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Neuro Pharmacology > Pharmacological Treatment of Headaches > Flashcards

Pharmacological Treatment of Headaches Flashcards

1
Q

What are causes of Secondary HA’s?

A
  1. Often Intracranial (deep, aching, dull, not throbbing)
    - Brian injury
    - Tumor or infection
    - Hangover
    - Kidney of liver disease
    - Dental problems
    - Caffeine withdrawal
    - HYPERTENSION
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2
Q

What is a Sinus HA?

A

Pain behind browbone and/or cheekbones.

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3
Q

What is a Cluster HA?

A

Pain is in and around one eye.

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4
Q

What is a tension HA?

A

Pain is like a band squeezing the head.

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5
Q

What is a migraine HA?

A

Pain, nausea and visual changes are typical of classic form.

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6
Q

What is a primary HA?

A
  • Not caused by underlying condition.
  • 90% of all HA.
  • Females 3X more likely
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7
Q

What are symptoms of migraine?

A
  1. Recurrent, paroxysmal attacks of throbbing, pulsating pain, usually unilateral, combined w/ autonomic disturbances.
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8
Q

What is the HIT-6?

A
  1. Headache Impact Test.
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9
Q

What is characteristic of episodic migraines?

A
  1. 0-14 HA days/mo
  2. 2.5% progress to chronic
  3. Contributing factors:
    - Obesity
    - Smoking
    - High caffeine
    - Sleep disorder
    - Opioid use #1 cause of conversion.
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10
Q

What are the 5 phases of complete migraine attack?

A
  1. Prodrome
  2. Aura
  3. HA
  4. Resolution
  5. Recovery
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11
Q

What is the diagnostic criteria of migraine w/o aura?

A
  1. Recurrent HA
  2. Untreated or unsuccessfully treated HA duration of 4-72 hr AND
  3. at least 2 of following:
    - Unilateral
    - Pulsating
    - Moderate or severe intensity
    - Aggravation by routine physical activity.
  4. Associated with one of the following:
    - Nausea/vomiting
    - Photophobia or phonophobia.
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12
Q

What is diagnostic criteria for migraine w/ aura?

A
  1. Aura less than 60 min before pain.
  2. Visual disturbances are the most common element of migraine aura.
    - blurred cloudy vision
    - Scotoma
    - Scintillating zigzag lines
    - Flashes of light
  3. Sensory, speech and/or language, motor, brainstem.
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13
Q

What is characteristic of chronic migraine?

A
  1. Tension-like or migraine-like HA occurring more than 15 days/mo for greater than 3 months w/ migraine features more than 15 days/mo
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14
Q

Consecutive stages in migraine attack?

A
  1. Cortical spreading depression
  2. Extracranial & Intracranial arterial constriction (during aura)
  3. Extracrania & Intracranial arterial dilation & decreased electrical activity (during attack)
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15
Q

What is Cortical Spreading Depression?

A
  1. Self propagating.
  2. Brief neuronal excitation w/ glutamate and ATP flux and large efflux of K from IC to EC.
  3. Long-lasting inhibition spreads across brain 2-3mm/min.
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16
Q

Where is cortical spreading depression seen?

A

Brain regions where greatest neuron to glia ratio.

-Perhaps insufficient glia to take up released K+

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17
Q

What are the overall effects of cortical spreading depression?

A
  1. Changes in Extracranial blood flow.
  2. dilation of middle meningeal artery due to leakage of blood borne factors.
  3. Opening of BBB
  4. Leakage of plasma proteins.
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18
Q

What is the vascular theory of Migraines?

A
  1. 5-HT release preceding pain phase
    - acts on 5HT2 post-synaptic receptors on blood vessels cause vasoconstriction.
  2. 5-HT deficiency during pain phase
    - extracranial arterial dilation, associated with decrease of 5-HT release from platelets.
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19
Q

What does extracranial arterial constriction do?

A
  1. Decrease regional blood flow

2. May increase prostaglandin production and release.

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20
Q

What is the neurogenic theory of migraines?

