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{{Cluster headache}}
{{Cluster headache}}
{{CMG}} {{AE}} {{SME}}
{{CMG}} {{AE}} {{SAI}}, {{SME}}
 
== 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==
Cluster headaches are classified as [[vascular headache]]s. The intense pain is caused by the [[dilation]] of blood vessels which creates pressure on the [[trigeminal nerve]]. While this process is the immediate cause of the pain, the [[etiology]] (underlying cause or causes) is not fully understood.  
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>


<div align="left">
*[[Hypothalamus]]
<gallery heights="175" widths="175">
** The site of the [[circadian]] pacemaker in the [[suprachiasmatic nucleus]]
Image:Gray778.png|Trigeminal nerve is shown in yellow.
**[[Posterior]] [[hypothalamus]] activation is most commonly involved with the onset of [[cluster headache]]
Image:Gray777.png|Detailed view of ophthalmic nerve, shown in yellow.
** Alterations in hypothalamic and pituitary molecules (orexin, melatonin, and luteinizing hormone)
</gallery>
* Autonomic system
</div>
** 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


===Hypothalamus===
<br />
Among the most widely accepted theories is that cluster headaches are due to an abnormality in the [[hypothalamus]]; a British specialist of the disease, Dr. Goadsby has developed this theory. This can explain why cluster headaches frequently strike around the same time each day, and during a particular season, since one of the functions the hypothalamus performs is regulation of the [[Circadian rhythm|biological clock]]. [[Metabolic]] abnormalities have also been reported in patients. 


The hypothalamus is responsive to light&mdash;[[Circadian rhythm|daylength and photoperiod]]; [[olfactory]] stimuli, including [[pheromone]]s; [[steroid]]s, including [[sex steroids]] and [[corticosteroid]]s; neurally transmitted information arising in particular from the [[heart]], the [[stomach]], and the [[reproductive system]]; [[autonomic]] inputs; [[blood]]-borne stimuli, including [[leptin]], [[ghrelin]], [[angiotensin]], [[insulin]], [[pituitary]] [[hormone]]s, [[cytokine]]s, [[blood plasma]] concentrations of [[glucose]] and [[Osmole (unit)|osmolarity]]; [[Stress (medicine)|stress]]; ''etc''. These particular sensitivities may underlay the causes, triggers, and methods of treatment of cluster headaches.
===Genetics===


<gallery heights="150" widths="150" perrow="3" caption="Neuroimaging">
* 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>
image:PET1.jpg
* Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies.
image:PET2.jpg
image:PET3.jpg
  image:VBM1.jpg
  image:VBM2.jpg
  image:VBM3.jpg
</gallery>
''top row:'' '''Positron Emission Tomography (PET) shows brain areas being activated during pain'''


''bottom row:'' '''Voxel-based morphometry (VBM) shows brain area structural differences'''
===Triggers===
 
The following trigger factor may be involved in the pathogenesis of cluster headache:
The above [[Positron emission tomography]] pictures indicate the brain areas which are activated during pain only, compared to the pain free periods. These pictures show [[brain]] areas which are always active during pain in yellow/orange colour (called "pain matrix"). The area in the centre (in all three views) is specifically activated during cluster headache only. The bottom row [[Voxel-based morphometry]] (VBM) pictures show [[structural]] brain differences between cluster headache patients and people without headaches. Only one area is different: This area is identical with the area of CH specific pain. This area is the [[hypothalamus]].<ref>May et al.: PET and MRA findings in cluster headache and MRA in experimental pain ''Neurology'' 2000;'''55''':1328-1335, PMID 11087776.</ref><ref> Dasilva AF, Goadsby PJ, Borsook D: Cluster headache: a review of neuroimaging findings. ''Curr Pain Headache Rep.'' 2007;'''11(2)''':131-6. PMID 17367592.</ref>
* [[Nitroglycerin]] (glyceryl trinitrate)  
*Alcohol
*Nicotine dependence or smoking
* Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume)
* Decreased tolerance to heat, and becoming overheated may act as a trigger.


===Genetics===
=== Associatade Condition: ===
There is a [[genetics|genetic]] component to cluster headaches, although no single [[gene]] has been identified as the cause. 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>
Cluster headaches may also be associated with or secondary to other conditions such as:
However, genetics appears to play a much smaller role in cluster headache than in some other types of headaches.


===Triggers===
* Hypothalamic and pituitary tumors
[[Nitroglycerin]] (glyceryl trinitrate) can sometimes induce cluster headaches in sufferers in a manner similar to spontaneous attacks. Ingestion of [[Ethanol|alcohol]] is recognized as a common trigger of cluster headaches when a person is in cycle or susceptible. Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume) is also recognized as a trigger for cluster headaches. Some patients have a decreased tolerance to heat, and becoming overheated may act as a trigger. Napping causes a headache for some sufferers. The role of diet and specific foods in triggering cluster headaches is controversial and not well understood.
* Meningiomas (anywhere from the cavernous sinus to the upper cervical spine)
* Carotid artery dissections
* Vascular malformations
* Sleep apnea


==References==
==References==
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Revision as of 21:52, 25 June 2020

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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
  • 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


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 dissections
  • Vascular malformations
  • Sleep apnea

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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)


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