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Flashcards in Lec 65 Migraines Deck (37)
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Can symptoms differentiate between primary and secondary headache?

symptoms alone cannot differentiate!


What are IHS criteria for migraine without aura?

- at least 5 attacks
- attacks last 4-72 hrs
- headache with 2 of: unilateral, pulsating, moderate/severe, avoidance of physical activity
- during headache N/V and/or photophobia
- not attributed to another disorder


What are criteria for migraine with aura?

- headache same as non-aura PLUS
- aura has no motor weakness and consists of: fuly reversible visual OR sensory symptoms OR dysphasic speech
- homonymous visual symptoms OR unilateral sensory symptoms OR develops over 5 minutes


When does aura occur?

can be before, during, or without headache


are migraines unilateral or bilateral? how long does it last?

usually unilateral
lasts 4-72 hours


What is episodic vs chronic migraine?

episodic = less than 15 days per month
chronic = more than 15 days per month


What percent of migraine pts have auras?

~ 20%
- most common = visual


What is CSD?

cortical spreading depression = wave of neuronal depolarization followed by suppression neuronal activity with corresponding blood flow change moved across cortex at 3mm/min

linked to migraine course/clinical feat


What is prevalence of migraine?

43% of women, 18% of men likely associated with estrogen

-- pre-puberty = equal between sexes


What causes migraine? triggers?

migraine is hereditary polygenic

migraine has many triggers = exertion, dietary, sleep disturbances, head trauma, hormones, meidcation


What diseases have co-morbidity with migraine?

mitral valve prolapse, stroke, epilepsy, sever psychiatric


What is association vascular changes and migraine?

vascular changes occur but they are not primary cause

migraine aura associated with vasoconstriction, headache with vasodilation

researches debating the relationship


What type of blood flow before/during headache?

- aura/migraine begin during hypo-perfusion phase
- then get hyper-perfusion as headache continues
- hyper-perfusion may outlast headache apin


How can you provoke CSD?

chemical, electrical, mechanical stimuli


What is role of CSD in migraine?

plays an important role in genesis of migraine attack [but not exclusive to migraine]


Can you feel sensation of brain parenchyma?

NO! but you can feel it from dura mater/vessels, blood vessels, and CNs


What innervates intracranial contents about the tentorium cerebelli?

trigeminal nerve


What innervates intracranial contents below the tentorium cerebelli?

CN2, 3, 7, 9, 10


What are 2 common misdiagnosis of pts who have migraine

tension headache: pt with neck pain = due to referred pain by CN V

sinus headache = pt with tearing, rhinorrhea, nasal congestion cause by trigeminal-ANS reflex


What is the trigeminocervical complex?

- runs from the medulla down into C3 where blends gradually into cervical dorsal horns
receives fibers from upper cervical roots and sends them to thalamus and collateral to ANS nuclei in brainstem and hypothalamus
- thalamic neurons project to S1 and limbic
- TNS also synaptically connects to parasympathetic superior salivatory nucleus [SSN] in pons


What innervates meningeal vessels?

parasympathetic superior salivatory nucleus [SSN] in pons via greater superficial petrosal


What is important about TNC as a convergence of different sensory info?

- pain from face and head referrred to neck
- pain from neck referred to face V1 distribution


When is ipsilateral greater occipital nerve [at C2] tender? importance for treatment?

during migraine OR cluster headache

- give occipital nerve block at C2 to terminate acute headache


What happens to midbrain during migraine attack?

- periaqueductal gray in midbrain is activated


What are premonitory symptoms?

- symptoms that occur hours to day before a migraine attack [irritability, food cravings, fatigue, excess yawning, etc]

- suggest hypothalamic involvement


What is the cortical spreading depression [CSD] theory of migraines?

- wave of neuronal depolarization moves 3 mm/min through cortex accompained by transiet hyperemia then oligemia and suppression of neuronal activity
- Ca waves propagate through glia affecting vascular activity
- as wave of depolarization moves, release inflammatory factors [NO, H, K, arachadonic acid] --> activates meningeal nociceptors + trigeminal neurons release stuff --> pain, inflammation


What is the trigeminovascular reflex?

occurs with CSD

trigeminal neurons that supply dural vessels release CGRP [calcitonin gene-releated peptide], substance P and neurokinin A] --> vessel dilation and inflamation --> "peripheral sensitization" of trigeminal neuron --> carries pain centrally


What is the trigeminoparasympathetic reflex?

through polysnaptic connects with SSN, parasympathetic fibers innervating dural vessels release ACh, NO, VIP [vasoactive intestinal polypeptide] --> miosis, ptosis, red eye, lacrimation, rhinorrhea


What happens if you treat during early stage of attack when there is only peripheral sensitization?

migraine can be fully termianted


What is peripheral vs cetnral sensitization?

peripheral = activation of first order trigeminal neuron

central = activation of sexond and third order trigemino-thalamic and thalamo-cortical neruons
- glutamatergic and NO transmission involved