Headache & HA Pharmacology Flashcards

1
Q

Trigeminal Neuralgia

A

Intense pain of short duration occurring in the distribution of the trigeminal nerve

Causes: Idiopathic (primary), vascular compression (secondary), demyelination (secondary)

Treatment: anti-epileptics, baclofen, surgery

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2
Q

Headache Red Flag Acronym

A
S - Systemic Symptoms 
N - Neurologic Symptoms/Signs 
O - Onset that is sudden, abrupt
O - Older (>50 years) 
P - Previous HA history (first headache or pattern change)
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3
Q

Which intracranial structures receive pain innervation?

A

Meninges

Blood vessels - dural sinuses, meningeal vessels, intracranial cerebral arteries

Dermis

Innervated by the trigeminal system (C2-4)

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4
Q

Migraine - Diagnostic Criteria

A

At least 5 recurring headaches, lasting 4-7 hours, characterized by at least 2 of the following:

Unilateral
Pulsating
Moderate to severe intensity
Pain increases with physical activity

+ Nausa/vomiting, photophobia, and/or phonophobia

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5
Q

Phases of Migraine

A

Premonitory - alterations in mood, alertness, appetite up to 24 hours before headache

Aura - experienced by 30%; most often visual, unilateral, gradually developing, lasting 5 minutes - 1 hour

Headache

Resolution

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6
Q

Tension Headache - Diagnostic Criteria

A

At least 10 episodes of headache that last 30 minutes to 7 days; each episode accompanied by at least 2 of the following:

Pressing/tightening sensation
Mild to moderative severity
Bilateral 
Not aggravated by physical activity
Lack of nausea/vomiting 
Only photophobia OR phonophobia; not both
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7
Q

Tension Headache - Treatment

A

Prophylactic: tricyclic antidepressants, SSRIs

Abortive: Aspirin, acetaminophen, NSAIDs

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8
Q

Cluster Headache - Diagnostic Criteria

A

At least 5 episodes of severe, unilateral, periorbital/temporal pain recurring at least every other day up to 8x/day; one of the following ANS signs must be present ipsilaterally:

Lacrimation
Nasal congestion
Rhinorrhea
Eyelid edema
Ptosis
Miosis
Facial swelling
Ear fullness
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9
Q

Cluster Headache - Prophylactic Treatment

A

Calcium channel blockers
Lithium
Anti-epileptics

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10
Q

Cluster Headaches - Abortive Treatment

A

Oxygen
Lidocaine
Corticosteroids
Nerve Blocks

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11
Q

Idiopathic intracranial hypertension - Definition

A

Idiopathic elevated ICP with normal CSF, normal neuroimaging, normal neurological exam except for 6th nerve palsy and papilledema

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12
Q

Idiopathic intracranial hypertension - Clinical features

A

Elevated ICP with:

HA that worsens with exertion 
HA that is worse upon wakening, or awakens patients from sleep
Nausea/Vomiting
Transient visual obscurations
Photopsias 
Diplopia
Vision loss 
6th Nerve Palsy
Papilledema
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13
Q

Giant Cell Arteritis

A

Mainly a disease of the elderly; 95% of cases occur with headache and associated features: jaw claudication, temporal scalp tenderness, blindness, joint pain, fever, malaise, weight loss

Diagnosed by temporal artery biopsy; ESR and CRP are often elevated

Treatment - Steroids

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14
Q

Phases of migraine pathophysiology

A
  1. Cerebral vasoconstriction and ischemia; serotonin release from neurons and platelets
  2. Cerebral vasodilation and pain; neurons in the trigeminal complex release substance P and CGRP that trigger vasodilation and neuroinflammation of pial and dural vessels, which stimulates nociceptive fibers of the trigeminal nerve

Culminates in cortical spreading depression, a self-propagating wave of neuronal depolarization associated with decreased cortical blood flow which triggers aura and activates trigeminal nerve afferents in the meninges

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15
Q

Triptans - Mechanism in migraine treatment

A

5HT1B/1D receptor agonists; causes vasoconstriction of cerebral vessels, reversing vasodilation-induced throbbing headache; inhibition of vasodilatory and inflammatory peptide release; prevention of activation of pain fibers in trigeminal nerves