A
  1. Changes in activity in locus coeruleus.
  2. Excitation of efferent neurons in trigeminal nuclei
  3. Release of vasoactive substances
  4. Vasodilation or arteries of dura mater & plasma protein extravasation (edema)
  5. Pain & Inflammation
  6. Sometimes excessive contraction of posterior neck muscles.
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21
Q

What do meningeal nociceptors mediate?

A

Throbbing pain of migraine.

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22
Q

What do central trigeminovascular neurons mediate?

A

Cutaneous allodynia

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23
Q

What happens with Triptan overuse?

A

Increase frequency of migraines, by neural adaptation, producing sensitization, perhaps explaining medication overuse headache.

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24
Q

What is the 3 step approach to migraine treatment?

A
  1. Non-specific Tx for mild migraine.
  2. Specific Tx for moderate-severe pain associated w/ some impairment of function.
  3. Prophylaxis in a migrainer
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25
Q

What is Non-specific treatment of Migraines?

A
  1. Mild Analgesics
    - ASA, APAP, NSAIDs
  2. Combination products
    - Fiorinal, Fioricet, Excedrin
  3. Isometheptine (alpha, beta agonists vasoconstrictor)
    - dichloralphenazone
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26
Q

What are opioid non-specific treatment of acute migraine attacks?

A
  1. Butorphanol nasal spray (Stadol)
    - abuse, dependence, increased risk of transformed migraine
    - ONLY as last resort.
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27
Q

What is Metoclopramide (Reglan)?

A
  1. Anti-emetic/gastro (pro-) kinetic agent.
    - Pro-kinetic to enhance gastric emptying, enhance absorption of oral agents.
    - Reduce N&V
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28
Q

What is the MOA of Pro-kinetic agents?

A
  1. 5-HT3 receptor antagonist and 5-HT4 receptor agonist to facilitate ACh release from enteric neurons.
  2. Peripheral DA2 antagonist on cholinergic enteric neurons.
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29
Q

How does Metoclopramide act as an anti-emetic?

A
  1. Central DA2 antagonist

- Inhibits chemoreceptor trigger zone (CTZ) in area postrema.

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30
Q

What is Ondansetron? MOA?

A
  1. Anti-emetic, modest prokinetic

2. Inhibit 5-HT3 receptors in GI tract and in CTZ.

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31
Q

What are Neuroleptics?

A
  1. AKA “antipsychotic”
  2. Phenothiazines (Promethazine)
  3. DA2 antagonists.
32
Q

What are other non-specific Tx of Acute Migraine Attack?

A
  1. Lidocaine
  2. Sedation
  3. Heat to relax tense muscles. Cold to constrict blood vessels.
  4. Hyperbaric oxygen
33
Q

What is used for specific treatment for moderate-severe pain of migraines?

A
  1. To directly arrest the process:
    - Ergots
    - Triptans
34
Q

What are the proposed MOAs of ergotamine and Triptans?

A
  1. Agonists at presynaptic 5-HT1D & 5-HT1B receptors that decrease release of pro-inflammatory NT and neuropeptides. (CGRP & Substance P)
  2. 5-HT1B activation to constrict cerebral and coronary arteries.
35
Q

What is the ADME of Ergotamine?

A
  1. Poor oral bioavailability (F less than 1% due to extensive first pass metabolism)
    - Sublingual also poor F.
    - Rectal suppositories w/ caffeine.
36
Q

What does the addition of caffeine to Ergotamine do?

A

Increase solubility to increase rate and extent of ergotamine absorption.

37
Q

What are the side effects of Ergotamine?

A
  1. N&V (probably due to DA activity)
  2. Peripheral and probably cardiac vasoconstriction.
  3. Increased frequency of medication overuse migraines.
38
Q

What are some complications of Ergots and related compounds?

A
  1. Severe HA due to rebound or withdrawal
  2. Retropentoneal fibrosis
  3. Gangrene
39
Q

Characteristics of Dihydroergotamine (D.H.E. 45)

A
  1. Injectable (IV,IM,SC)
  2. Agonists at multiple 5-HT, DA, NE receptors.
  3. Oral F = 0.001-0.015
  4. Quite effective esp. IV,IM,SC
  5. Migranal (nasal spray)
  6. ALSO USED FOR MIGRAINE PROPHLYAXIS.
40
Q

What are the contraindications of Ergots?

