Headache

Question 1

Most common type of headache

Answer 1

Tension

Question 2

Most common type of headache presenting to physician

Answer 2

Migraine

Question 3

7 causes of secondary headaches

Answer 3

1) Intracranial HTN (idiopathic or secondary)
2) Intracranial hypotension
3) SAH
4) GCA
5) CNS infection (meningitis/encephalitis)
6) Cranial neuralgias
7) Brain tumor

Question 4

What are 11 historical red flags for a headache?

Answer 4

1) Onset after age 50
2) Worse on awakening** (may be secondary to increased ICP)
3) WHOML (thunderclap - sudden onset is worse than just hearing WHOML)
4) Change in typical headache pattern
5) History of Cancer
6) Fever
7) Visual loss (other than as part of an aura)
8) Diplopia
9) Change in personality
10) New onset seizures
11) History of HIV

Question 5

What are 8 physical exam red flags for a headache?

Answer 5

1) Fever
2) Meningeal irritation
3) Papilledema
4) Enlarged blind spot
5) Loss of visual acuity
6) Tender temporal artery
7) Focal neuro findings
8) Alteration of arousal

Question 6

Normal ICP

Answer 6

5-20

Question 7

How does laying down increase ICP?

Answer 7

More blood in head.

Note: When sleeping, total minute ventilation decreases. The increases serum CO2 which lowers pH. This causes vessels in brain to dilate leading to higher ICP.

***If your ICP is already elevated at baseline, you’d get a HA when you wake up

Question 8

Which cranial nerve is most susceptible to increases in ICP?

Answer 8

CN 6 (diplopia)

Question 9

Signs of compressive lesion to CN3?

Answer 9

They affect parasympathetic fibers first - pupils will be dilated initially

Question 10

IHS criteria for migraine

Answer 10

Must be recurrent

Not explained by secondary disorder

Must have 2 out of 4 of:

1) Unilateral
2) Pulsating
3) Moderate to severe intensity
4) Aggravated by routine physical activity

Must have 1 out of 2 of:

1) Nausea and/or vomiting
2) Photophobia AND phonophobia

Question 11

Migraine aura

Answer 11

Most migraines DONT have aura, but if there is an aura there are usually several features they share

Develops over minutes

HA should begin within an hour

Older adults may get “acephalic” migraines

Typically visual - fortification spectra, scintillating scotoma, phosphenes, metamorphopsia

Can be non-visual - numbness from hand to mouth, aphasia, unilateral weakness, slurring of speech

Aura is thought to be from cortical spreading depression due to vasoconstriction

Question 12

Abortive tx of migraines

Answer 12

OTC - aspirin, NSAIDs, Acetaminophen, excedrin (must take at high doses), naproxen (Aleve) has longer half-life than ibuprofen

Rx:
1st line: Triptans - vasoconstrict abnormally dilated vessels. Can be PO, SQ, nasal. They work better when taken as soon as you feel HA starting. AVOID IN PTS WITH CAD, CVA, PREGNANCY, COMPLICATED MIGRAINES

2nd line: Antiemetics, corticosteroids

3rd line: opiates

Relying on pain meds for HA can cause rebound HAs - USE A TRIPTAN

Question 13

Prophylactic tx of migraines

Answer 13

For 2 or more debilitating attacks per month

B-blockers (propranolol and nadilol)

TCAs (Amitryptiline - anticholinergic action)

Antiepileptics (Topiramate -side effect is weight loss, tingling, teratogen cleft lif/Valproate - side effect is teratogenic neural crest)

2nd line: Verapimil, ARBs, SSRIs

Avoid known triggers

BoTox for chronic migraines - more than 14 HAs per month can get 31 injections q3mo

Question 14

Typical migraine characteristics - 8 factors

Answer 14

1) Onset - teenage to age 40 occuring anytime during day
2) Location - Half of face; frontal, usual in or about eye or cheek
3) Precipitating factor - fatigue, stress; hypoglycemia; diet (tyramine, alcohol); sunlight; hormonal change (menstruation)
4) Freq - 2-4 per month or sporadic; can be cyclic with menstruation
5) Sex distrib - 70 female/30 male
6) Duration of attack - head pain 4 hours, aura to postdrome 24-36hrs
7) Pain type and severity - begins as dull ache, progress to stabbing pain; intense
8) Associated sx - n/v; photophobia, visual obscuration

