Cluster headache pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| (12 intermediate revisions by 3 users not shown) | |||
| Line 3: | Line 3: | ||
{{CMG}} {{AE}} {{SAI}}, {{SME}} | {{CMG}} {{AE}} {{SAI}}, {{SME}} | ||
== Overview == | ==Overview== | ||
The clear pathogenesis of [[cluster headache]] is still unknown. Various thought processes and pathophysiologic mechanism are considered to be involved in the pathogenesis. Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of [[cluster headache]]. Three brain systems are thought to be involved: [[hypothalamus]], [[Autonomic nervous system|autonomic]] system and [[trigeminal nucleus]]. [[Orexin receptor|Orexin]]/hypocretin receptor 2 (HCRTR2) [[gene]] mutations are found to be particularly associated with [[cluster headaches]] in a couple of separate independent studies. [[Cluster headaches]] may also be associated with or secondary to other conditions such as: [[Hypothalamic]] and [[pituitary tumors]], [[meningiomas]] (anywhere from the [[cavernous sinus]] to the upper [[cervical spine]]), [[Carotid artery dissection|carotid artery]] dissections, [[vascular malformations]] and [[sleep apnea]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
The clear pathogenesis of [[cluster headache]] is still unknown. Various thought processes and pathophysiologic mechanism are considered to be involved in the pathogenesis. Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of [[cluster headache]].<ref name="pmid25492975">{{cite journal |vauthors=Barloese M, Jennum P, Lund N, Knudsen S, Gammeltoft S, Jensen R |title=Reduced CSF hypocretin-1 levels are associated with cluster headache |journal=Cephalalgia |volume=35 |issue=10 |pages=869–76 |date=September 2015 |pmid=25492975 |doi=10.1177/0333102414562971 |url=}}</ref><ref name="pmid3620514">{{cite journal |vauthors=Kauppinen RA, Sihra TS, Nicholls DG |title=Aminooxyacetic acid inhibits the malate-aspartate shuttle in isolated nerve terminals and prevents the mitochondria from utilizing glycolytic substrates |journal=Biochim. Biophys. Acta |volume=930 |issue=2 |pages=173–8 |date=September 1987 |pmid=3620514 |doi=10.1016/0167-4889(87)90029-2 |url=}}</ref><ref name="pmid2663174">{{cite journal |vauthors=Murialdo G, Fanciullacci M, Nicolodi M, Filippi U, De Palma D, Sicuteri F, Polleri A |title=Cluster headache in the male: sex steroid pattern and gonadotropic response to luteinizing hormone releasing hormone |journal=Cephalalgia |volume=9 |issue=2 |pages=91–8 |date=June 1989 |pmid=2663174 |doi=10.1046/j.1468-2982.1989.0902091.x |url=}}</ref><ref name="pmid28128461">{{cite journal |vauthors=Láinez MJ, Guillamón E |title=Cluster headache and other TACs: Pathophysiology and neurostimulation options |journal=Headache |volume=57 |issue=2 |pages=327–335 |date=February 2017 |pmid=28128461 |doi=10.1111/head.12874 |url=}}</ref<nowiki><ref name="pmid21864072"></nowiki>{{cite journal |vauthors=Holle D, Obermann M |title=Cluster headache and the hypothalamus: causal relationship or epiphenomenon? |journal=Expert Rev Neurother |volume=11 |issue=9 |pages=1255–63 |date=September 2011 |pmid=21864072 |doi=10.1586/ern.11.115 |url=}}</ref><ref name="pmid15549574">{{cite journal |vauthors=Bussone G, Usai S |title=Trigeminal autonomic cephalalgias: from pathophysiology to clinical aspects |journal=Neurol. Sci. |volume=25 Suppl 3 |issue= |pages=S74–6 |date=October 2004 |pmid=15549574 |doi=10.1007/s10072-004-0257-9 |url=}}</ref><ref name="pmid29493566">{{cite journal |vauthors=May A, Schwedt TJ, Magis D, Pozo-Rosich P, Evers S, Wang SJ |title=Cluster headache |journal=Nat Rev Dis Primers |volume=4 |issue= |pages=18006 |date=March 2018 |pmid=29493566 |doi=10.1038/nrdp.2018.6 |url=}}</ref> | |||
*[[Hypothalamus]] | |||
**The site of the [[circadian]] pacemaker in the [[suprachiasmatic nucleus]] | |||
**[[Posterior]] [[hypothalamus]] activation is most commonly involved with the onset of [[cluster headache]] | |||
* Hypothalamus | **Alterations in [[hypothalamic]] and [[pituitary]] molecules (orexin, melatonin, and luteinizing hormone) | ||
** The site of the circadian pacemaker in the suprachiasmatic nucleus | *[[Autonomic nervous system|Autonomic]] system | ||
** Posterior hypothalamus activation is most commonly involved with the onset of cluster headache | **The [[Superior salivary nucleus|superior salivatory nucleus]] and the sphenopalatine ganglion, which includes molecules such as vasoactive intestinal peptide (VIP) | ||
** Alterations in hypothalamic and pituitary molecules (orexin, melatonin, and luteinizing hormone) | **Depending upon the setting, stimulation of [[ganglion]] may stimulate or abort an episode of [[cluster headache]] | ||
* Autonomic system | *[[Trigeminal nucleus]] | ||
