Migraine pathophysiology: Difference between revisions
No edit summary |
|||
| Line 2: | Line 2: | ||
{{Migraine}} | {{Migraine}} | ||
{{CMG}} | {{CMG}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
Migraine was once thought to be initiated by problems with [[blood vessels]]. This theory is now largely discredited.<ref name="CohenNeuroimaging">{{cite journal | author=Cohen AS, Goadsby PJ| title=Functional neuroimaging of primary headache disorders | journal=Curr Pain Headache Rep | year=2005 | pages=141-146 | volume=45 | issue=9 }}</ref> Current thinking is that a phenomenon known as [[cortical spreading depression]] is responsible for the disorder.<ref name="LauritzenM">{{cite journal | author=Lauritzen M. | title=Pathophysiology of the migraine aura. The spreading depression theory. | journal=Brain | year=1994 | pages=199-210 | volume=117 | issue=1 | id=PMID 7908596}}</ref> In [[cortical spreading depression]], [[neuron|neurological activity]] is depressed over an area of the [[cerebral cortex|cortex]] of the brain. This situation results in the release of [[inflammation|inflammatory]] mediators leading to irritation of [[cranial nerve]] roots, most particularly the [[trigeminal nerve]], which conveys the sensory information for the face and much of the head.This view is supported by [[neuroimaging]] techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.In 2005, research<ref name="PFOSchwerzmann">{{cite journal | author=Schwerzmann M, Wiher S, Nedeltchev K, Mattle HP, Wahl A, Seiler C, Meier B, Windecker S | title=Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks | journal=Neurology | year=2004 | pages=1399-401 | volume=62 | issue=8 | id=PMID 15111681}}</ref> was published indicating that in some people with a [[patent foramen ovale]] (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines reduce in frequency if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.Migraine headaches can be a symptom of [[Hypothyroidism]]. | Migraine was once thought to be initiated by problems with [[blood vessels]]. This theory is now largely discredited.<ref name="CohenNeuroimaging">{{cite journal | author=Cohen AS, Goadsby PJ| title=Functional neuroimaging of primary headache disorders | journal=Curr Pain Headache Rep | year=2005 | pages=141-146 | volume=45 | issue=9 }}</ref> Current thinking is that a phenomenon known as [[cortical spreading depression]] is responsible for the disorder.<ref name="LauritzenM">{{cite journal | author=Lauritzen M. | title=Pathophysiology of the migraine aura. The spreading depression theory. | journal=Brain | year=1994 | pages=199-210 | volume=117 | issue=1 | id=PMID 7908596}}</ref> In [[cortical spreading depression]], [[neuron|neurological activity]] is depressed over an area of the [[cerebral cortex|cortex]] of the brain. This situation results in the release of [[inflammation|inflammatory]] mediators leading to irritation of [[cranial nerve]] roots, most particularly the [[trigeminal nerve]], which conveys the sensory information for the face and much of the head.This view is supported by [[neuroimaging]] techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.In 2005, research<ref name="PFOSchwerzmann">{{cite journal | author=Schwerzmann M, Wiher S, Nedeltchev K, Mattle HP, Wahl A, Seiler C, Meier B, Windecker S | title=Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks | journal=Neurology | year=2004 | pages=1399-401 | volume=62 | issue=8 | id=PMID 15111681}}</ref> was published indicating that in some people with a [[patent foramen ovale]] (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines reduce in frequency if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.Migraine headaches can be a symptom of [[Hypothyroidism]]. | ||
Revision as of 15:51, 19 February 2013
|
Migraine Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Migraine pathophysiology On the Web |
|
American Roentgen Ray Society Images of Migraine pathophysiology |
|
Risk calculators and risk factors for Migraine pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Migraine was once thought to be initiated by problems with blood vessels. This theory is now largely discredited.[1] Current thinking is that a phenomenon known as cortical spreading depression is responsible for the disorder.[2] In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.In 2005, research[3] was published indicating that in some people with a patent foramen ovale (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines reduce in frequency if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.Migraine headaches can be a symptom of Hypothyroidism.
References
- ↑ Cohen AS, Goadsby PJ (2005). "Functional neuroimaging of primary headache disorders". Curr Pain Headache Rep. 45 (9): 141–146.
- ↑ Lauritzen M. (1994). "Pathophysiology of the migraine aura. The spreading depression theory". Brain. 117 (1): 199–210. PMID 7908596.
- ↑ Schwerzmann M, Wiher S, Nedeltchev K, Mattle HP, Wahl A, Seiler C, Meier B, Windecker S (2004). "Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks". Neurology. 62 (8): 1399–401. PMID 15111681.