Question 15

Migraine prevalence in children

Answer 15

even in boys and girls. Only in adults do you see the female predominance

Question 16

Common migraine triggers

Answer 16

1) Chocolate, cheese, red wine, citrus, coffee, tea, tomatoes, potatoes, irregular meals
2) Excessive/insufficient sleep
3) Changes in hormone balance in women (menses, pill, menopause)
4) Stress or relaxation after a period of stress
5) Caffeine withdrawal
6) Physical activity
7) Smoking
8) Flashing lights or noise
9) Weather - high pressure conditions, hot dry winds, change of season, exposure to sun and glare
10) Sexual arousal
11) Smells - paint, fumes from car heaters or perfume

Question 17

Evaluation of migraine

Answer 17

Complete H and P. If history is consistent with migraine then just go to treatment.

If atypical then use caution (male migraine under age 50, neuro exam abnormal) then can do workup that may include the following

1) Routine blood tests
2) Sed rate
3) LP
4) Imaging

Question 18

Routine blood tests in setting of headache

Answer 18

Vasculitis, toxic exposures, metabolic diseases, severe HTN, infectious processes can all be associated with HA

CBC, HIV testing, vasculitis screen, thyroid function, serum protein electrophoresis can be ordered

Question 19

Sed rate in setting of headache

Answer 19

In HA patients older than 60, temporal arteritis should be considered. It affects medium and large vessels of the upper body esp temporal vessels.

Can be coupled with pain/stiffness of neck, shoulders, back, and sometimes pelvic girdle. HA is one sided at temporal region

Major complication is vision loss

Question 20

LP in setting of HA

Answer 20

Consider in patients with new onset HA with fever, stiff neck, or AMS

If ddx includes SAH or pseudotumor cerebri, an LP should also be considered

If LP is done to workup a HA then the patient should have a scan performed before the LP (unless bacterial meningitis is a serious possibility) - in cases where meningitis is suspected to LP immediately unless there’s papilliedema

Question 21

Imaging in setting of HA

Answer 21

MRI

CT may be adequate to detect a space-occupying lesion, shift in midline structures, brain herniation, or presence of SAH

Question 22

Postspinal HA

Answer 22

25% of patients get HA after LP

Better when laying down and worse when sitting/standing up.

Can be associated with nausea and vomiting

Improve with bedrest and fluids

If don’t improve, an epidural blood patch can be done

Question 23

Postcoital cephalgia

Answer 23

Both before or after orgasm

Equal in men and women

Sudden, pulsatile HA often entire head

Usually benign (2% SAH)

Simple NSAID before sex is enough

Question 24

Pseudotumor cerebri

Answer 24

Increased ICP without evidence of CNS malignancy

HA often associated with visual disturbances

Usually a woman who is obese with menstrual irregularities

All have papilledema

Diplopia maybe from CN VI palsy (otherwise normal neuro exam and MRI)

LP shows high opening pressure only

Not entirely benign bc of risk of vision loss

Standard tx = acetozolamide

Consider VPS or optic nerve sheath fenestration in severe or refractory cases

Question 25

Acute glaucoma

Answer 25

Sudden orbital or eye pain in face of nausea and vomiting Pain can begin after the use of anticholinergic drugs High IOP is the hallmark of acute angle-closure glaucoma

Question 26

Carotid dissection

Answer 26

Orbital or neck pain associated with neuro findings suggestive of carotid disease. Horner syndrome (when sympathetic innervation to eye disrupted) on ipsilateral dissected carotid side Trauma to neck or vigorous movements to neck will often trigger the dissection

Question 27

Brain tumor

Answer 27

HAs from brain tumor are like typical tension or migraine headaches. Quite frequent and can occur on a daily basis, often awakening the patient from sleep Neuro exam can be normal but can reveal focal deficits as well as papilledema. HA is presenting feature in 40% of brain tumor patients