** The superior salivatory nucleus and the sphenopalatine ganglion, which includes molecules such as vasoactive intestinal peptide (VIP) | **Trigeminovascular system | ||
** Depending upon the setting, stimulation of ganglion may stimulate or abort an episode of cluster headache | ***[[Trigeminal nucleus]] plus Large cranial blood vessels and [[meninges]] | ||
* Trigeminal nucleus | **The Trigeminocervical complex | ||
** Trigeminovascular system | ***[[Trigeminal nucleus]] plus upper [[cervical]] dorsal horns | ||
*** Trigeminal nucleus plus Large cranial blood vessels and meninges | **[[Trigeminal nucleus]] is usually associated with the pain component of [[cluster headaches]] | ||
** The Trigeminocervical complex | **This system includes molecules such as [[calcitonin gene-related peptide]], [[pituitary]] [[adenylate cyclase]]-activating peptide | ||
*** Trigeminal nucleus plus upper cervical dorsal horns | |||
** Trigeminal nucleus is usually associated with the pain component of cluster headaches | |||
** This system includes molecules such as calcitonin gene-related peptide, pituitary adenylate cyclase-activating peptide | |||
<br /> | <br /> | ||
| Line 32: | Line 28: | ||
===Genetics=== | ===Genetics=== | ||
* First-degree relatives of sufferers are more likely to have the condition than the population at large.<ref>{{cite journal | author = Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S | title = Genetics of cluster headache: an update. | journal = J Headache Pain | volume = 6 | issue = 4 | pages = 234-6 | year = 2005 | month = September 2005 | id = PMID 16362673}} </ref> | *First-degree relatives of sufferers are more likely to have the condition than the population at large.<ref>{{cite journal | author = Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S | title = Genetics of cluster headache: an update. | journal = J Headache Pain | volume = 6 | issue = 4 | pages = 234-6 | year = 2005 | month = September 2005 | id = PMID 16362673}} </ref> | ||
* Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies. | *[[Orexin]]/[[Hypocretin (orexin) receptor 2|hypocretin]] receptor 2 (HCRTR2) gene mutations are found to be particularly associated with [[cluster headaches]] in a couple of separate independent studies. | ||
===Triggers=== | ===Triggers=== | ||
The following trigger factor may be involved in the pathogenesis of cluster headache: | |||
* [[Nitroglycerin]] (glyceryl trinitrate) | *[[Nitroglycerin]] (glyceryl trinitrate) | ||
*Alcohol | *Alcohol | ||
*Nicotine dependence or smoking | *Nicotine dependence or smoking | ||
* Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume) | *Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume) | ||
* Decreased tolerance to heat, and becoming overheated may act as a trigger. | *Decreased tolerance to heat, and becoming overheated may act as a trigger. | ||
=== | ===Associatade Condition:=== | ||
Cluster headaches may also be associated with or secondary to other conditions such as: | Cluster headaches may also be associated with or secondary to other conditions such as: | ||
* Hypothalamic and pituitary tumors | *[[Hypothalamic]] and [[pituitary tumors]] | ||
* Meningiomas (anywhere from the cavernous sinus to the upper cervical spine) | *[[Meningiomas]] (anywhere from the [[cavernous sinus]] to the upper [[cervical spine]]) | ||
* Carotid artery | *[[Carotid artery dissection|Carotid artery]] dissection | ||
* Vascular malformations | *[[Vascular malformations]] | ||
* Sleep apnea | *[[Sleep apnea]] | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WikiDoc Help Menu}} | |||
{{WikiDoc Sources}} | |||
[[Category:Ailments of unknown etiology]] | [[Category:Ailments of unknown etiology]] | ||
[[Category:Headaches]] | [[Category:Headaches]] | ||
| Line 61: | Line 60: | ||
[[Category:Diseases]] | [[Category:Diseases]] | ||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
Latest revision as of 07:47, 30 August 2020
|
Cluster Headache Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cluster headache pathophysiology On the Web |
|
American Roentgen Ray Society Images of Cluster headache pathophysiology |
|
Risk calculators and risk factors for Cluster headache pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2], Saumya Easaw, M.B.B.S.[3]
Overview
The clear pathogenesis of cluster headache is still unknown. Various thought processes and pathophysiologic mechanism are considered to be involved in the pathogenesis. Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of cluster headache. Three brain systems are thought to be involved: hypothalamus, autonomic system and trigeminal nucleus. Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies. Cluster headaches may also be associated with or secondary to other conditions such as: Hypothalamic and pituitary tumors, meningiomas (anywhere from the cavernous sinus to the upper cervical spine), carotid artery dissections, vascular malformations and sleep apnea.
