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105 Cards in this Set
- Front
- Back
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Why Learn About Headache?
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Headache disorders are common
45 million people in the US regularly experience headache Headaches are costly and time consuming (when a patient has a migraine they go to work thinking they will get better, but the migraine gets worse so there is a olss of productivity) Poor use of emergency rooms and healthcare $ 1999 study: cost to employers $13 billion a year in absences & job productivity Cost of treating migraine (not including OTC) $1 billion per year Migraineurs: 2 X as many medical claims and 2.5 X as many pharmaceutical claims than non-sufferers VA study showed yearly cost of migraine management $3,195+/- and an annual ER cost of $2,446 |
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Migraine Status
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28 million Americans
21 million women 7 million men ~ 50 % the problem is severe and disabling Most not diagnosed and not treated w/ prescription medications 1 ot 10 patients that have migraines do not have a formal diagnosis and then have MOH |
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Primary HA (know)
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Migraine with aura (classic): vascular
Migraine without aura (common): vascular Tension-type headache: muscle contraction Cluster headache: vascular (less common, but most common in men, there is a heriditary component) Due to HA no underlying cause |
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are cluster HA more common in males or females (know)
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males
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aura protion of a migraine is ___________ component that usually ___________ the migraine
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vasucular
preceeds |
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Secondary HA (know)
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due to a secondary cause
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Causes of secondary HA (know)
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Non-cephalic infection
Metabolic disorders Disorders of face & neck Cranial neuralgias Head trauma Vascular disorders Non-vascular disorders Toxic substances |
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International Headache Society Criteria for Migraine w/o Aura (know)
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At least Five attacks fulfilling the following characteristics:
*HA lasting 4 to 72 h *HA has 2 of the following *Unilateral location (can move to both sides) *Pulsating quality (ususally in temproal area) *Moderate (inhibits ADLs) or severe intensity *Aggravated by routine physical activity During HA, at least 1 of the following (generally not held to all of these below) *Nausea and/or vomiting *Photophobia or phonophobia |
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International Headache Society Criteria for Migraine w/ Aura
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At least two attacks fulfilling three or more of the following:
At least one fully reversible aura symptom At least one aura symptom developing gradually over 4 minutes, or two in succession No aura symptom lasting > 60 minutes; if more than one aura symptom is present, expected duration is proportionally increased Migraine headache follows aura within 60 minutes; it may begin with or before the aura |
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Physical Examination for Migraine
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Vital Signs: temperature, blood pressure, pulse, cardiac status (murmurs, rubs, bruits), lung status (clear, COPD, etc.) (making sure the patient is not having a stroke)
Optic-fundi, visual fields, pupillary reaction (make sure there is not a bleed in the back of the brain) Indication of possible co-morbid illness Screening neurological exam (ataxia?? Brainstem problems?) Detailed cervical and spinal exam |
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The Headache History
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Circumstance/suddenness of onset
Age at onset Intensity/characterization/ location of pain Duration/frequency/course Preceding & associated symptoms Provoking/aggravating factors Impairment/impact Ameliorating factors Medications (past & present) Medical history Family history Psychosocial conditions THIS IS REALLY IMPORTANT TO DETERMINE TYPE OF HA |
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Migraine in General
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Multifactorial
Autosomal dominant Environmental Gender distribution is equal in childhood Adults: women 3:1 Likely represents the aggravating influence of estrogen Most develop migraine in the first 3 decades of life Migraine is usually an inherited disorder. Most believe that migraine is a syndrome with multiple genetic and environmental implications and variations. Gender distribution is approximately = in childhood. In adults it affects women 3:1 The dominance of women likely represents the influence of estrogen |
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Migraine Triggers (know)
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increase or decreasein sleep (diffferent from what the patient is used to, consistency plays a role)
Dehydration Stress Emotional letdown Missing meals Medications EtOH Weather changes Smoking Strong perfumes Many foods and preservatives: nuts, chocolate, caffeine (too much or too little), bacon, aged cheese, avocados, pizza, prepared foods, tannens in red wine (sulfides) |
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Fortification spectra
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aura term
objects appear surrounded by luminous angles |
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photopsia
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aura term
shimmering, sparkling, flashing light in one visual field usually (unilateral) |
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formication
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aura term
burning, prickling sensations without external stimuli neurological component nerves getting sensitized |
