Cluster headache is a neurological disease that involves as its
most prominent feature an immense degree of pain.
Cluster headache can affect people of any age but are most
common between adolescence and middle age.
Onset is generally between the age of 20 – 50.
No specific cause has been found for the disorder.
Some people who experience Cluster headache are heavy
Alcohol provokes attacks in about 70% of patients certain foods,
Emotional factors (Stress), Tobacco chewing precipiate the pain.
Men are affected seven to eight times more than women.
Hereditary factors are usually absent.
1) Episode cluster Headache.
2) Chronic Cluster Headache.
Episode Cluster Headache
Episode cluster Headache is characterised by cluster periods of
7 days to 1 year with periods of remission of more than 14 days upto
months or years and occasional minibouts.
Chronic Cluster Headache
Chronic cluster headache is characterised by absence of
remission for year or short remission of less than 14 days, increased
frequently of attacks, and relative resistance to pharmacotherapy.
Patho Physiology of Cluster Headache
Although a unifying pathophysiology explained of cluster
headache is not yet available.
Any attempt to understand this syndrome must taken into
account the three cardinal feature of the disorder – pain – periodicity
– autonomic features.
To recognize the significance a basic under standing of the
neurovascular anatomy is essential. Cephalic pain is relayed to the
central nervous system through nociceptive ophthalmic branches of
the trigeminal nerves which innervates pain – sensitive intracranial
structural such as duramater and dural blood vessels.
When the trigemenial nerves, fibers activated
Calciotonin generated peptide (Trigeminal vascular
Dilation of dural blood vessels.
Activation of the trigeminal vascular system in cluster headache
has been corroborated by evidence demonstrating markely elevated
blood level of CGRP in the external jugular vein.
A number of observation have indicated vasodilation of the
opthalomic artery during cluster headache attack. These include
tonometry, corneal indentation, pulse amplitude studies and the
thermography showing focul hyperthermia. Doppler studies
showing decreased velocities.
Hypothalamus may be the site of activation in this disorder.
The posterior hypothalamus contains cells that regulate
autonomic functions, and the anterior hypothalamus contains
cells that constitute the principal circadian pacemaker in
Activation of both is necessary to explain the symptoms of
No consistant blood flow changes accompany attacks of pain.
There is little genetic predisposition.
It can be concluded tentatively that both migraine and cluster
headache result from abnormal Serotonergic