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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
Serotonin Agonists MOA?
Lead to vasoconstriction which decreases pain Activate serotonin receptors on trigeminal neurons and inhibit release of vasodilating compounds
26
Examples of Serotonin Agonists?
Sumatriptan (Imitrex) Zolmitriptan (Zomig) Eletriptan (Relpax)
27
What is considered overuse of Serotonin Agonists?
used 2-3x/wk, may ;ead to daily dull headache or migraine overuse HA
28
2nd line abortive therapy in severe attack migraine? MOA?
Ergotamines: less effective and more adverse effects than triptans Non-selective serotonin (5-HT1) agonists
29
Examples of Ergotamines:?
Dihydroroergotamine (Migranal) Ergotamine/Caffeine (Cafergot)
30
When should opioids be used?
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
What are some adjunct tx for migraine attack?
Antiemetics: Metoclopramide (Reglan) Prochlorperazine (Compazine) Promethazine (Phenergan) Hydration
32
When should preventative migraine therapy be started?
For patients with frequent (≥ 3 attacks/month), recurring and disabling symptoms Migraines last over 48 hours Acute treatments are contraindicated, ineffective, or overused
33
What are some preventative meds for migraine therapy?
Valproic acid Propranolol Verapamil Amitriptyline Venlafaxine
34
Botulinum Toxin use? MOA?
chronic migraine blocks release of substance P and CGRP Inhibits peripheral signals to CNS and blocks central sensitization
35
What is the most common primary headache disorder?
tension headaches
36
tension HA epidemiology?
mid teens- <50 y/o M >F (3:2)
37
Risk factors for tension HAs?
Stress & anxiety Too little or too much sleep Obstructive sleep apnea Depression Muscular tension Cervical spondylosis-arthritic changes within C-spine
38
Proposed tension HA etiology?
Peripheral activation and sensitization of pericranial myofascial nociceptors Decrease nociceptor threshold Stimuli that are normally innocuous are misinterpreted as pain
39
Clinical findings of tension HA?
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
Is Photophobia / phonophobia common with tension HAs? N/V?
NO NO
41
1st line therapy for acute attack tension HA?
NSAIDs, Acetaminophen, ASA
42
Chronic tension HA? Tx?
>7-9 HA/mo Amitriptyline (Elavil) Non pharm therapy: CBT, relaxation training, EMG, PT, acupuncture, spinal manipulation
43
Cluster HA epidemiology?
>30 y/o with peak in 40s M > F
44
Risk factors for cluster HAs
1st degree relative (14 fold increase) Prior head injury Cigarette smoking High alcohol consumption Male gender Type A personality
45
Etiology of cluster HAs?
Hypothalamic activation with secondary activation of the trigeminal-autonomic reflex
46
What triggers initial cluster HAs?
Disorder of circadian rhythm Sleep (reduced oxygenation) Volatile smells Vasodilators Smoking Sildenafil
47
Cluster HA presentation?
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
What are some autonomic components of cluster headaches?
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
Tx for cluster HA, acute attack?
1st line: 100% O2 Sumatriptan (Imitrex)/zolmitriptan (Zomig) Prednisone taper Intranasal lidocaine
50
Triptans are contraindicated in...
HTN and vascular disease
51
Prophylaxis tx for cluster HAs?
CCB, Verapamil, is most effective
52
What is a secondary HA?
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
What are some subclasses of secondary HAs?
post concussion, analgesic rebound, pseudotumor cerebri, temporal arteritis, trigeminal neuralgia, SAH
54
What is a concussion?
a mild traumatic brain injury may have sxs related to: cognitive-sensory, vestibular-somatic, sleep arousal, affective
55
Should you order a CT to r/o concussion?
NO primary use to rule out intracranial hemorrhage
56
What are some variables that predict ICH in peds pts?
LOC: Relative risk GCS < 15: Focal neurological defect
57
How are concussions managed?
Rest: physical rest and cognitive rest Tylenol for HA
58
Describe Drug (analgesic) rebound HA
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
Associated sxs for drug rebound HA
+/- nausea, asthenia, dif. concentrating, memory problems, irritability
60
What is considered analgesic overuse?
regular intake >10 days per month for > 3 months
61
What is pseudotumor cerebri?
aka idiopathic intracranial hypertension chronically elevated intracranial pressure HA is MC presenting sxs
62
Describe HA associated with pseudotumor cerebri
variable and non specific pain of unusual severity intermittent or persistent +/- exacerbation w/ changes in posture +/- relief w/ NSAIDS and or rest
63
pseudotumor primarily affects...
women of childbearing age
64
Associated sxs of pseudotumor cerebri
transient visual obscurations intracranial noises photopsia BP, retrobulbar pain, diplopia, sustained visual loss
65
Pseudotumor cerebri PE findings?
Pepilledema visual field loss Abducens (CN VI) palsy
66
Tx for pseudotumor cerebri?
weight loss for obese pts decrease salt intake carbonic anhydrase inhibitors (Acetazolamide) Loop diuretics (furosemide) Serial LPs, optic nerve fenestration, CSF shunting
67
Describe temporal arteritis
AKA giant cell arteritis MC systemic vasculitis Peak incidence 70-79 y/o
68
Temporal arteritis clinical presentation?
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
Temporal arteritis PE?
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
Temporal arteritis work up?
Hallmark: elevated ESR and CRP Gold standard: temporal artery biopsy (refer to vascular surgeon)
71
Should you start tx for temporal arteritis before biopsy?
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
How long should pts with temporal arteritis be on high dose steroids?
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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