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cluster HA charateristics
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Usually male
Onset: 27-30 years Duration: 15 minutes-3 hours Excruciating Unilateral location (almost always Nausea & vomiting rare Awakens from sleep with headache Can not remain still and usually paces strong family hx generally occur at the same time of year and cluster together not induced by stress |
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Tension Type Headache
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Attacks >/= 15 days/month (180 days/years)
Pain does not prohibit activities Dull and band like Bilateral No nausea/vomiting, photophobia, or phonophobia usually stressed induced mild to moderate pain |
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Pathophysiology of migranes
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The migraine generator: brain stem
Reticular activating system: brain stem Stimulates brain stem nuclei (Vegas - parasympathetic) This stimulates nitric oxide and plasma protein release from the meningeal blood vessels Meningeal blood vessels Release nitric oxide (vasodilator) Plasma proteins + (NO) = irritation of trigeminal nerve |
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the migraine generator
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brain stem
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meingeal blood vessels are CNS or PNS component of a migraine
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PNS
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phases of a migraine
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Peripheral trigeminal nerve, when stimulated releases vasodialtors (know)
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Calcitonin gene-related peptide (CGRP): potent vasodilator
Substance P (SP) Neurokinin-A (NKA) causing: Plasma protein extravasation & inflammation “Neurogenic Inflammation” |
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Central brain stem trigeminal nuclei conduct pain through the...
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Central pain transmission through the thalamus
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path of a migraine
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trigger-->brain stem --> long gangli--> meningeal blood vessels (peripheral)--> relase of vasodilators--> trigeminal nerve-- brain stem (central)--> thalamus --> N/V, central sensitization--> pain/migraine
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picture of the integrates hypothesis of a migraine
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The fourth key event of a migraine
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is the transmission of pain signals by trigeminal nuclei to higher cortical centers where migraine pain is felt.
The trigeminal system is the sensory system that innervates the pain sensitive vessels in the head and dura mater. It essentially is a vasodilatory system, as well as having a primary involvement in sensory functions |
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Goals of Migraine Therapy
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To attain a pain-free status
To reduce or prevent disability Improve quality of life Avoid headache medication escalation Educate and enable patients to manage their disease |
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acute/abortive goals of migraine therapy
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Reduce the intensity and duration of pain & symptoms
No effect on aura and must take at onset of pain |
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preventative goals of migraine therapy
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To prevent or reduce the occurrence of migraine
> 2 attacks/mo or prolonged/refractory to short-term treatment Patient does not want to have the headache at all |
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behavioral therapy for migraines
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Avoid Triggers
Biofeedback Stress Reduction Application of ice (when feel it starting) Stop smoking Sleep and relaxation Most effective w/ recurrent migraines 50% reduction in migraine if used appropriately |
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preventative therapy of migraines (most commonly used agents)
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Most commonly used agents
Beta-blockers Calcium channel blockers Antidepressants (TCA) Antiepileptic drugs (AEDs) NSAIDS (don't typically use because of MOH) Cox-2 Inhibitors Celecoxib (Celebrex®) 200 mg daily Cyproheptadine Methysergide (only compounded) (potent vasoconstrictor, category X and can cause fibrosis throughout the body) |
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what are the AEDs that are FDA approved for migrains (know)
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valproate and topiramate
Depacon (IV valproate) is used in status migrainus) |
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what is the big SE of cyproheptadine
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central mediated weight gain
so it is not commonly used |
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also effective preventative migraine therpay
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Estrogen replacement agents
Angiotensin-converting enzyme inhibitors Angiotension receptor blockers (Candesartan) Clonidine Fish oil supplements (omega 3) Feverfew (50 to 100 mg/d) Magnesium (300mg/d) Riboflavin (400 mg/d) Coenzyme Q-10 (100 mg TID) Butterbur (Petadolex 150 /d decreases by 50 %) (food supplement) Acupuncture Botulinum Toxin every 3 months Leukotriene antagonists |
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beta blockers and migraine
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Beta-blockers = efficacy to calcium channels blockers
80% effective Propranolol: FDA approved for prophylaxis w/ or w/o aura Initial dose 20-40 mg three times daily; often need 120-360 mg daily (extended release) doses are at lower end initially the they may need to be tirtrated up all beta blockers are used |
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other beta blockers used for migraine (konw timolol)
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(effective but not FDA approved)