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16
Q

Triptans - Pharmacokinetics

A

Oral ROA; intranasal/SC preparations available

Sumatriptan has poor CNS penetration; newer triptans are more lipophilic and achieve higher brain concentrations

Short duration (2-4 hours); can see recurrence rate of 20-40%

17
Q

Triptans - Adverse Effects

A
Paresthesias
Flushing
Dizziness
Drowsiness
Fatigue 
Heaviness, tightness, pressure in chest 

Rarely: Coronary vasospasm, angina, MI, cardiac arrhythmia

18
Q

Triptans - DDIs

A

Should not be used within 24 hours after an ergot alkaloid because vasoconstriction may be additive

Should not be used concurrently with an MAOI (risk of serotonin syndrome)

Increased risk of serotonin syndrome with SSRIs or SNRIs

19
Q

Ergot Alkaloids - Mechanism in migraine

A

5HT1B/1D agonists

Similar to triptans but somewhat less effective/more toxic; third line agent

20
Q

Ergot Alkaloids - Pharmacokinetics

A

ROA: Oral, sublingual, intranasal, parenteral, rectal

21
Q

Ergot Alkaloids vs. Triptans - Benefits/Risks

A

Ergot Alkaloids are less effective/more toxic than Triptans but provide longer duration of effect and relatively milder side effects

22
Q

Ergot Alkaloids - Adverse Effects

A
Nausea/vomiting
Diarrhea
Muscle Cramps 
Paresthesias
Vertigo 

Rarely, vascular occlusion/gangrene due to a1-adrenergic mediated vasoconstriction

23
Q

Ergot Alkaloids - DDIs

A

Non-selective B-blockers - causes severe peripheral ischemia due to combination of alpha-vasoconstriction + blockade of Beta-2 vasodilation

Should not be used within 24 hours of Triptans - vasoconstriction may be additive

Contraindicated with strong inhibitors of CYP3A4 (itraconazole, macrolides, protease inhibitors) - increased risk of vasospasm

24
Q

Use of B-Blockers in migraine prophylaxis

A

I.e. Propanolol and Timolol - first line

Reduces frequency and severity of migraine in 60-80% of patients

Adverse Effects: Fatigue, exercise intolerance, orthostatic hypotension; CI ina sthma, cardiac conduction disturbances, heart failure

25
Q

Use of hypertensives in migraine prophylaxis

A

First line - Beta Blockers (Propanolol, Timolol)

Also some evidence that ACEIs/ARBs and Calcium Channel Blockers may be useful

26
Q

Use of anti-depressants in migraine prophylaxis

A

I.e. TCADs (Amitriptyline)

Second line prophylactic agent; useful in patients with insomnia or depression

Side effects: Sedation, dry mouth, constipation, tachycardia, weight gain, urinary retention

27
Q

Use of anticonvulsants in migraine prophylaxis

A

I.e. Valproate, Topiramate (FDA approved) - first line

Reduce migraine frequency by 50% in 50% of patients; efficacy similar to Propanolol

28
Q

Use of Botox in migraine prophylaxis

A

Use indicated in chronic migraine (15+ headache days per month, lasting at least 4 hours/day)

Adverse effects: Headache, neck pain, generalized muscle weakness, ptosis

29
Q

Use of dietary supplements in migraine prophylaxis

A

Riboflavin (vitamin B2)

Feverfew

30
Q

Role of 5-HT1B/1D agonists in migraine treatment

A

Prevents initial vasodilatory effect of 5HT
Vasoconstriction of extracerebral vessels
Decreased neuropeptide (CGRP, SP) release
Inhibition of trigeminal neuron activation

31
Q

Serotonin Syndrome - Signs & Symptoms

A
Neuromulscular effects (clonus)
ANS changes
Mental status changes (agitation, delirium, hypervigilance)
32
Q

Methysergide - use in migraine prophylaxis

A

5HT2 blocker - blocks serotonin-mediated vasodilation that initiates the migraine attack

Role in refractory migraine with high attack frequency