attacks per month of disabling
pounding pain over one temple, with nausea and sensitivity to light. She says that her headaches
can be triggered by lack of sleep and made worse by physical exertion, and are more common
during menstrual bleeding. Untreated, they last for 2 days. On four occasions, headaches were
preceded by the gradual appearance of a shimmering, zigzag line that enlarged, moved to the
peripheral visual field, and then faded away over 45 minutes. Examination is normal.
Vignettes
Common Vignette 2
A 40-year-old man complains of a 1-year history of twice-monthly global headache, worse on
the left side in the postauricular region. It comes on gradually and, at its most severe, the vision
in his left eye becomes distorted. He often has to stop watching television as the picture
becomes "blurry." His nose becomes blocked, although sometimes he has a "runny nose." He
takes a nonsteroidal anti-inflammatory drug (NSAID) that helps a little, but he feels that his
head is about to explode at times. When the headache occurs, he needs to go into a dark quiet
room and sleep until it resolves. He reports the problem is "really getting him down," and he is
having difficulties with his employer due to loss of work time.
Vignettes
Other Presentations
Typical migraine aura (a complex of reversible visual, sensory, or speech symptoms) is
pathognomonic of migraine, but occurs in only 15% to 30% of patients. Aura typically occurs
just before or at onset of headache, developing over 5-20 minutes and lasting less than 60
minutes, but it may not occur every time. Aura can also occur during the headache. Aura
includes positive phenomena (visual sparkles, flashing lights, tingling) and negative phenomena
(visual loss or scotomata, numbness, speech disturbance).
•Features that should increase suspicion of a dangerous
underlying headache or migraine mimic can be
summarized using the mnemonic "SNOOP":
•Systemic symptoms: fever, weight loss
•Neurologic symptoms or abnormal signs: confusion,
impaired alertness or consciousness

Dangerous •Onset: sudden, abrupt, or split-second


•Older: new-onset and progressive headache, especially in
modifies patients aged >50 years
•4 "P"s
•Pattern change (increased frequency)
•Papilledema
•Precipitating factors (valsalva, etc)
•Positional aggravation.
Abortive Therapeutic Options
Acute mild-moderate symptoms: nonpregnant ibuprofen: 800 mg as a single dose at onset, then
1st: nonsteroidal anti-inflammatory drug (NSAID) 400-800 mg orally every 4-6 hours when required,
maximum 2400 mg/day
Primary options »
OR »
aspirin: 900-1000 mg as a single dose at onset, then
325-975 mg orally every 4-6 hours when required, naproxen: 500-1000 mg as a single dose at onset,
maximum 4000 mg/day then 250-500 mg orally twice daily when required,
maximum 1250 mg/day Secondary options » celecoxib:
OR » 200 mg orally twice daily when required
diclofenac potassium: 50 mg as a single dose OR »
(powder for oral solution) at onset, then 50 mg orally
(immediate-release) three times daily when required indomethacin: 50-200 mg/day orally (immediate-
release) given in 2-3 divided doses »
OR »
Acute treatment of migraine with NSAIDs is most
effective when the medication is used early, while the
headache is mild. »
Several NSAIDs are presumed to be effective;
aspirin, naproxen, and indomethacin are the most
commonly used members of this class. NSAID use is
Prevention Eligibility
to headache days per month and degree of disability
considerations outlined earlier, patients are
candidates for preventive treatments if they have the
following conditions[1]:
•Attacks significantly interfere with patients' daily
routines despite acute treatment
•Frequent attacks (≥ 4 MHDs)
•Contraindication to, treatment failure, or overuse of
Prevention acute treatments; overuse is defined as:
• 10 or more days per month for ergot
Eligibility derivatives, triptans, opioids, combination
analgesics, and a combination of drugs from
different classes that are not individually
overused
• 15 or more days per month for nonopioid
analgesics, acetaminophen, and nonsteroidal
anti-inflammatory drugs (NSAIDs; including
aspirin)
•Adverse events from acute treatments
Preventive Therapeutic Options
References
• BMJ best practice
• Epocrates
• Case Challenges in the Comprehensive Management of Frequent Headache (MEDSCAPE)
https://www.medscape.org/viewarticle/950351_1

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