Atenolol: 50 - 200 mg daily Metoprolol: 50 - 200 mg daily (twice daily if conventional, daily if extended release) Nadolol: 20 - 240 mg daily Timolol: 5 - 30 mg daily (FDA approved for prophylaxis in adult) |
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beta blockers MOA and risks when used for migraines
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MOA: unknown
Risks: cardiovascular, asthma, CNS (sedation, confusion, etc.) May require several months of treatment for full benefit they reduse HR and BP so they reduce exercise capacity and you would not want to give to a patient with already low BP they alos cause fatigue and sexual dysfunciton |
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CCB as preventaitive therapy for migraines
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Verapamil: 40 mg tid initially then gradually increase to 80 mg tid to qid
Diltiazem: 30 mg tid initially, then gradually increase to 60 -120 mg tid Amlodipine: 5 mg qd Nimodipine: 20 - 40 mg tid to qid Nifedipine: 10 mg tid Flunarizine: 10 mg qd doses not on exam |
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CCB MOA for migraine
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Calcium channel blockers
MOA: most likely an interaction with CNS neurotransmission May require 3 weeks – 2 months for full benefit of efficacy don't know how they really work consider the SE such as constipation |
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antidepressants and preventative migraine therapy
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Antidepressants
Amitriptyline: 10 - 300 mg qd, start low go slow; may be given @ hs Nortriptyline: 10 to 150 mg qd @ hs MOA: inhibition of 5-HT2 receptor Risks: anticholinergic effects, CNS (sedation, confusion, etc.) weight gain TCA are not recommended for the elderly because of sedation |
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AEDS and migraine prevention
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Valproate (Depakote®) is FDA approved: 250-1500 mg divided bid to tid, start low go slow
Topiramate (FDA approved): remember can cause kidney stones, word confusion and parasthesias Levetiracetam, gabapentin, pregabalin |
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Cyproheptadine (Periactin®)
and migraine prevention |
4 - 16 mg divided bid
Potent serotonin and histamine antagonist MOA: unknown Risks: sedation, anticholinergic, weight gain Remember weight gain not commonly used |
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Methysergide (Sansert®) and migraine prevention
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2 – 6 mg in divided doses
MOA: serotonin receptor antagonist Risks: retroperitoneal, endocardial, pleuropulmonary fibrosis (w/ prolonged therapy) Slowly taper off over 2-3 weeks to avoid rebound Drug holiday: for 3-4 weeks after 6 months of therapy; (prevents fibrosis) may cause rebound Only available as a compounded agent |
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NSAIDS and migraine prevention
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may cause rebound:
Aspirin: 300 mg qd or qod Fenoprofen (Nalfon®): 600 mg tid Ibuprofen: 300 - 600 mg tid Ketoprofen (Orudis®): 50 or 75 tid Meclofenamate: 50 mg tid Mefenamic acie (Ponstrel®): 500 mg tid Naproxen/Naproxen sodium: 550/500 mg bid be careful |
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Premere™ and migraine prevention
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Premere™ for patent foramen ovale (PFO)
In patients with PFO there is a link with migraine w/aura MOA: potentially unfiltered blood may contain triggers for migraine Chemicals in blood Blood clots leakage between the atria in the heart this filters the blood many patients have PFO when they have a migraine with an aure fits between the atria |
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5-HT1B/1D receptor agonists
names |
Sumatriptan (Imitrex®)
Naratriptan (Amerge®) Zolmitriptan (Zomig®) Rizatriptan (Maxalt®) Almotriptan (Axert®) Frovatriptan (Frova®) Eletriptan Hydrobromide (Relpax®) Sumatriptan/Naproxen (Treximet®) |
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what receptors does imitrex hit
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5HT 1B/1D/1F
since it interacts with more receptors it has more SE |
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recommended use of the triptans
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Acute, moderate to severe migraine
Cluster headache: imitrex injectable has the fastest onset and pain doesn't generally last more than 3 hours so want fast acting) Menstrual migraine abortive therapy |
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MOA of the tirptans
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Neuronal inhibition, blocks depolarization of sensory afferents at the trigeminal nerve, thus blocking vasoactive peptide release and neurovascular inflammation of the meningeal and dural vasculature
Central neuronal inhibition within the trigeminal nuclei in the brainstem Zolmitriptan crosses the BBB Naratriptan and rizatriptan minimally cross the BBB Sumatriptan’s ability to cross BBB is questionable Vasoconstriction of meningeal, dural, and cerebral arteries Does not affect regional cerebral blood flow, since the small vessels controlling cerebral blood flow are not constricted |
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triptans work in what 3 areas of the migraine pathway
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1. brainstem level (CNS)
2. when the neuropeptides are released at the dura level 3. trigeminal nerve |
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the longer you wait to take a triptan the _______ they take to work
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longer
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what formulation has the quickest onset of action
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SQ
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Are doses on the exam for HA
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NO
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Sumatriptan (Imitrex®)
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Receptor site: 5-Ht1b/1d/1f
Duration of action: short Onset: PO 30-90”, SC 10”, NS 15-90” Bioavailability: PO 15%, NS 17%, SC 97% t½: PO 2 hrs, NS 2 hrs, SC 2 hrs Metabolism: MAO-A |
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1B stands for...
