Cluster headache pathophysiology

Jump to navigation Jump to search

Cluster Headache Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Classification

Differentiating Cluster Headache from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Treatment

Medical Therapy

Primary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Cluster headache pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Cluster headache pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA onCluster headache pathophysiology

CDC on Cluster headache pathophysiology

Cluster headache pathophysiology in the news

Blogs on Cluster headache pathophysiology

Directions to Hospitals Treating Cluster headache

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

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. Usually it involves three brain systems: 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

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.[1][2][3]

  • 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.[4]
  • 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. 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. 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)


Template:WikiDoc Sources