Question 28

SAH

Answer 28

3 main etiologies 1) leakage of AVM 2) Leakage of ruptured aneurysm 3) Trauma Debilitating HA that's WHOML. Sudden onset with nausea, vomit, stiff neck Can look like a migraine Associated with blood in subarachnoid space which is usually seen on MRI or CT An LP will confirm (blood or xanthochromic staining) 50% do not survive Most common etiology is rupture of berry aneurysms off arterial circle of willis Hunt-Hess grading system for prognosis based on severity of HA, level of consciousness, focal signs

Question 29

4 drugs used in abortive therapies for migraines

Answer 29

1) Triptans 2) Ergotamine derivatives 3) Dihydroergotamine 4) Midrin

Question 30

Triptans

Answer 30

They work at 5HT-1D serotonin receptors as agonists 80% effective in treatment of individual attack They can be given again as early as 4hrs if there's another HA No more than 3x in 24hrs Side effects are nausea, vomiting, numbness/tingling of fingers and toes Contra is history of CAD, HTN If patient has hemiplegia or blindness as an aura in a migraine attack then do not use

Question 31

Ergotamine derivatives

Answer 31

Consider when patients fail triptans Usually sublingual

Question 32

Dihydroergotamine

Answer 32

Episodic migraine that has become more chronic and intractable can respond to intramuscular or IV DHE Given with metochlopramide

Question 33

Midrin

Answer 33

Between abortive and ppx 3 parts: acetominophen, dichloralphenazone (muscle relaxant), isometheptene mucate (vasoconstrictor) Take 2 tabs if abortive at onset of HA or aura then 1 tab per hour for 3 more hours Can be scheduled for chronic muscle tension headaches

Question 34

Retinal migraine

Answer 34

Eye pain and vision loss

Question 35

Abdominal migraine

Answer 35

abdominal pain, nausea, vomiting, diarrhea

Question 36

Basilar migraine

Answer 36

Dizziness, confusion, lack of balance

Question 37

Ophthalmoplegic migraine

Answer 37

eye pain and oculomotor weakness

Question 38

hemiplegic migraine

Answer 38

temporary stroke-like symptoms

Question 39

Tension HA

Answer 39

Mild-moderate intensity - does not prohibit activities like a migraine does Pressing quality Bilateral Not aggravated by activity No nausea,vomit Photophobia or phonophobia but not both Migraine-tension spectrum Treat with NSAIDs and nonpharm approach

Question 40

Cluster HA

Answer 40

Male predominance 5x Severe, unilateral, orbital, lasting up to 3hrs (usually 90 mins) with trigeminal autonomic features like conjunctival irritation, tearing, nasal congestion, miosis, ptosis, eyelid edema Typically cluster over a period of weeks then remit Treatment = oxygen, triptan, DHE (acute); lithium, corticosteroid, verapamil (ppx) Think 1-2 times per day at night in men lasting 1-2 months

Question 41

Intracranial hypotension

Answer 41

It's a CSF leak! Remarkable history in that the HAs completely disappear when supine but reemerge when upright Quite disabling Felt to be due to traction on the dural nerves when ICP low Can be spontaneous or post-dural puncture** Related to size of spinal needle used, not amount of CSF removed Tx = epidural blood patch (99% effective)

Question 42

GCA

Answer 42

subacute HA at older age with temporal artery and scalp tenderness Visual loss with risk of anterior ischemic optic neuropathy causing possible permanent blindness Systemic symptoms, polymyalgia rheumatica Jaw claudication High ESR needed for dx Bx important to determine duration of tx tx with prednisone 1mg/kg/day

Question 43

Intracerebral mass

Answer 43

Initially patient may have diffuse or localizing HA caused by local traction of the dura Remember that the brain has no pain receptors If ICP is high - HA are dull, constant and usually worse on awakening - HA becomes worse with coughing/valsalva - Associated with papilledema - Pt may develop "false localizing VI palsy"

Question 44

Trigeminal neuralgia

Answer 44

Brief, lightning-like lancinating pain typically in V2 or V3 distribution in the mouth, triggered by any activity using the mouth like breathing, chewing or swallowing Exam is normal including sensation Mainstay of tx is carbamazepine Trigem nerve decompression in refractory cases In a young person, think MS Deep boring, throbbing pain is more likely dental carries Remember that carbamazepine is an auto-inducer - will see initial effect then it might induce its own metabolism. Just increase the dose

