Cluster headache pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[2]


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.


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 biological clock. Metabolic abnormalities have also been reported in patients.

The hypothalamus is responsive to light—daylength and photoperiod; olfactory stimuli, including pheromones; steroids, including sex steroids and corticosteroids; 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 hormones, cytokines, blood plasma concentrations of glucose and osmolarity; stress; etc. These particular sensitivities may underlay the causes, triggers, and methods of treatment of cluster headaches.

top row: Positron Emission Tomography (PET) shows brain areas being activated during pain

bottom row: Voxel-based morphometry (VBM) shows brain area structural differences

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.[1][2]


There is a 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.[3] However, genetics appears to play a much smaller role in cluster headache than in some other types of headaches.


Nitroglycerin (glyceryl trinitrate) can sometimes induce cluster headaches in sufferers in a manner similar to spontaneous attacks. Ingestion of alcohol is recognized as a common trigger of cluster headaches when a person is in cycle or susceptible. Exposure to hydrocarbons (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.


  1. May et al.: PET and MRA findings in cluster headache and MRA in experimental pain Neurology 2000;55:1328-1335, PMID 11087776.
  2. Dasilva AF, Goadsby PJ, Borsook D: Cluster headache: a review of neuroimaging findings. Curr Pain Headache Rep. 2007;11(2):131-6. PMID 17367592.
  3. 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)