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blood vessel
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how does the half life of a triptan affect when the dose can be repeated (know)
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doses can be repeated if necessary
repeat dose sooner than later with a short half life triptan |
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Sumatriptan/naproxen sodium (Treximet®)
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Fixed-dose combination tablet containing sumatriptan 85 mg and naproxen sodium 500 mg
Sumatriptan - 5HT-1 agonist, with high affinity for 5HT-1B/1D subtypes of the serotonin receptor Naproxen sodium - exhibits analgesic effect by inhibiting prostaglandin synthetase. Approved for acute treatment of migraine headaches in adults. The combination of both substances contributes to the relief of migraine through pharmacologically different mechanisms of action |
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Zolmitriptan (Zomig®)
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Receptor site: 5-HT1b/1d
Dose: 2.5-5 mg at onset, MR in 2 hrs if needed (max 10 mg/d) Availability: 2.5 mg tablets, 2.5 and 5 mg ZMT (melt) – gastric absorption, 5 mg nasal spray (NS) Duration of action: short Onset: 60 minutes Bioavailability: 48% t½: 3 hrs Metabolism: P450/MAO-A |
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what does 1D stand for
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dura matter
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are the melt tablets (triptans) more or less quickly absorbed
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they do not get activated more quickly and may even have some lag time because the absorbed through the GI tract
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what flavor are the MLT
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mint
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what flavor are the ZMTs
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orange
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what is the benefit of using a melt triptan
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when a patient has N/V using a melt tablet allows them to take the tablet without wter
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Naratriptan (Amerge®)
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Receptor site: 5-HT1b/1d
Dose: 2.5 mg, MR in 4 hrs if needed (max 5 mg/d) Availability: 1 and 2.5 mg tablet Duration of action: long Onset: 1 to 3 hrs Bioavailability: 63-74% t½: 6 hrs Metabolism: P450 |
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Rizatriptan (Maxalt®)
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Receptor site: 5-HT1b/1d
Dose: 5-10 mg at onset, MR in 2 hrs if needed (max 30 mg/d, ? 40 mg/d ) Availability: 5 and 10 mg oral tablet, 5 and 10 mg oral disintegrating tablet (MLT) Duration of action: short Onset: 30-90” Bioavailability: 40% t½: 2 hrs Metabolism: MAO-A Patients taking propranolol should receive 2.5-5 mg dose initially Max 15 mg/d AUC increases by 70% MLT: Mint-flavored, orally disintegrating tablet 5 and 10 mg Gastric absorption Time to maximum concentration is slightly longer than PO: 1.6-2.5 hrs vs. 30-90” |
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Rizatriptan (Maxalt®) MOA
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MAO-A
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longest half life triptan
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frova
26 hours |
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Almotriptan (Axert®)
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Receptor site: 5-HT1b/1d
Dose: 6.25-12.5 mg, MR in 2 hrs (max 25 mg/d) Availability: 6.25 and 12.5 mg oral tablet Duration of action: short Onset: 30” to 2 hrs Bioavailability: 70 - 80% t½: 1-2 hrs Metabolism: liver CYP 3A4, 2D6, MAO May be better tolerated than other triptans |
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Frovatriptan (Frova®)
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Receptor site: 5-HT1b/1d
Dose: 2.5 mg, MR in 2 hrs if needed, (max 7.5 mg/d) Availability: 2.5 mg oral tablet Duration of action: long Onset: ~ 3 hrs Bioavailability: 29.6% t½: 26 hrs |
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Frovatriptan (Frova®) Metabolism
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Metabolism: renal, and CYP 1A2 hepatic
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marketing for Frovatriptan (Frova®)
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Marketed as an alternative for patients who require repeat dosing w/other migraine therapies; potentially menstrual migraine
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Birth control and Frova
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increase Cmax and AUC of frova so there is a potential for more SE
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Eletriptan Hydrobromide (Relpax®)
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Receptor: 5-HT 1b/1d
Dose: 20 mg or 40 mg (decide based on ID response), MR in 2 hrs if needed (max 80 mg/d) Duration of action: terminal half-life is 4 hrs Onset: 1.5 hrs Bioavailability: 50%, increased AUC 20-30% after high fat meal t½: 4 hrs |