Question 45

Sentinel bleed

Answer 45

Often seen in SAH Intermittent aneurysmal SAH causing lesser HA that precedes the WHOML that happens with rupture

Question 46

Major complication of SAH

Answer 46

vasospasm Irritation causes constriction of major cerebral arteries, vasospasm, lethargy, and delayed cerebral infarction Occurs mostly with aneurysms rather than other causes of SAH Peaks btw 4 and 14 days TCD can be used to detect a change in flow velocity in an affected MCA

Question 47

Acute communicating hydrocephalus

Answer 47

Complication occuring from SAH bc of obstruction of subarachnoid granulations in the venous sinuses by the subarachnoid blood. CT shows enlarged lateral, third, fourth ventricles with clinical signs of HA, vomit, blurry/double vision, somnolence and syncope

Question 48

Risk factors for SAH

Answer 48

1) age (avg age is 50) 2) Female 3) HTN (chronic severe with diastolic more than 110) 4) Smoking 5) Liver disease 6) Vasculitis 7) Collagen vascular disease (Marfan) 8) infx - mycotic aneurysm 9) oral contraception 10) PCKD 11) Fibromuscular dysplasia Usually a history of recent moderate HA 60% occur during physical or emotional strain, head trauma, defecation or coitus

Question 49

Physical exam findings in SAH

Answer 49

Can see neurogenic pulm edema (bibasilar crackles), tachycardia Compression of ipsilateral CN 3 causing mydriasis, ptosis, impaired EOMs (often seen with posterior communicating artery origin) Could see contralateral hemiparesis and complex partial seizures with secondary generalization. This is from extension of hemorrhage with edema and MCA vasospasm HypoNa (high atrial natriuetic factor, cerebral salt wasting and/or SIADH) ECG changes - QT prolongation, T inversion, arrhythmia

Question 50

Most common sites of SAH aneurysm

Answer 50

Anterior circulation (75%) 1) anterior communicating artery 2) bifurcation of internal carotid with MCA Fibromuscular dysplasia is associated with 25% of aneurysm patients PCKD is related to 3% of cases

Question 51

Imaging for SAH

Answer 51

HCT non con - hyperdensity within the cerebral convexities, cisterns and parenchyma Sensitivity is highest 24h after event with half still seen after 1w Neg CT in 10-15% of cases and should be further assessed with LP (look for xanthochromia - yellowish CSF)

Question 52

CSH for SAH

Answer 52

yellowish or bloody Can also be negative in 10-15% - prognosis is better in this case Most sensitive 12h after incident

Question 53

Grade 1 SAH

Answer 53

Alert with mild HA and nuchal rigidity 5% chance of deteriorating 3-5% mortality risk

Question 54

Grade 2 SAH

Answer 54

Mod-severe HA and nuchal rigidity 6-10% mortality risk

Question 55

Grade 3 SAH

Answer 55

Similar to grade 2 but with drowsiness, confusion, and mild focal deficit

Question 56

Grade 4 SAH

Answer 56

Stupor and mod-severe hemiparesis

Question 57

Grade 5 SAH

Answer 57

comatose with signs of severe ICP increease 80% chance of deteriorating 25-30% rebleed 50-70% mortality Delayed vasospasm is a potentially serious complication in 20% of cases

Question 58

SAH treatment

Answer 58

Grade 1 and 2 - observed after diagnostic measures Emergent angiography is warranted if ruptured aneurysm is suspected and neurosurg is required Endovascular coiling indicated to reduce rebleeding in low-grade cases - superior to clipping Clipping should be done in first 48h after onset or be delayed 2w to avoid the window of greatest risk for vasospasm, esp in high grade cases Mainstay of medical management to reduce spasm is Triple H (hypertension, hypervolemia, hemodilution) to maintain cerebral perfusion and nimodipine (CCB). Address other complications like metabolic issues (SIADH, hyponatremia, cerebral salt wasting), respiratory and cardiac complications, seizures, and hydrocephalus

Question 59

Best formulation for pediatric migraine

Answer 59

Nasal sumatriptan As any migraine, try high dose NSAIDs first (10mg/kg ibuprofen or 15mg/kg tylenol) Cyproheptadine for ppx