Headache Flashcards
Estrogen and migraines
Estrogen increases the likelihood and frequency of migraine headaches
Mechanistically, this is thought to be due to its influence on nitric oxide levels
For this reason, it is most common in 20-40 year old females.
Migraine prodrome vs migraine aura
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Prodrome:
- Nonspecific phenomena that occur hours to days prior to headache onset
- May be psychological (euphoria, depression, irritability) or constitutional (increased urination, increased defecation, anorexia)
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Aura:
- Transient frank neurologic dysfunction
- Gradually develop over minutes and last 5-60 minutes
- Classically occurs immediately before head pain, but may occur during headache or without headache in affected patients
Some classical migraine auras
- Scintillating scotomas: zigzag luminous images, flashing lights with zigzag pattern, distortion of images
- Smells
- Tastes
- Nausea
Features of the classical migraine headache
- Unilatreal
- Pulsating in quality
- Lasts 4 hours - several days
- Associated symptoms of nausea, photophobia, and phonophobia
- Desire to seek rest in a quiet, dark place
Cortical spreading depression theory
- Important in both migraine and seizure spreading
- As disrupted cellular calcium homeostasis and chemical cascades propagate, trigeminal neurons signal dural vessels to release calcitonin gene-related peptide (CGRP), substance P, and neurokinin A
- These mediators lead to inflammation and dilation of blood vessels, resulting in pain signals which are sent to the brain
If you think a patient’s headache is due to temporal arteritis, what do you do?
- Give empiric corticosteroids
- Send them to the ED
- Here they will get a screening ESR and CRP
- If elevated, they will get further workup including temporal artery biopsy
Features of a tension headache
- Bilatreal
- Band-like tightness/pressure quality
- Sometimes precranial tenderness
- Not associated with nausea, vomiting
- May be associated with phonophobia or photophobia, but usually not both
Studies that one might order for suspected secondary headache
- CT
- LP
- Biopsy
Headache red flags
- Fever
- Focal deficit
- New-onset in age > 50
- Thunderclap headache (instantaneous onset worst headache of life)
- Progressive N/V that is worse in morning
Analgesic rebound headache criteria for diagnosis
- Use of analgesics > 10 times per month
- Headaches occur when in withdrawal period after analgesic use
Cluster headache
- Pathology: vascular
- Presentation: Asymptomatic for months, then experience a “cluster” of headaches 8-10 times per day
- Features: Unilateral eye pain, Horner’s syndrome, rhinorrhea, lacrimation, conjunctival injection
- Diagnosis: Clinical, but one-time brain MRI or CT is necessary to rule out other etiologies.
- Treatment:
- Abortive: Oxygen (nasal cannula). If this fails, triptans.
- Maintenance: Verapamil
Migraine therapy
-
Abortive:
- 1st line: NSAIDs
- 2nd line: Triptans, ergots (but be careful in CAD), OR midrin
- NOT butalbital – no longer recommended
-
Maintenance:
- 1st line:
- Beta blockers: Propranolol
- Anticonvulsants: Topiramate, valproate, divalproex, gabapenti
- 2nd line:
- Combinations: Midrin
- CCBs: Verapamil
- Antidepressants: Amitryptiline, duloxetine, nortryptiline
- 3rd line: Methysergide maleate, lithium carbonate, clonidine, captopril
- 4th line: Botox injections q3 months
- 1st line:
Idiopathic intracranial hypertension aka pseudotumor cerebri
- Path: Increased ICP, for no discernable reason
- Presentation: Female patient with increased ICP and papilledema, but THEN imaging is negative for any etiology
- Often some form of visual disturbance is present, such as blurry vision when standing up quickly – untreated disease can lead to blindness
- Causes: OCPs
- Dx: Negative CT and/or MRI to rule out intracranial mass-occupying lesion. LP with opening pressure > 25 cm H2O with relief after LP
- Tx:
- 1st line: Acetazolomide and weight loss.
- Refractory or bridging to acetazolomide: Repeated LPs
- Truly chronic, refractory cases: VP shunt. Optic nerve fenestration (may help preserve vision)
If sinusitis does not respond to anticongestants, consider. . .
. . . migraine as a mimic of sinusitis
It is actually VERY common. In fact, 80% of patients with “sinus headache” actually have migraines, NOT sinusitis.
If you have strong clinical suspicion for SAH despite a negative CT, you should. . .
. . . do an LP to look for xanthochromia
You WILL have to differentiate between migraine and SAH on the test.
Why is “new onset headache in a patient over age 50” a red flag sign for headaches?
Because this is the demographic of patients at risk for temporal arteritis
Lab data that support a diagnosis of temporal arteritis in someone with a case of TA vs migraine
Elevated ESR, CRP, and thrombocytosis
Platelets in temporal arteritis
Platelets may be elevated in temporal arteritis, AND this elevation correlates with the risk of vision loss
If there is strong clinical suspicion for temporal arteritis, . . .
. . . you should treat with corticosteroids immediately – prior to even confirming the diagnosis with a biopsy
“Headache that awakens the patient from sleep”
Concerning for brain tumor
How are triptans optimally used to abort migraines?
At the first sign that a migraine is coming on, such as during an aura in the case of migraine with aura
They can still help once the migraine has begun, but are less effective than if used ASAP
How much triptan can someone take for a prolonged migraine?
Can be used q4 hours PRN, but not more than three doses per 24 hours