Cluster Headache- Aetiology, Types, Pathogenesis And Pathophysiology

Cluster headache is a neurological disease that involves as its

most prominent feature an immense degree of pain.


Migrainous neuralgia

Histamine cephalagia

Histamine headache

Reader’s syndrome


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.

Types :

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


Substance P

Calciotonin generated peptide (Trigeminal vascular


neurogenic inflammation

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

migrainous neuralgia

 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