Headache Disorders Flashcards

1
Q

What are the three types of primary headaches?

A
Migraine (w/ and w/out auroa)
Tension-type headache
Cluster headache (and other trigeminal autonomic cephalalgias)
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2
Q

What can cause a secondary headache?

A
Head and/or neck trauma
Cranial or cerebral vascular disorder
Substance abuse or withdrawal
INfection
Disorder of homeostasis
DIsorder of cranium, neck, ears, eyes, nose, sinus, mouth, or other facial or cranial structures
Psychiatric disorders
Cranial neuralgias, central and primary facial pain, and other headaches.
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3
Q

What is the most prevalent type of primary headache?

A

Tension-type headache

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4
Q

Which two types of primary headaches are more common in women and which one is the most common in men?

A

Migraines and tension headaches occur more in women

Cluster headaches occur more in men

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5
Q

What primary headache is more common in spring/fall and at night?

A

Cluster headaches

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6
Q

What is the vascular hypothesis for migraines?

A

Vasoconstriction in the cerebrum causes aura.
Aura related to changed in blood flow in the cranial vessels reduces blood flow by 25-35%
Followed by vasodilation in the extra cranial and intracranial vessels leading to headache pain.
Serotonin is believed to play important role in migraine development. Many meds used to tx migraines are agonists of the serotonin receptors, causing vasoconstriction, based on the theory that migraine pain result of cranial artery vasodilation.

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7
Q

What is the neuronal dysfunction hypothesis?

A

Pain of a migraine is through to originate from trigeminovascular system of the cerebrum
The trigeminovascular system is an initiator and promotor of tissue inflammation & when activation it releases neuropeptides that cause vasodilation and inflammation.

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8
Q

What are the modifiable risks for migraines?

A
Attack frequency
Central sensitization
Obesity
Medication Overuse
Stress snoring
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9
Q

What are the non-modifiable risks for migraines?

A

Sex-female
Low education/socioeconomic status
Head Injury

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10
Q

What are the medications that are common triggers of migraines?

A
Cocaine
Nicotine
NTG
Hormones
NTG
Hormones
Indomethacin
Cimetidine
Nifedipine
Fluoxetine
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11
Q

What are the Dietary factors that are common triggers of migraines?

A
ETOH
chocolate
aspartame
monosodium glutamate
caffeine
Tyramine
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12
Q

What are the environmental factors that are common triggers of migraines?

A
Bright flashing lights
Loud noises
Strong odors
Tobacco smoke
High Altitude
Weather changes
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13
Q

What are the lifestyle factors that are common triggers of migraines?

A

Sleeping disorders
Dieting/skipping meals
Strenuous exercise

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14
Q

What are the hormonal factors that are common triggers of migraines?

A

Menopause
Menses
Pregnancy

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15
Q

What are the psychological factors that are common triggers of migraines?

A

Anxiety
Depression
Stress

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16
Q

What is the criteria for a migraine w/out aura (common migraine)?

A

Must have 2 of the following: aggravated by routine physical activity, pulsating, unilateral, moderate or severe pain
And
At least 1 of the following_ N/V, photophobia/phonophobia

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17
Q

What is the criteria for a migraine w/ aura (classic migraine)?

A

Criteria at least 2 of the following:
Homonymous visual sx, unilateral sense sx
At least 1 aura sx develops over >/=5 min and/or different aura sx develop in succession over >/=5 min.
Each sx lasts >/= 5min and < / = 60 min
Aura consists of > / = 1 of the following:
Fully reversible visual sx (+ or -)
Fully reversible dysphasic speech disturbance
Fully reversible sensory sx (+ or -)
Approximately 15%; aura allow dx

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18
Q

What are the long-term goals of migraine treatment therapy?

A

Decrease the number and severity of future migraines
Improves patients quality of life
Supporting the resumption of normal activities Reducing ADRs.

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18
Q

What are the 3 nonpharmacologic treatment?

A
Ice to head w/ periods of rest and sleep in a dark, quiet environment
Avoid triggers
Behavioral interventions (relaxation therapy, biofeedback, cognitive therapy)
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18
Q

What is step-therapy?

A

ACP-ASIM 1st line therapy
NSAIDs (nonsteroidal anti-inflammatory drug) or combo (opiate or migraine drug)
Migraine specific agents if no response to NSAIDS
Involves non-oral route if N/V, guard against medication overuse, educate patients

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18
Q

What is stratified therapy?

