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Foundations II-Neurology > Headaches > Flashcards

Headaches Flashcards

1
Q

What are the primary headaches?

A

migraine

tension-type headache

cluster headache

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2
Q

What can be used to quantify the level of disability of HAs?

A

HIT questionnaire (headache impact test)

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3
Q

What are some HA red flags?

A
  • Abrupt onset “thunderclap”
  • trauma associated HA w/ neurological deficit/progressively worsening sxs
  • focal neuro sxs or abn. findings
  • change in previously existing HA presentation
  • systemic sxs/illness
  • new onset in a pt with cancer or HIV
  • new onset after age 50
  • wakes from sleep
  • jaw claudication/temporal tenderness
  • posture/exercise/valsalva provoked
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4
Q

Red flags are usually associated with…

A

secondary HA

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5
Q

Most common headache leading to pts seeking medical attention?

A

migraine headache

~90% report some HA related disability, 53% are severely disabled or need bed rest during an attack

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6
Q

Risk factors for migraine headache?

A

female, white ethnicity, low SES, fam hx, obesity, hx anxiety or depression

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7
Q

Migraine etiology?

A

trigger–> brainstem neuronal hyper excitability–> increase in nerve cell activity and increased blood flow

alteration in neuropeptide levels (serotonin/norepinephrine)

increased blood vessel dilation and inflammation of adjacent dura matter –> activation of trigeminal nerve pain receptors

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8
Q

What are some common migraine triggers?

A

emotional stress, hormones in women, not eating, weather, sleep disturbances

-can lower threshold for development of migraine

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9
Q

When estrogen levels are low, there is a ….incidence of migraines

A

lower

inverse relationship between estrogen level and migraine

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10
Q

When does migraine prodrome occur? What are some sxs?

A

sxs appear 24-48 hrs prior to HA (75%)

yawning, depression, irritability, food cravings, constipation, neck stiffness

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11
Q

Describe migraine aura

A

occurs in 25%

gradual development over ~5 mins, lasts 5-60mins

can be visual (shimmering/scintillating shapes)

sensory (tingling on one side of face)

language (dif. finding words)

Motor (weakness on one side of face/body)

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12
Q

Describe a migraine HA

A

4-72 hrs

typically unilateral, throbbing of pulsating quality, moderate to severe pain (progressively increases)

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13
Q

migraine associated sxs?

A

N +/- V, photophobia, phonophobia, osmophobia (sensitivity to odors), cutaneous allodynia (sensitivity to touch)

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14
Q

Describe migraine resolution/post-dromal state

A

up to 24 hrs

sudden head movement causes transient HA

fatigue, concentration difficulty, not feeling like norm. self

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15
Q

What are the types of migraine HAs?

A

migraine w/out aura “common migraine” (75%)

migraine w/ aura “classic migraine”

chronic migraine >8d/mo for > 3mos

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16
Q

Dx criteria for migraine w/out aura?

A

at least 5 attacks
- HA lasting 4-72 hrs
+2 of: unilateral, pulsating, mod/severe pain, aggravation by or avoidance of routine activity

+ 1 during headache: N/V, photophobia/phonophobia

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17
Q

Patient with retinal migraines present with?

A

vision loss on visual field exam

monocular field defect

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18
Q

What is a brainstem aura?

A

aura of fully reversible visual, sensory and/or speech/language sxs

+ 2 or more: dysarthria, vertigo, tinnitus, hypacusis, diplopia, ataxia, decreased LOC

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19
Q

What is a hemiplegic migraine?

A

aura consisting of both of the following:

  • fully reversible motor weakness
  • fully reversible visual, sensory and/or speech language sxs
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20
Q

Tx options for migraines?

A

Acute (abortive), preventive

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21
Q

Describe abortive migraine tx

A

take during an attack

reduces pain, associated sxs and disability, stops progression

-works better the sooner it is taken

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22
Q

1st line med for abortive migraine therapy? 2nd line? 3rd line?

A

NSAIDs

Acetaminophen

ASA/Acetaminophen/Caffeine (Excedrin)

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23
Q

Which abortive therapy for migraines is a common cause of med-overuse HA?

A

Excedrin

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24
Q

1st line abortive therapy in severe attack migraine?

A

Serotontin (5-HT1) Agonists “Triptans” 1st line

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25
Q

Serotonin Agonists MOA?

