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35 Cards in this Set
- Front
- Back
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Recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually dev gradually over 5-20 min. and last for less than 60 min.
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migraine with aura
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Recurrent, 4-72 hr, Pain is unilateral, pulsating, intensity moderate to severe, aggravated by mvmt
Nausea, photophobia, photophonia |
migraine without aura
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Complex of neurological symptoms that occur before migraine HA
3 types of aura |
1. Visual auras are the most common
–Photopsia 2. Sensory aura is next common – smell and/or hearing abnormalities •3. Motor weakness & aphasia are least common |
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Pathophysiology of Aura:
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Cortical spreading depression: wave of neuronal and glial depolarization
Long-lasting suppression of neural activity Occur in visual cortex contralateral to visual aura Arises in primary visual cortex → spreading scintillating scotoma → starts at center of VF and propagates to periphery (10-15 min) Neural event = migraine “trigger” |
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pathophysiology of migraine headache (4 main processe)
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extracranial arterial vasodilation
extracranial neurogenic inflammation peripheral sensitization central sensitization |
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convergence theory
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trigeminal nucleus caudalis and great occipital nerve C1 and C2
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extracranial arterial vasodilation
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-vasodilation of meningeal BV activates CNV
-release of vasoactive peptides from nerve terminals -causes FURTHER dilation of blood vessels |
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extracranial neurogenic inflammation
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-more peptide release from nociceptive fibers
-increase in circulating neuropeptides → inflammatory response: vasodilation, swelling, histamine release |
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peripheral sensitization
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-CN V afferents release CGRP at peripheral nerve endings
-activation of vascular CGRP Rs or Rs on mast cells -vasodilation and neuroinflammation respectively |
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central sensitization
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-afferent stimulation of CN V1,2 from meningeal BV
-afferent stimulation continues via second order neurons from trigeminal nucleus caudalis to VPM of thalamus it is the levels of the trigeminal nucleus caudalis that central sensitization occurs -high level of activity from nociceptor afferents (primarily C fibers) -activity dependent increase in excitability from trigeminal ganglia -trigeminal nucleus caudalis is overstimulated and decreases in threshold to generate AP (dev of hyperalgesia) and allodynia -decease of inhibitory local circuits → increased release of vasoactive peptides into trigeminovascular system (feedforward mechanism) in brainstem, CN V afferents release CGRP onto 2nd order neurons CGRP facilitates pain transmission |
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Central pathways involved in pain modulation:
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-PAG receives inputs from other brain regions
-inhibitory projection to nucleus raphe magnus -serotonin projections from raphe to dorsal horn of SC |
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hypothesis of pain modulation
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Trigger factors overexcite cortical neurons
This decreases discharge rate of PAG and ultimately NRM -disinhibition of brain regions that normally gate/control/diminish pain *through direct activation of interneurons *through activation of Abeta and subsequent activation of interneurons |
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therapeutic approach to treating migraines
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Constrict BV:
5HT1b on BV Inhibit neuropeptide release: 5HT1d on CNV endings -break vasodilator cycle -promote normalization block receptor activation of TNC -5HT1d and 5HT1F receptors on TNC -interrupts pain signal transmission -could prevent development of central sensitization CGRP (calcitonin gene related peptides) antagonists |
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acute
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purpose of tx of pts with primary headache is to relieve symptoms as quickly as possible with abortive meds
-early tx prevents central sensitization and dev of hyperalgesia and allodynia •Triptans (DOC) |
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ACUTE-triptans
Sumatriptan (Imitrex) – prototype of Triptans |
5-HT1B / 1D / 1F agonists
•–Nasal, tablet, sc injection –Approximately 70% of patients report significant relief following a subcutaneous dose –Peak plasma concentration is reached within 12 minutes(SC, subcutaneously) or in 2 hrs with oral admin •PROBLEMS –Side effects are minor –Rebound headache, want gradual disuse –Side effects •Pain, stinging or burning at the injection site •Dizziness, muscle weakness, neck pain •Coronary side effects are the most significant –Coronary arteries have 5HT1B <<<<< 5HT2A Contraindications –Do not give i.v. (potential to cause coronary vasospasm) – patients with signs or symptoms of ischemic heart disease or Prinzmetal's angina –Finally, sumatriptan should not be used concurrently with ergot-containing compounds or given within 24 hr |
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acute tx for migraines
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triptans
ergotamine tartrateihydroergotamine OTC/NSAIDS/analgesics |
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CCRP antagonists
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Gepants
Olcegepant taken IV Telcagepant |
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prophylactic treatment
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taken daily to prevent occurence of headaches
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what are the prophylactic meds used for migraines?
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beta-blockers
tricyclic antidepressants calcium channel blockers anti-epileptic drugs (anti-seizure) |
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3 types of tension headaches
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infrequent
episodic chronic |
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what does a tension HA feel like?
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pain that is dull, throbbing, aching, dullness, heaviness, tightness in head scalp, beck
muscle tightness in areas mild to moderate pain intensity pain is BILATERAL and often diffuse |
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pathophysiology of tension headaches
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dysfunction of pain modulatory systems
sensitization of nociceptive pathways: spinal horn and peripheral mm convergence of nociceptor inputs in TNC: lamina I and V of SC afferent from neck and shoulder muscles myofacial afferents on TNC |
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acute tx for tension ha
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analgesics
antipyretics NSAIDs nonsedating muscle relaxants |
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prophylactic treatment
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antidepressants
fewer side effects less research support |
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cluster headaches 2 types
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episodic and chronic
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sx of cluster headaches
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Pain starts quickly, no warning; 2-15 min.
•Excruciating, deep, nonfluctuating •Occurs at night •Pain around eye & temple •Unilateral & same side •Lacrimation from the eye • Blocked nasal passage •Red eye •Sweating and pallor of the Forehead and cheek • In general, a modest bradycardia occurs during an attack •Transitory, pupillary meiosis and lid ptosis |
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dx criteria for general cluster
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severe to very severe unilateral orbital, supraorbital and temporal pain lasting 15-180 min if untreated
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episodic cluster
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Periods lasting 7 days - 1 yr separated by pain-free periods lasting 1 mo or longer
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chronic cluster
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Attack lasting for more than 1 yr w/o remission or with remissions lasting < I month
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pathophysiology of cluster HA
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1. trigeminal distribution of pain
2. ipsilateral cranial autonomic features 3. circadian pattern of attacks (regulated by suprachiasmatic nucleus of hypothalamus), serotonergically modulated |
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acute treatment for cluster headaches
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oxygen
sumatriptan ergotomain tartate |
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transitional prophylaxis for cluster HA
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corticosteroids
ergotamine tartate |
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maintenance and long-term prophylaxis for cluster HA
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FIRST-LINE MEDICATIONS
–Calcium channel blockers •Verapamil (Calan, Covera, Isoptin) –Lithium Carbonate Ergotamine and lithium •SECOND-LINE MEDICATIONS –Antiepileptic drugs (AEDs) •Topiramate (Topamax) •Divalproex sodium / sodium valproate (Depakote) •Gabapentin (Neurontin) –Melatonin |
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hypothalamic deep brain stimulation
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Therapeutic targeting with DBS of the posterior hypothalamic grey matter
•Extremely efficacious in the treatment of patients with refractory cluster headache •10-20% of patients |
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occipital nerve stimulation
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Less invasive than DBS
•After 17.5 months •Majority of patients reported greatly improved (90%) to mild improvement (20%) •Relief was observed within hrs to days Adverse effects: electrode drift and battery depletion and pain returns if device is off Safe, alternative approach |