A
  1. Pregnancy category X.
  2. Peripheral vascular disorders.
  3. Severe HTN
  4. Coronary ischemic heart disease.
  5. Impaired hepatic or renal function.
  6. Sepsis.
41
Q

Characteristics of Triptans?

A
  1. Structurally similar to 5-HT
  2. Highly selective 5-HT1 agonists, esp. 5-HT1D and 5-HT1B.
  3. Receptors located pre-juntionally on the peripheral and central ends of sensory trigeminal neurons and have NO vasoconstrictor action.
  4. Hyperpolarize nerve terminals, Inhibit trigeminal impulse.
42
Q

What is the site of action for Triptans?

A
  1. Trigeminal nerve, outside the brain.

2. Early use helps block development of central sensitization symptoms.

43
Q

Characteristics of Sumatriptan (Imitrex) PO?

A
  1. F=.14-.17 due to 1st pass of 80%
  2. 50-100mg onset of action 30-60 min, peak plasma 1-2 hr , 50-60% efficacy.
    half life 1.7hr Duration 2hr.
44
Q

Characteristics of Sumatriptan (Imitrex) SC?

A
  1. F= 0.97
  2. 6mg onset of action 10 min, peak plasma 12 min, 70% efficacy.
  3. Needle free injection (Sumavel) onset of action 10 min.
45
Q

Characteristics of Sumatriptan (Imitrex) patch?

A

Single use, battery powered
5-20 mg
Onset of action 15 min.

46
Q

What is Treximet?

A

85mg sumatriptan, 500 mg Naproxen

10 mg sumatriptan, 60 mg Naproxen.

47
Q

What are the side effects of Sumatriptan?

A
  1. Subcutaneous injection site reactions.

2. Tightness in chest, throat tightening, coronary vasoconstriction. 5-HT1B agonist effect.

48
Q

Which 2nd gen. Triptans have superior relief at 2 hours compared to Sumatriptan?

A
  1. Rizatriptan

2. Eletriptan

49
Q

Which 2nd gen. Triptans have superior sustained freedom from pain?

A
  1. Rizatriptan
  2. Eletriptan
  3. Almotriptan
50
Q

Which 2nd gen. Triptans have superior consistency of effect compared to sumatriptan?

A
  1. Risatriptan (++)

2. Almotriptan

51
Q

What 2nd gen. Triptans have increased tolerability compared to sumatriptan?

A
  1. Naratriptan (++)

2. Almotriptan (++)

52
Q

Characteristics of Zolmitiptan?

A
  1. Nasal spray
  2. 2.5 (up to5) mg at onset
  3. Equal F compared to oral tablet
  4. May repeat after 2hr. Not to exceed 10mg/24hr.
53
Q

What are drug interactions of Triptans?

A
  1. Avoid concurrent use w/ other triptans & ergots.
  2. SSRIs cause serotonin syndrome
  3. MAOIs (within 2wks D/C) causes HTN
    - All but Naratriptan.
54
Q

What are cautions of Triptans?

A
  1. Should not be used in prego.
  2. Can cause strokes and MI in ppl w/ arteriosclerotic vascular diseases, high bp, coronary artery disease, and poorly controlled diabetes.
55
Q

What are contraindications of Triptans?

A
  1. Ischemic coronary artery disease, stroke, TIAs.
  2. Cerebral & peripheral vascular disease.
  3. Uncontrolled HTN.
  4. Others w/ specific drugs.
56
Q

What Beta Blockers are used for migraine prophylaxis?

A
  1. Propranolol (80-240 mg/d) and Timolol (20mg and up)

2. 50% of patients experience 50% efficacy = 25% therapeutic gain.

57
Q

What is the MOA of Beta Blockers for Migraine prophylaxis?

A
  1. Unknown.

2. Does not correlate with beta blockade or intrinsic sympathetic activity.

58
Q

What Antidepressants are used for Migraine Prophylaxis?

A
  1. Tricyclic Antidepressants.