A

Lead to vasoconstriction which decreases pain

Activate serotonin receptors on trigeminal neurons and inhibit release of vasodilating compounds

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26
Q

Examples of Serotonin Agonists?

A

Sumatriptan (Imitrex)

Zolmitriptan (Zomig)

Eletriptan (Relpax)

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27
Q

What is considered overuse of Serotonin Agonists?

A

used 2-3x/wk, may ;ead to daily dull headache or migraine overuse HA

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28
Q

2nd line abortive therapy in severe attack migraine? MOA?

A

Ergotamines: less effective and more adverse effects than triptans

Non-selective serotonin (5-HT1) agonists

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29
Q

Examples of Ergotamines:?

A

Dihydroroergotamine (Migranal)

Ergotamine/Caffeine (Cafergot)

30
Q

When should opioids be used?

A

only as rescue meds

only if pt cannot take/does not respond to other tx

  • Regular use can lead to tolerance, opioid-induced hyperalgesia, and medication overuse headaches
  • Potential for abuse and dependence
31
Q

What are some adjunct tx for migraine attack?

A

Antiemetics:

Metoclopramide (Reglan)

Prochlorperazine (Compazine)

Promethazine (Phenergan)

Hydration

32
Q

When should preventative migraine therapy be started?

A

For patients with frequent (≥ 3 attacks/month), recurring and disabling symptoms

Migraines last over 48 hours

Acute treatments are contraindicated, ineffective, or overused

33
Q

What are some preventative meds for migraine therapy?

A

Valproic acid

Propranolol

Verapamil

Amitriptyline

Venlafaxine

34
Q

Botulinum Toxin use? MOA?

A

chronic migraine

blocks release of substance P and CGRP

Inhibits peripheral signals to CNS and blocks central sensitization

35
Q

What is the most common primary headache disorder?

A

tension headaches

36
Q

tension HA epidemiology?

A

mid teens- <50 y/o

M >F (3:2)

37
Q

Risk factors for tension HAs?

A

Stress & anxiety

Too little or too much sleep

Obstructive sleep apnea

Depression

Muscular tension

Cervical spondylosis-arthritic changes within C-spine

38
Q

Proposed tension HA etiology?

A

Peripheral activation and sensitization of pericranial myofascial nociceptors

Decrease nociceptor threshold

Stimuli that are normally innocuous are misinterpreted as pain

39
Q

Clinical findings of tension HA?

A

Daily or episodic headaches that last from 30 minutes to 7 days

Bilateral location

Pressing / tightening quality (non-pulsating)

Mild or moderate intensity

May have increased tenderness of pericranial myofascial tissue

40
Q

Is Photophobia / phonophobia common with tension HAs? N/V?

A

NO

NO

41
Q

1st line therapy for acute attack tension HA?

A

NSAIDs, Acetaminophen, ASA

42
Q

Chronic tension HA? Tx?

A

> 7-9 HA/mo

Amitriptyline (Elavil)

Non pharm therapy: CBT, relaxation training, EMG, PT, acupuncture, spinal manipulation

43
Q

Cluster HA epidemiology?

A

> 30 y/o with peak in 40s

M > F

44
Q

Risk factors for cluster HAs

A

1st degree relative (14 fold increase)

Prior head injury

Cigarette smoking

High alcohol consumption

Male gender

Type A personality

45
Q

Etiology of cluster HAs?

A

Hypothalamic activation with secondary activation of the trigeminal-autonomic reflex

46
Q

What triggers initial cluster HAs?

A

Disorder of circadian rhythm

Sleep (reduced oxygenation)

Volatile smells

Vasodilators

Smoking

Sildenafil

47
Q

Cluster HA presentation?

A

15-180 mins up to 8 times/day

unilateral orbital, supraorbital and/ or temporal pain described as severe, piercing, exploding, penetrating

Individuals are agitated and restless, often pacing around the room

also contain autonomic component

can be episodic or chronic

48
Q

What are some autonomic components of cluster headaches?

A

Must have at least 1 on the affected side:

  • conjunctival injection or lacrimation
  • nasal congestion/rhinorrhea
  • forehead and facial sweating
  • sensation of fullness in the ear
  • miosis (constriction) and/or ptosis (drooping)
49
Q

Tx for cluster HA, acute attack?

