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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.  
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.  


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Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of cluster headache.


===Hypothalamus===
* Hypothalamus
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 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
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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.
<br />
 
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 the yellow/orange color (called "pain matrix"). The area in the center (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>


===Genetics===
===Genetics===


* 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>
* 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 receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies.
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===Triggers===
===Triggers===


* [[Nitroglycerin]] (glyceryl trinitrate) can sometimes induce cluster headaches in sufferers in a manner similar to spontaneous attacks.
* [[Nitroglycerin]] (glyceryl trinitrate)  
* Ingestion of [[Ethanol|alcohol]] is recognized as a common trigger of cluster headaches when a person is in cycle or susceptible.
*Alcohol
* Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume) is also recognized as a trigger for cluster headaches.
*Nicotine dependence or smoking
* Some patients have a decreased tolerance to heat, and becoming overheated may act as a trigger.
* Exposure to [[hydrocarbon]]s (petroleum [[solvents]], perfume)  
* Napping causes a headache for some sufferers.
* Decreased tolerance to heat, and becoming overheated may act as a trigger.
* The role of diet and specific foods in triggering cluster headaches is controversial and not well understood.


=== Associations: ===
=== Associations: ===

Revision as of 02:16, 26 May 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

Cluster headaches are classified as vascular headaches. 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.

Pathophysiology

Cluster headaches are classified as vascular headaches. 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.

Generally 3 brain systems are mostly found to be involved or associated with the pathophysiology of cluster headache.

  • 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


Genetics

  • First-degree relatives of sufferers are more likely to have the condition than the population at large.[1]
  • Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies.

Triggers

  • 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.

Associations:

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. ↑ 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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