Migraine pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 6: Line 6:


==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]].
Migraines are believed to be a neurovascular disorder<ref name=Bart10>{{cite journal |author=Bartleson JD, Cutrer FM |title=Migraine update. Diagnosis and treatment |journal=Minn Med |volume=93 |issue=5 |pages=36–41 |date=May 2010 |pmid=20572569 }}</ref> with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.<ref name=HA29>The Headaches Chp. 29, Pg. 276</ref> Some researchers feel [[neuron]]al mechanisms play a greater role,<ref>{{cite journal|last=Goadsby|first=PJ|title=The vascular theory of migraine – a great story wrecked by the facts|journal=Brain : a journal of neurology|date=January 2009|volume=132|issue=Pt 1|pages=6–7|pmid=19098031|doi=10.1093/brain/awn321}}</ref> while others feel blood vessels play the key role.<ref>{{cite journal|last=Brennan|first=KC|coauthors=Charles, A|title=An update on the blood vessel in migraine|journal=Current Opinion in Neurology|date=June 2010|volume=23|issue=3|pages=266–74|pmid=20216215|doi=10.1097/WCO.0b013e32833821c1}}</ref> Others feel both are likely important.<ref>{{cite journal|last=Dodick|first=DW|title=Examining the essence of migraine – is it the blood vessel or the brain? A debate|journal=Headache|date=April 2008|volume=48|issue=4|pages=661–7|pmid=18377395|doi=10.1111/j.1526-4610.2008.01079.x}}</ref> High levels of the neurotransmitter [[serotonin]], also known as 5-hydroxytryptamine, are believed to be involved.<ref name=HA29/>
 
===Aura===
[[Cortical spreading depression]] or spreading depression of [[Aristides Leão|Leão]] is bursts of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura.<ref name=HA28>The Headaches, Chp. 28, pp. 269–72</ref> There are a number of explanations for its occurrence including activation of [[NMDA receptor]]s leading to calcium entering the cell.<ref name=HA28/> After the burst of activity the blood flow to the [[cerebral cortex]] in the area affected is decreased for two to six hours.<ref name=HA28/> It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.<ref name=HA28/>
 
===Pain===
The exact mechanism of the head pain which occurs during a migraine is unknown.<ref name=Olesen2009>{{cite journal|last=Olesen|first=J|coauthors=Burstein, R; Ashina, M; Tfelt-Hansen, P|title=Origin of pain in migraine: evidence for peripheral sensitization|journal=Lancet neurology|date=July 2009|volume=8|issue=7|pages=679–90|pmid=19539239|doi=10.1016/S1474-4422(09)70090-0}}</ref> Some evidence supports a primary role for [[central nervous system]] structures (such as the [[brainstem]] and [[diencephalon]])<ref>{{cite journal|last=Akerman|first=S|coauthors=Holland, PR; Goadsby, PJ|title=Diencephalic and brainstem mechanisms in migraine|journal=Nature Reviews Neuroscience|date=2011-09-20|volume=12|issue=10|pages=570–84|pmid=21931334|doi=10.1038/nrn3057}}</ref> while other data support the role peripheral activation (such as via the [[sensory nerve]]s that surround [[blood vessel]]s of the head and neck).<ref name=Olesen2009/> The potential candidate vessels include [[dura mater|dural arteries]], [[Pia mater|pial arteries]] and extracranial arteries such as those of the [[scalp]].<ref name=Olesen2009/> The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.<ref>{{cite journal|last=Shevel|first=E|title=The extracranial vascular theory of migraine – a great story confirmed by the facts|journal=Headache|date=March 2011|volume=51|issue=3|pages=409–17|pmid=21352215|doi=10.1111/j.1526-4610.2011.01844.x}}</ref>


==References==
==References==

Revision as of 19:25, 7 February 2014

Migraine Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Triggers

Differentiating Migraine from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Treatment

Medical Therapy

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Migraine pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Migraine pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Migraine pathophysiology

CDC on Migraine pathophysiology

Migraine pathophysiology in the news

Blogs on Migraine pathophysiology

Directions to Hospitals Treating Migraine

Risk calculators and risk factors for Migraine pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

Migraines are believed to be a neurovascular disorder[1] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.[2] Some researchers feel neuronal mechanisms play a greater role,[3] while others feel blood vessels play the key role.[4] Others feel both are likely important.[5] High levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.[2]

Aura

Cortical spreading depression or spreading depression of Leão is bursts of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura.[6] There are a number of explanations for its occurrence including activation of NMDA receptors leading to calcium entering the cell.[6] After the burst of activity the blood flow to the cerebral cortex in the area affected is decreased for two to six hours.[6] It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.[6]

Pain

The exact mechanism of the head pain which occurs during a migraine is unknown.[7] Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon)[8] while other data support the role peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck).[7] The potential candidate vessels include dural arteries, pial arteries and extracranial arteries such as those of the scalp.[7] The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.[9]

References

  1. ↑ Bartleson JD, Cutrer FM (May 2010). "Migraine update. Diagnosis and treatment". Minn Med. 93 (5): 36–41. PMID 20572569.
  2. ↑ 2.0 2.1 The Headaches Chp. 29, Pg. 276
  3. ↑ Goadsby, PJ (January 2009). "The vascular theory of migraine – a great story wrecked by the facts". Brain : a journal of neurology. 132 (Pt 1): 6–7. doi:10.1093/brain/awn321. PMID 19098031.
  4. ↑ Brennan, KC (June 2010). "An update on the blood vessel in migraine". Current Opinion in Neurology. 23 (3): 266–74. doi:10.1097/WCO.0b013e32833821c1. PMID 20216215. Unknown parameter |coauthors= ignored (help)
  5. ↑ Dodick, DW (April 2008). "Examining the essence of migraine – is it the blood vessel or the brain? A debate". Headache. 48 (4): 661–7. doi:10.1111/j.1526-4610.2008.01079.x. PMID 18377395.
  6. ↑ 6.0 6.1 6.2 6.3 The Headaches, Chp. 28, pp. 269–72
  7. ↑ 7.0 7.1 7.2 Olesen, J (July 2009). "Origin of pain in migraine: evidence for peripheral sensitization". Lancet neurology. 8 (7): 679–90. doi:10.1016/S1474-4422(09)70090-0. PMID 19539239. Unknown parameter |coauthors= ignored (help)
  8. ↑ Akerman, S (2011-09-20). "Diencephalic and brainstem mechanisms in migraine". Nature Reviews Neuroscience. 12 (10): 570–84. doi:10.1038/nrn3057. PMID 21931334. Unknown parameter |coauthors= ignored (help)
  9. ↑ Shevel, E (March 2011). "The extracranial vascular theory of migraine – a great story confirmed by the facts". Headache. 51 (3): 409–17. doi:10.1111/j.1526-4610.2011.01844.x. PMID 21352215.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Migraine_pathophysiology&oldid=940296"