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Eletriptan Hydrobromide (Relpax®) metabolism
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Metabolism: P450, CYP 3A4
Do not use within 72 hrs of a potent 3A4 inhibitor Propranolol increases the AUC of Eletriptan by 10-33% Should not be given to patients with severe hepatic impairment, use with caution in patients with mild to moderate impairment ( AUC by 34%) |
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triptan pk table
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Importance of Dose-Delivery Form for the triptans
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Treat each patient as an individual
Migraine-related decrease in GI-motility reduces oral absorption of medications N/V make it difficult for patients to take some formulations 70% nausea, 40% vomit Antiemetics should be considered (may also help HA) Onset is most important |
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what happens with GI and migrianes
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it slows down and therefore absorption is decrease
stasis of the gut |
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dose delivery forms and the triptans
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Self-injection
Fastest onset Inconvenient, uncomfortable, poor coordination Rectal suppository Inconvenient, uncomfortable Intranasal Unpleasant taste and rhinitis Oral/oral disintegrating tablet Gastric absorption |
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SE of the triptans
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Adverse drug reactions (as a class)
Chest pressure, heaviness Flushing/dizziness Paresthesia Drowsiness Nausea Neck pain or stiffness More serious ADRs include vasospasm, and potentially arrhythmias and myocardial infarction |
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contraindications of the triptans
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Coronary artery disease/Hypercholesterolemia
Prinzmetal’s angina/Diabetes/Hepatic disease Complicated/hemiplegic migraine (basilar migraines Breastfeeding/Pregnancy MAO-I use (sumatriptan, rizatriptan, zolmitriptan, almotriptan) within 2 weeks of discontinuation Use within 24 hours of other vasoconstrictors/ergots SSRIs: risk of Serotonin Syndrome- relative contraindication (higher risk with long acting triptans) |
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serotonin syndrome and triptains
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risk of Serotonin Syndrome- relative contraindication (higher risk with long acting triptans)
counsel patient on sypmtoms: muslce rigidity, increase in core temp, confusion, increase in BP can be life threatening |
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Early verses Late Treatment for migraines and the triptans
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75% of patients develop cutaneous allodynia in later stage of migraine
If treated within 30 min, before skin is sensitized triptans work well If wait 1 or 2 hrs to treat, and skin is hypersensitive, triptans only reduce pain For other 25% of patients tripans work without regard to when they are taken |
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triptan non-responders
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Need to treat at least 3 headache episodes
If fail 2 or 3, try different triptan Non-responder to one triptan does NOT correlate with non-response to another triptan |
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combo therapy for migraines
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IV Prochlorperazine 10 mg + IV Diphenhydramine 12.5 mg + 0.5 ml SQ NS (for blind)
NS 2.25 ml IV (placebo) + 6 mg SQ Sumatriptan Mean pain reduction at 80 minutes was statistically significant (P < 0.05) with use of combination therapy |
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abortive therapy fro migraines
isometheptene (midrin) |
Isometheptene (Midrin®): mild to moderate pain
Isometheptene 65 mg + dichloralphenazone 100 mg + APAP 325 mg 2 tablets at onset, 1 tablet ever 1 hr until relieved Max 5 per 12 hrs or 8 per day |
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abortive therapy for migraines antiemetics
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Antiemetics: mild to moderate pain; adjunct
Chlorpromazine IM or IV Metoclopramide IM, IV or PR (getting the drug to the small intestine where it is absorbed, becasue during a migraine GI function slows) Has a role in pregnancy Prochlorperazine IM, IV or PR 1st line therapy in ED or office; PR adjunct (good for pregnancy) |
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abortive therapy for migraines corticosteroids
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rescue therapy in status
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abortive therapy for migraines analgesics
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Analgesics (limit to 3 per week)
NSAIDS: mild to moderate, 1st line, rebound, N/V Cox-2 inhibitors Narcotic: limit to rescue medication, ED, rebound/depend |