A

1st line: 100% O2

Sumatriptan (Imitrex)/zolmitriptan (Zomig)

Prednisone taper

Intranasal lidocaine

50
Q

Triptans are contraindicated in…

A

HTN and vascular disease

51
Q

Prophylaxis tx for cluster HAs?

A

CCB, Verapamil, is most effective

52
Q

What is a secondary HA?

A

HA attributed to some underlying pathologic process

i.e. trauma/injury to the head/neck, cranial or cervical vascular disorder, a substance or its withdrawal, infection, psychiatric disorder

53
Q

What are some subclasses of secondary HAs?

A

post concussion, analgesic rebound, pseudotumor cerebri, temporal arteritis, trigeminal neuralgia, SAH

54
Q

What is a concussion?

A

a mild traumatic brain injury

may have sxs related to: cognitive-sensory, vestibular-somatic, sleep arousal, affective

55
Q

Should you order a CT to r/o concussion?

A

NO

primary use to rule out intracranial hemorrhage

56
Q

What are some variables that predict ICH in peds pts?

A

LOC: Relative risk

GCS < 15:

Focal neurological defect

57
Q

How are concussions managed?

A

Rest: physical rest and cognitive rest

Tylenol for HA

58
Q

Describe Drug (analgesic) rebound HA

A

med overuse HA

typically preceded by episodic HA disorder

MC related to acute symptomatic meds: opiods, Butalbital/analgesic combinations, ASA/Acetaminophen/caffeine combinations

resolves/reverts to previous pattern w/in 2 mos after discontinuation of analgesia

59
Q

Associated sxs for drug rebound HA

A

+/-

nausea, asthenia, dif. concentrating, memory problems, irritability

60
Q

What is considered analgesic overuse?

A

regular intake >10 days per month for > 3 months

61
Q

What is pseudotumor cerebri?

A

aka idiopathic intracranial hypertension

chronically elevated intracranial pressure

HA is MC presenting sxs

62
Q

Describe HA associated with pseudotumor cerebri

A

variable and non specific

pain of unusual severity

intermittent or persistent

+/- exacerbation w/ changes in posture

+/- relief w/ NSAIDS and or rest

63
Q

pseudotumor primarily affects…

A

women of childbearing age

64
Q

Associated sxs of pseudotumor cerebri

A

transient visual obscurations

intracranial noises

photopsia

BP, retrobulbar pain, diplopia, sustained visual loss

65
Q

Pseudotumor cerebri PE findings?

A

Pepilledema

visual field loss

Abducens (CN VI)
palsy

66
Q

Tx for pseudotumor cerebri?

A

weight loss for obese pts

decrease salt intake

carbonic anhydrase inhibitors (Acetazolamide)

Loop diuretics
(furosemide)

Serial LPs, optic nerve fenestration, CSF shunting

67
Q

Describe temporal arteritis

A

AKA giant cell arteritis

MC systemic vasculitis

Peak incidence 70-79 y/o

68
Q

Temporal arteritis clinical presentation?

A

abrupt or insidious onset of HA (usually localized to temporal or occipital area)

Neck/torso/shoulder/pelvic girdle pain consistent w/ polymyalgia rheumatica

Jaw claudication

fever

general sxs: malaise, weight loss, night sweats, myalgias

69
Q

Temporal arteritis PE?

A

1/2 with tenderness over SF temporal a.

nodularity/thickening of the SF temporal a.

gentle pressure on scalp may elicit pain

complete eye exam should be performed r/o arthritic anterior ischemic optic neuropathy (10% develop central retinal a. occlusion)

70
Q

Temporal arteritis work up?

A

Hallmark: elevated ESR and CRP

Gold standard: temporal artery biopsy (refer to vascular surgeon)

71
Q

Should you start tx for temporal arteritis before biopsy?

A

YES

start on high dose corticosteroid therapy due to impending danger of blindness

Prednisone 40-60mg if bx within 1 wk

Prednisone 80-100mg in pts with visual sxs

(improvement usually within 72 hrs)

72
Q

How long should pts with temporal arteritis be on high dose steroids?

A

enough for sxs to resolve. Taper steroids while continuing to monitor CRP/ESR. Keep on stable dose until inflammation resolves

(some pts require 5 yrs)

Foundations II-Neurology (9 decks)

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