Migraine

what are the steps to treating migraine?

1. First of line drugs are NSAIDS 2. If it does respond to NSAIDS, you move on to triptans or ergo alkaloids 3. Depending on the degree of nausea, might need nonoral route and you also need to address the nausea vomiting symptoms. 4. see if you have use preventive therapy to help them. 5. first line prophylaxis treatment are timolol, propanol, amitriptlin, vaproate, topiramatate, and gabapentin. 6. engage them in formulating a management plan.

What are environmental factors and physiological factors??

glare from light, time zone shift, high altitude, barometric pressure changes. stress and fatigue, excitement and insomia, exposure to cold or heat, menstrual cycle.

What's menstrual headache?

in relation to the menstrual cycle, more severe, persists longer, and more resistant to therapy

Difference between migraine headache and tension headache?

migraine is unilateral, throbbing, worsening pain with routine activity. Moderate to severe intensity. At least has *nausea/vomiting or photophobic and phonophobia*. On the other hand, tension headache is bilateral usually, pressing, tightening, or nonpulsable. Does *NOT HAVE* nausea or vomiting and photophobia/phonophobia at the same time.

what's cluster headache?

5 attacks, with the frequency of 5-8 attacks on the same day.

what NT is the key mediator of the pathogenesis of migraine?

5-HT

Causes of migraines?

CSD from a focal point of vasoconstriction followed by vasodilation. Events eventually lead to the release of endogenous substances that cause inflammation, making trigeminal nerve fibers more sensitive to pain. Neuronal and vascular theory.

What are the genes involved in migraine?

FHM1, FHM2, FHM3, result from channelpathies.

what are the chemical triggers of migraine?

MSG, nitrates/nitrites, oral contraceptive use, smoking, and phenylethalmine.

Difference between seizure and migraines?

both by neocortical cellular excitability, but in migraine transition to CSD (cortical spreading depression) vs. hypersynchronous activity. Both can be caused by channelopathis, and be triggered by photic stimulation. Some antiepileptics can be used for migraine.

what beings the migraine attacks?

cortical spreading depression and vasoconstriction/dilation both result in headache, sympathetic activation, and triggering central sensoory symptoms and peripheral autonomic symptoms.

what's CSD?

cortical spreading depression is the slow spread of depolarization of cortical neurons with large efflux of K+, which trigger in migraine symptoms.

what are the typical manifestations of migraine?

debilitating throbbing pain around the eyes and temples lasting for hours, nausea , and heightened sensitivity to light or sound. Some experience aura.

What are the two types of migraines?

migraine with aura (20%) always associated with a prodrome (aura) and is unilateral. Also called classic, premonitory aura may begin as long as 24H before the onset of pain, and often accompanied by photophobia, phonophobia, polyuria, and diarrhea, and disturbances of mood and appetite. Migraine without aura (80%) not preceded by prodrome and is unilateral. array of vague symptoms, mental fuzziness, mood changes, and fatgue. Variable.

what are the dietary trigger of migraine?

tyramine, chocolate, and alcohol