Headache Tx Flashcards
Note the triptans and the ergots
Describe migraines
they are unilateral for the most part and described as having a gradual onset with a cesendo pattern of severity with aggrevation with physical activity. Commonly associated with N/V, photophobia, and aura
pts often prefer to rest in quiet dark rooms
these last typically 4-72 hrs
Describe tension HAs
bilateral in nature, described as pressure or tightness that waxes and wanes and variable in their duration
Describe cluster HAs
unilteral HAs beginning around the eye or temple and described as quick onset reaching crescendo in minutes with excruciating pain lasts 0.5-3 hrs
Patients are often restless during this time and may experience eye redness, ipsilateral lacrimination, sweating, Horner syndrome, or rhinorrhea
How can non-migranous tension HAs be tx?
usually self-medicated with NSAIDs
How can non-migranous cluster HAs be tx?
Note that these are very rare and more prevealent in male smokers 25-50 yo (vasodilation casuses pain and autonomic dysfunction)
Rx: Nasal or SC triptans or ergots + “burst + taper” steroid, like prednisone
How is prophylaxis of migraine achieved?
topiramate, valproate,
propranolol, timolol, or metoprolol
What is the usual tapering up of tx for increasing severity of HA?
start with NSAIDs for mild, then add a short-acting triptan for increasing severity
What triptan is the most effective and has the fastest onset?
S.C. sumatriptan (all PO products are equally effective and Naratriptan and Frovatriptan have longer DOA but slower onset)
How do migraine arise?
The initiating event is uncertain but may be abnormal neuronal discharge set off by emotional or biochemical disturbances. This leads to localized ‘spreading depression” which causes the aura and may also lead to sensitization of central pain pathways
In migraine without aura, the primary event is excitiation (cause unknown) of nociceptive nerve terminals in the meningeal vessels, leading to a cycle of neurogenic inflammation
What NTMs are thought to be involved in the pathogenesis of migraine?
A number of triggers can lead to release of serotonin, nor, dopamine, GABA, glutamate, nitric oxide, CGRP, substance P, and estrogen and these NTMs produce a localized sterile inflammatory response leading to dilation of meningfeal blood vessels and activation of the trigeminal nucleus which collectively produce symptoms
Thus, drug tx is aimed at mitigating the action of these inflammatory mediators
The most effective migraine drugs act upon what NTM receptors?
serotonin (CGRP targeting drugs cause too many AEs)
How do NSAIDs modulate these inflammatory NTMs?
through their effects on PGs, they reduce the production of inflammatory signals that would trigger MAPK upregulation and the increased neuronal production of CGRP and substance P for release from nerve endings
Likewise, all triptans produce selective carotid vasocnstriction (via 5-HT1B receptors) and presynaptic inhibition of the trigminovascular inflammatory responses implicated in migraine (via 5-HT1D/5-HT1F receptors)
What NSAIDs are commonly used for migraine tx?
ketoprofen
Fenoprofen
Nabumetone
Ibuprofen
Naproxen
AEs of NSAIDs?
gastric irritation
additive nephrotoxicity, especially in the elderly
DDIs of NSAIDs?
they attenuate diuretics, BBs, ACEIs, vasodilators, central a2 agonists, peripheral a1 agonists, and ARBs
What are some compound NSAID preps?
Acetaminophen/butalbital/caffeine
Aspirin/butalbital/caffeine
G6PD deficiency may be improtant with chronic high doses of acetaminophen
Note that butalbital is strongly linked to analgesic overuse syndrome
How do triptans work?
serotonin agonists, particularly on 1B and 1D receptors in the CNS
Note how ergots cause peripheral vasoconstriction in moderate doses but in large doses, it paralyzes motor nerve endings of the sympathetic nervous system
AEs of ergots?
contraindicated with vasospastic predisposing conditions such as peripheral vascular or CAD, sepsis, MI, uncontrolled HTN, etc.
-teratogenic and contraindicated in lactation
How should tx of migraine in pregnancy be approached?
this is a common problem particularly in the 1st trimester and ergots are contraindicated and other tx should only be given when unavoidable
Give acetaminophen for attacks in 1st trimester,
What is allodynia?
hypersensitivity to stimuli during migraine that would otherwise not induce a rxn
Note that triptans do NOT provide relief from allodynia so need to give narcotics (debate continues about whether this is appropriate; possible option is IM ketorolac)
How should migraine prophylaxis be handled?
1st line give Amitriptyline, valproic acid, propanolol/timolol, or topiramate and if not successful after 2-3 months, adjust the dose and then change
If a change doesnt bring results, then add 2 first line agents
What is another tx option for migraine?
Boxin (botulinum toxin A)
What are the criteria for analgesic overuse syndrome?
What causes analgesic overuse syndrome?
The mechanisms may be related to the bodies’ adaptation to drug at the receptor, leading to changes in receptor density and transmitter synthesis. In either instance, cellular adaptation occurs