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abortive therapy for migraines lidocaine
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Lidocaine 4 % solution 15 drops
Short duration of action, HA recurrence Ipsilateral (same side) nostril to HA, extend, rotate contralateral |
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abortive therapy for migraines AEDs
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drug (not covered in guidelines)
IV valproate (Depacon®): moderate-severe, ED rescue works well when cannot use another vasocontrictor not a lot of SE not sedating |
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abortive therapy for migraines narcotics
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Meperidine
50-100 mg IM/SC every 3-4 hrs PRN Butorphanol NS (Stadol®) 1mg = 1 spray in one nostril/d; MR > 4 hrs Max 3-4 sprays/d Butalbital +/- APAP 1-2 tablets every 4-6 hrs Max 4 tablets/d, up to 2 times/wk |
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ergots recommended use
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Moderate to severe migraine, including menstrual migraine
Cluster headache Intractable migraine Intractable, chronic daily headache |
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what receptors do ergots target
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2HT (1A, 1B, 1D, 2A, 2c)
causing: Nausea/Emesis/Dysphoria 1B and 1D are the anti-migraine adrenergic (alpha 1 and 2) causing: Unnecessary Vascular Effects Asthenia Dizziness D2 (which cause a lot of N/V so have to pretreat with antiemetics) |
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when a mediction targets more receptors what happens
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more SE
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MOA of ergot derivatives
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High affinity for the 5-HT1b, 5-Ht1d, 5-HT1f, 5-HT2 receptors
Affinity at alpha and beta receptors and D2 receptors Vasoconstriction via stimulation of arterial smooth muscle through 5-HT receptors Reuptake inhibition of noradrenaline at sympathetic nerve endings Reduction of vasogenic/neurogenic inflammation (via influence on serotonin receptors) |
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Vascular effects vary between ergotamine and dihydroergotamine (DHE)
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DHE have less SE and vascular effects
Arterioconstriction (chest pain): ergotamine > DHE Blood pressure: ergotamine = increased DHE = variable N/V |
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what pregnancy are ergot derivatives
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X
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ergot abortive therpay for migraines
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Ergotamine Tartrate (ET)
Ergomar® and Ergostat®: sublingual tablets Bellergal-S®, Bel-Phen-Ergot S®, Phenerbel-S® 0.6 mg with belladonna alkaloids (0.2 mg) and oral phenobarb (40 mg) Cafergot®, Ercaf®, Wigraine® 1.0 mg with oral caffeine (100 mg) 2 mg then, 1 mg every 30 min PRN; max 6 mg/d or 10 mg/wk Ergo-Caff PB® 1 mg with belladonna (0.125 mg), caffeine (100 mg), oral phenobarb (30 mg) |
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abortive therpay for migraines DHE
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Dihydroergotamine Mesylate (DHE)
IV or IM (DHE 45®) Migranal® Nasal Spray: 4 mg/ml NS with caffeine 1 spray (0.5 mg) each nostril Repeat in 15 min Total dose per attack is 2 mg |
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Ergot derivatives SE
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nasal irritation, fatigue, diarrhea, dizziness, dry mouth, N/V, taste perversion
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Ergot derivatives contraindications
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pregnancy category X
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Ergot derivatives drug interactions
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major interactions with other vasoconstrictors, “triptans”, antibiotics (erythromycin increases concentration of ergots)
don't use a triptan and a ergot derviative within 24 hours of each other without cardiac monitoring |
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new drug class for migraines
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CGRP inhibitor
Not yet approved by FDA Telcagepant (MK-0974) Abortive therapy Phase III clinical trial Studied and found just as effective as Zomig® with less side effects* May be permanently on hold due to increased liver function tests (LFTs) |
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conclusions on migraines
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Migraine is a widespread, serious health problem
Of all migraineurs with severe attacks, only 38% have been diagnosed, and most self-treat Absenteeism and diminished productivity incur a significant economic burden New treatment which is more efficacious, and well-tolerated has improved migraine therapy Choose the best medication for the person |
