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Neurology > Headache > Flashcards

Headache Flashcards

1
Q

Most common type of headache

A

Tension

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2
Q

Most common type of headache presenting to physician

A

Migraine

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3
Q

7 causes of secondary headaches

A

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

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4
Q

What are 11 historical red flags for a headache?

A

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

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5
Q

What are 8 physical exam red flags for a headache?

A

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

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6
Q

Normal ICP

A

5-20

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7
Q

How does laying down increase ICP?

A

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

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8
Q

Which cranial nerve is most susceptible to increases in ICP?

A

CN 6 (diplopia)

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9
Q

Signs of compressive lesion to CN3?

A

They affect parasympathetic fibers first - pupils will be dilated initially

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10
Q

IHS criteria for migraine

A

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

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11
Q

Migraine aura

A

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

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12
Q

Abortive tx of migraines

A

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

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13
Q

Prophylactic tx of migraines

A

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

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14
Q

Typical migraine characteristics - 8 factors

A

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

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15
Q

Migraine prevalence in children

A

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

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16
Q

Common migraine triggers

A

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

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17
Q

Evaluation of migraine

A

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

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18
Q

Routine blood tests in setting of headache

A

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

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19
Q

Sed rate in setting of headache

A

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

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20
Q

LP in setting of HA

A

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

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21
Q

Imaging in setting of HA

A

MRI

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

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22
Q

Postspinal HA

A

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

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23
Q

Postcoital cephalgia

A

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

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24
Q

Pseudotumor cerebri

A

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

25
Q

Acute glaucoma

A

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

26
Q

Carotid dissection

A

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

27
Q

Brain tumor

A

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

28
Q

SAH

A

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

29
Q

4 drugs used in abortive therapies for migraines

A

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

30
Q

Triptans

A

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

31
Q

Ergotamine derivatives

A

Consider when patients fail triptans

Usually sublingual

32
Q

Dihydroergotamine

A

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

Given with metochlopramide

33
Q

Midrin

A

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

34
Q

Retinal migraine

A

Eye pain and vision loss

35
Q

Abdominal migraine

A

abdominal pain, nausea, vomiting, diarrhea

36
Q

Basilar migraine

A

Dizziness, confusion, lack of balance

37
Q

Ophthalmoplegic migraine

A

eye pain and oculomotor weakness

38
Q

hemiplegic migraine

A

temporary stroke-like symptoms

39
Q

Tension HA

A

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

40
Q

Cluster HA

A

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

41
Q

Intracranial hypotension

A

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)

42
Q

GCA

A

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

43
Q

Intracerebral mass

A

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”
44
Q

Trigeminal neuralgia

A

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

45
Q

Sentinel bleed

A

Often seen in SAH

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

46
Q

Major complication of SAH

A

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

47
Q

Acute communicating hydrocephalus

A

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

48
Q

Risk factors for SAH

A

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

49
Q

Physical exam findings in SAH

A

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

50
Q

Most common sites of SAH aneurysm

A

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

51
Q

Imaging for SAH

A

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)

52
Q

CSH for SAH

A

yellowish or bloody

Can also be negative in 10-15% - prognosis is better in this case

Most sensitive 12h after incident

53
Q

Grade 1 SAH

A

Alert with mild HA and nuchal rigidity

5% chance of deteriorating

3-5% mortality risk

54
Q

Grade 2 SAH

A

Mod-severe HA and nuchal rigidity

6-10% mortality risk

55
Q

Grade 3 SAH

A

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

56
Q

Grade 4 SAH

A

Stupor and mod-severe hemiparesis

57
Q

Grade 5 SAH

A

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

58
Q

SAH treatment

A

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

59
Q

Best formulation for pediatric migraine

A

Nasal sumatriptan

As any migraine, try high dose NSAIDs first (10mg/kg ibuprofen or 15mg/kg tylenol)

Cyproheptadine for ppx

Neurology (14 decks)

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