- Amitryptyline (10-150mg/day –Only antidepressants conssistantly effective.

59
Q

What is the MOA of antidepressants for Migraine Prophylaxis?

A
  1. Block NE & 5-HT re-uptake.

2. Migraine: Perhaps via interaction w/ 5-HT receptors.

60
Q

What antiepileptic drugs are used for migraine prophylaxis?

A

Aberrant physiological state of abnormal neuronal heyperexcitability.

  1. Phenytoin (200-300mg/d)
  2. Valproic acid(250-1000mg/d)
  3. Topiramate (FDA approved)
  4. Gabapentinoids and Pregabalin
  5. All at anti-convulsant doses
61
Q

What is done for Menstrual Migraine Prophylaxis?

A
  1. Naproxen (275 mg tid, start 3-7 days before and through menses)
  2. Hormonal manipulation w/ lowest dose estrogen oral contraceptives taken continuously
  3. Regular sleep, avoid migraine triggers, use relaxation techniques.
  4. PG migrainers (propranolol, verapamil, topiramate)
  5. NOT Valproate or Ergots.
62
Q

Why are post-synaptic 5-HT2a receptor antagonists used for migraine prophylaxis?

A
  1. Block 5-HT induced temporal arterial vasoconstriction seen in early stage of migraine.
    - 2a receptors mainly in temporal arteries.
63
Q

Characteristics of Cyproheptadine (Periactin)?

A
  1. 5-HT2a antagonists and 5-HT1b agonist.

2. Latter may mediate its effects to constrict dilated blood vessels to reduce symptoms.

64
Q

Characteristics of Methysergide (Sansert)?

A
  1. An ergot alkaloid, generally avoided due to side effects.
65
Q

What are side effects of Methysergide?

A
  1. GI: reduce by gradual increase in dose.
  2. LSD like psychic disturbances
  3. Vasoconstriction
  4. Inflammatory fibrosis (w/ chronic Tx)
66
Q

How is Botox for Migraine Prophylaxis used?

A
  1. FDA approved in pts. w/ adult chronic migraine who suffer HA on 15 or more d/mo, each lasting more than 4 hrs.
  2. 155 U, 31 injections into 7 muscle groups. q12wks
  3. NMJ blocker (10% therapeutic gain)
67
Q

MOA of Memantine for Migraine Prophylaxis?

A
  1. A moderate affinity uncompetitive NMDA receptor antagonist, believed to work by competing w/ Mg in the synapse.
68
Q

MOA of Ketamine for Migraine Prophylaxis?

A
  1. NMDA receptor antagonist.

2. Effective in 1/2 of patients to reduce disruptive aura.

69
Q

How is Riboflavin used for Migraine prophylaxis?

A
  1. 400mg/d RDA 1.3f and 1.7m

2. Based on hypothesis that there is a mitochondrial energy deficit.

70
Q

How is Magnesium used for migraine prophylaxis?

A
  1. 200-600 mg/d RDA 280f and 350m

2. Affects 5-HT receptors, NMDA receptors, NO synthesis and release.

71
Q

How does Feverfew work?

A
  1. Decreases 5-HT release from platelets.
72
Q

How does Butterbur work?

A
  1. An extract (Petasin) has anti-inflammatory & Vasodilatory properties.
  2. MOA could be Ca channel blockade and inhibition of lipoxygenase pathway.
73
Q

What is the usual onset of a Cluster HA?

A

20-30 y/o. Peak 40-60.

74
Q

When do cluster HA attacks occur?

A
  1. Occur nightly during early REM sleep.
  2. Brief 15-180 min
  3. Severe, Sharp, stabbing pain, unilateral, near/behind eye.
75
Q

What is the treatment of cluster headaches?

A
  1. Mostly like migraines
  2. Inhaled 100% O2
  3. IV DHE45
  4. Sumatriptan
  5. Warfarin to an INR 1.5-1.9
76
Q

What is the prophylaxis treatment of cluster HA?

A
  1. Avoid triggers like alcohol
  2. Valproate
  3. Topiramate

Neuro Pharmacology (9 decks)

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