A

USHC 1st line therapy
Migraine specific agents in severe migraine
Involves non-oral route if N/V, guard against medication overuse, educate patients

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18
Q

What are the non-specific pharmacological treatments?

A

NSAIDs, analgesics, antiemetics (phenergan, compazine), corticosteroids

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18
Q

What are migraine-specific pharmacological treatments?

A

Ergot derivatives

5-HT1B/1D (seratonin agonists)

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18
Q

NSAIDs

A

Non-specific meds for migraines
FIrst line for mild to moderate migraines.
Inhibit prostaglandin synthesis (inhibits inflammation in trigeminovascular system)
Includes- ASA (aspirin), naproxen, ibuprophen, APAP + ASA + Caffeine (Excedrin Migraine)

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18
Q

What are the first line NSAIDs?

A

ASA (aspirin), naproxen, ibuprophen, APAP (acetaminophen) + ASA + Caffeine (Excedrin Migraine)

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18
Q

What are the short-term goals of migraine treatment therapy?

A

Decrease severity and duration, restore ability to function

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18
Q

Ergotamine acute side effects

A
N/V (pretreatment with antiemetic)
Diarrhea
Abdominal pain
Weakness
Leg cramps
Tremor
Dizziness
Syncope
Chest pain
Intermittent claudication
Syndrome of ergotism
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19
Q

what nonsepecific treatment for migraines involves a local anesthetic into the area where pain is felt?

A

Intranasal lidocaine

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19
Q

Which nonspecific treatment is reserved for severe migraine HA that is unresponsive to other treatments?

A

Opioids

Little data for use in migraines

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19
Q

Butorphanol (Stadol nasal spray)

A

Synthetic narcotic antagonist-agonist

Abuse potential

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20
Q

Barbiturate Combinations (hypnotics)

A

Non-specific migraine treatment
Combined w/ analgesics or codein
Potential for overuse, mod-severe migraine
EX- butalbital, aspirin & caffeine (fiorinal)

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21
Q

What are the drug interactions of barbiturate combinations (hypnotics)?

A

Effects reduced by barbiturates- phenotiazine, quinidine, cyclosporine, theophylline, & BETA BLOCKERS
Effects increased by barbiturates- chloramphenicol, benzodiazepines, CNS depressents

22
Q

Triptan Side effects

A
Dizziness
Fatigue
Flushing
Nausea
Chest tightness, pressure, heaviness, pain
Injection rxn
Taste perversion from nasal spray
23
Q

Ergotamine tartrate pharmacokinetics

A

Oral tablet and retal tablet

24
Q

Dihydroergotamine

A

Nasal spray

25
Q

Ergotamine acute side effects

A
N/V (pretreatment with antiemetic)
Diarrhea
Abdominal pain
Weakness
Leg cramps
Tremor
Dizziness
Syncope
Chest pain
Intermittent Claudication
Syndrome of Ergotism
26
Q

What does syndrome of ergotism consist of?

A

Peripheral ischemia, cold, numb extremities, diminished peripheral pulses.

27
Q

Ergotamine chronic side effects

A
Cerebral/peripheral ischemic disorders
Hypertension
TACHY/BRADY
Medication overuse HA
Renal D/O
Withdrawal signs: severe HA, N/V, malaise
28
Q

Ergotamine Contraindications

A
Sepsis
Renal/hepatic failure
Pregnancy/lactation
Gluacoma
Peptic ulcer disease
Uncontrolled HTN
CHD/Stroke/PVD
Potential interactions w/ protease inhibitors
USE OF TRIPTANS W/IN 24 HOURS
29
Q

Ergotamine Drug Interactions

A

CYP 3A4 substrate
Interactions w/ strong 3A4 inhibitors (azole antifungals, macrolides, protease inhibitors)
Triptans (additive vasoconstrictive effect)
Fluoxetine, fluvoxamine (competes for metabolism by 3A4)

30
Q

Triptans

A

Selective 5-HT1b/d agonists- intracranial vasoconstriction, inhibition of neuropeptide release from trigeminovascular nerves, interrupts pain signal w/in brain stem trigeminal nuclei
1ST LINE FOR MODERATE TO SEVERE MIGRAINE