Pathophysiology
The clear pathogenesis of cluster headache is still unknown. Various thought processes and pathophysiologic mechanism are considered to be involved in the pathogenesis. Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of cluster headache.[1][2][3][4][5][6]
- Hypothalamus
- The site of the circadian pacemaker in the suprachiasmatic nucleus
- Posterior hypothalamus activation is most commonly involved with the onset of cluster headache
- Alterations in hypothalamic and pituitary molecules (orexin, melatonin, and luteinizing hormone)
- Autonomic system
- The superior salivatory nucleus and the sphenopalatine ganglion, which includes molecules such as vasoactive intestinal peptide (VIP)
- Depending upon the setting, stimulation of ganglion may stimulate or abort an episode of cluster headache
- Trigeminal nucleus
- Trigeminovascular system
- Trigeminal nucleus plus Large cranial blood vessels and meninges
- The Trigeminocervical complex
- Trigeminal nucleus plus upper cervical dorsal horns
- Trigeminal nucleus is usually associated with the pain component of cluster headaches
- This system includes molecules such as calcitonin gene-related peptide, pituitary adenylate cyclase-activating peptide
- Trigeminovascular system
Genetics
- First-degree relatives of sufferers are more likely to have the condition than the population at large.[7]
- Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies.
Triggers
The following trigger factor may be involved in the pathogenesis of cluster headache:
- Nitroglycerin (glyceryl trinitrate)
- Alcohol
- Nicotine dependence or smoking
- Exposure to hydrocarbons (petroleum solvents, perfume)
- Decreased tolerance to heat, and becoming overheated may act as a trigger.
Associatade Condition:
Cluster headaches may also be associated with or secondary to other conditions such as:
- Hypothalamic and pituitary tumors
- Meningiomas (anywhere from the cavernous sinus to the upper cervical spine)
- Carotid artery dissection
- Vascular malformations
- Sleep apnea
References
- ↑ Barloese M, Jennum P, Lund N, Knudsen S, Gammeltoft S, Jensen R (September 2015). "Reduced CSF hypocretin-1 levels are associated with cluster headache". Cephalalgia. 35 (10): 869–76. doi:10.1177/0333102414562971. PMID 25492975.
- ↑ Kauppinen RA, Sihra TS, Nicholls DG (September 1987). "Aminooxyacetic acid inhibits the malate-aspartate shuttle in isolated nerve terminals and prevents the mitochondria from utilizing glycolytic substrates". Biochim. Biophys. Acta. 930 (2): 173–8. doi:10.1016/0167-4889(87)90029-2. PMID 3620514.
- ↑ Murialdo G, Fanciullacci M, Nicolodi M, Filippi U, De Palma D, Sicuteri F, Polleri A (June 1989). "Cluster headache in the male: sex steroid pattern and gonadotropic response to luteinizing hormone releasing hormone". Cephalalgia. 9 (2): 91–8. doi:10.1046/j.1468-2982.1989.0902091.x. PMID 2663174.
- ↑ Láinez MJ, Guillamón E (February 2017). "Cluster headache and other TACs: Pathophysiology and neurostimulation options". Headache. 57 (2): 327–335. doi:10.1111/head.12874. PMID 28128461.</ref<ref name="pmid21864072">Holle D, Obermann M (September 2011). "Cluster headache and the hypothalamus: causal relationship or epiphenomenon?". Expert Rev Neurother. 11 (9): 1255–63. doi:10.1586/ern.11.115. PMID 21864072.
- ↑ Bussone G, Usai S (October 2004). "Trigeminal autonomic cephalalgias: from pathophysiology to clinical aspects". Neurol. Sci. 25 Suppl 3: S74–6. doi:10.1007/s10072-004-0257-9. PMID 15549574.
- ↑ May A, Schwedt TJ, Magis D, Pozo-Rosich P, Evers S, Wang SJ (March 2018). "Cluster headache". Nat Rev Dis Primers. 4: 18006. doi:10.1038/nrdp.2018.6. PMID 29493566.
- ↑ Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S (2005). "Genetics of cluster headache: an update". J Headache Pain. 6 (4): 234–6. PMID 16362673. Unknown parameter
|month=ignored (help)