31
Q

Triptan- sumatriptan (imitrex)- ROA

A

SQ injection, oral tabs, nasal spray

31
Q

Beta-blockers MOA and contraindications

A

1st line agents for prophylactic treatment- agents include propranalol (inderal), metoprolol (lopressor), atenolol(tenormin), & nadolol
MOA- unknown theory is that it may regulate serotonin transmission in cortical pathways
Contraindications- pts w/ peripheral vascular disease, depression, asthma

32
Q

Triptans- Rizatriptan (Maxalt)-ROA

A

Oral tabs, oral disintegrating tabs

33
Q

Beta-blocker ADRs

A

Fatigue, vivid dreams, depression, impotence, BRADYCARDIA, HYPOTENSION

34
Q

If you have controlled HTN can you take triptans?

A

Yes, only those with UNCONTROLLED cannot

35
Q

Triptan Contraindications

A
Ergot alkaloid in last 24 hrs
MAOI in last two weeks
Ischemic heart disease/cerebrovascular
Uncontrolled HTN
Hemiplegic and basilar migraines
36
Q

What does MAOI do?

A

It inhibits the break down of DA, NE, and serotonin increasing the amounts of all of these leading to tachycardia and other cardiac abnormalities

37
Q

What does the triptan drug interaction MAOI result in?

A

Inhibits clearance of triptans

Risk of serotonin syndrome

38
Q

What does the triptan drug interaction w/ SSRIs result?

A

Risk of serotonin syndrome

39
Q

What does the tiptan drug interaction w/ ergotamine containing products result in?

A

Increased vasoconstrictive effects

40
Q

What is serotonin syndrome?

A

Hyperthermia, muscle rigidity, myoclonus, rapid change in mental status and vitals
Results from too much serotonin

41
Q

When is prophylactic drug therapy indicated?

A

Migraines occur 2-3 times monthly
Occur in a predictable pattern
Patients that aren’t able to tolerate or unable to take abortive therapies
Migraines are long lasting and lead to severe impairment (>3 days disability/month)

42
Q

If a patient is on prophylactic drug therapy trial and gets a headache in the first month should the trial be stopped?

A

No give the medication time to work, only stop the trial if a negative side effect is noted.

43
Q

Beta-blockers MOA and contraindications

A

1st line agents for prophylactic treatment- agents include propranalol (inderal), metoprolol (lopressor), atenolol(tenormin), & nadolol
MOA- unknown theory is that it may regulate serotonin transmission in cortical pathways
Contraindications- pts w/ peripheral vascular disease, depression, asthma

44
Q

Beta-blocker ADRs

A

Fatigue, vivid dreams, depression, impotence, BRADYCARDIA, HYPOTENSION

45
Q

What are beta-blockers used for and which ones are used?

A

1st line agents for prophylactic treatment of migraines- agents include propranalol (inderal), metoprolol (lopressor), atenolol(tenormin), & nadolol

46
Q

Tricyclic antidepressants (TCAs) MOA

A

Also used as 1st line agents for migraines- include imipramine (tofranil), nortriptyline (pamelor), & AMITRIPTYLINE (elavil)
MOA- antagonist of 5-HT2 receptors inhibiting the reuptake of serontonin and causing increased concentration of serotonin in the synaptic cleft

47
Q

What medications are used to tx intractable migraines?

A

DHE (dihydroergotamine)- SQ, IV, IM
Sumatriptan (imitrex)
Prchlorperazine (compazine) or chlorpromazine (thorazine)- antimigraine and antiemetic properties
Narcotics
Corticosteroids- suppress perivascular inflammation of resistant HA

48
Q

Tricyclic antidepressants (TCAs) ADRs and Drug interactions

A

ADRs-Sedation, constipation, blurred vision, HPOTN

Drug interactions- MAOIs

49
Q

Valproic acid (depakene) and divalproex sodium (depakote) MOA and contraindications

A

Anticonvulsant
MOA- increased activity of GABA inhibitory transmitter
Contraindications- liver-disease, monitor liver enzymes

50
Q

Valproic acid (depakene) and divalproex sodium (depakote) ADRs and drug interactions

A

Anticonvulsant
ADRs- tremor, weight gain, hair loss, nausea
Drug interactions- other anticonvulsants, CNS depressants, absence sz in combo w/ clonazepam

51
Q

What other anticonvulsants besides Valproic acid (depakene) and divalproex sodium (depakote) can be used in the prophylaxis of migraines?

A

Carbamazepine (tegretol), topiramate (topamax), gabapentin (neurontin)

52
Q

Methysergide (Sansert)

A

Should not be used unless nothing else worse and a patient has severe migraines due to black box warning of fatal pulmonary fibrosis
MOA- peripheral 5-HT inhibitor but central 5-HT agonist
Use only for 6 mo. followed by 3-4 week drug free period.
Effective but has serious side effects

53
Q

Botulinum Toxin Type A (Botox)

A

Prophylaxis of migraines
Inhibits acetylcholne release at the presynaptic cholinergic junction (inhibition of overactive peripheral neurons, possibly modulates substance P, and does not cross BBB)
Not FDA approved indication
Prophylactic effect seen 60-90 days after injection
Inconsistent clinical trials

54
Q

What are the effective natural products for migraine used in acute therapy?

A

Caffeine in combo w/ ASAP and ASA

55
Q

What are the possibly effective natural products for migraine used in prevention

A

Butterbur
Coenzyme Q-10 (can take 3 mo. to benefit)
Feverfew- difference in extraction method and bioavalability

56
Q

Which natural product is used for prevention of headaches associated with menstruation and female hormone changes?

A

Feverfew

57
Q

What are the possibly effective natural products for migraine used in prevention that are only useful if there is a deficiency?

A

Magnesium
Riboflavin (B2
Ineffective or insufficient evidence- fish oils, intranasal capsaicin, ginger, L-arginine, melatonin, olive oil

58
Q

What medications are used to tx intractable migraines?

A

DHE (dihydroergotamine)- SQ, IV, IM
Sumatriptan (imitrex)
Prchlorperazine (compazine) or chlorpromazine (thorazine)- antimigraine and antiemetic properties
Narcotics
Corticosteroids- suppress perivascular inflammation of resistant HA

59
Q

What distinguishes tension type headaches from migraines?

A

Bilateral location
Pressure/tightening (non-pulsating) quality
Not aggravated by routine physical activity

60
Q

Tension type Headache

A

Most prevalent type of chronic and recurrent HA
Pathophys is not well understood; but might have similar mechanism as migraine (muscle contractions, vasodilation, secondary to TMJ or cervical spondylosis)
HA lasts 30 minutes- 7 days with at least 2 of the following: bilateral location, pressure/tightening (nonplusating) quality, mild or moderate intensity, not aggravated by routine physical activity
Precipitants include anxiety, depression, situational stress

61
Q

What type of headache involved a BILATERAL feeling of band-like sensation around head, pain that is dull, steady, and worsening as the day progresses w/out N/V?

A

Tension type HA

62
Q

What are the non-pharmacologic treatments for tension type headaches?

A
Stress management
Relaxation training
Physical therapy
Counseling
Regulation of sleep/meal schedules
Acupuncture
63
Q

What is the pharmacologic tx of tension type headaches?

A

Analgesics w/ or w/out caffeine for mild-moderate (APAP, ASA, ibuprofen, naproxen)
Sedatives- butalbital (Fiorinal/fioricet)
Prophylactic- TRICYCLIC ANTIDEPRESSANTS- muscle relaxants (methocarbemol [robaxin], orphenadrine [norflex], cyclobenaprine [flexeril]
Botulinum toxin

64
Q

What sx are associated with a cluster headache?

A

Intense, non-throbbing, unilateral HA, behind the eye that is searing, stabbing, or burning and accompanied by ipsilateral lacrimation, nasal stuffiness, and facial flushing

65
Q

What type of headache occurs at night, lasts 30-90 minutes, occurs nightly for 2-3 months and then is gone only to return months or years later?

Hint - sx include Intense, non-throbbing, unilateral HA, behing the eye that is searing, stabbing, or burning and accompanied by ipsilateral lacrimation, nasal stuffiness, and facial flushing

A

Cluster headache

66
Q

Cluster HA- acute treatment

A
Imitrex SQ (nasal is less effective)
O2 inhalation
Ergotamine +/- caffeine
DHE-45
Lidocaine nasal spray 4%
67
Q

Cluster HA- prophylaxis

A
Verapamil (ca++ blocker)
Prednisone
Ergotamine
Methysergide
Lithium