Cluster Headache

Cluster Headache
    Synonyms : Eritroprocephalgia Bing, ciliary neuralgia/migrenous (Harris), Eitromelalgia head, Horton headache, histaminic cephalgia, petrosal neuralgia (Gardner), spenopalatin neuralgia, neuralgia Vidian and Sluders, hemicrania neuralgiformis periodically .

     Attacks of unilateral pain around the eyes, supraorbital and can spread temporal areas, the attack lasted 15-180 minutes and can be repeated. Accompanying symptoms can include conjunctival injection, lacrimation, nasal congestion, rhinorea, forehead and facial sweating, miosis, ptosis and edema eyelid area. Attacks can last for several weeks or several months. Then there was a period of remission for months or even years. There are about 10 %

The etiology of cluster headache are as follows :
     · Emphasis on the trigeminal nerve ( nerve V ) due to dilation of blood vessels around .
     · Swelling of the internal carotid artery walls .
     · The release of histamine .
     · Explosion of paroxysmal parasympathetic .
     · Abnormalities of the hypothalamus .
     · Decreased oxygen levels .
     · The influence of genetic

Suspected cluster headache trigger factors, among others :
     · Glyceryl trinitrate .
     · Alcohol .
     · Exposure to hydrocarbons .
     · Heat .
     · Too much or too less sleep .
     · Stress .

      Positron Emission tomography (PET) scanning and magnetic resonance imaging (MRI) help to clarify the causes of cluster headache are still poorly understood .

      Basic pathophysiology of the hypothalamic gray matter. In some families, an autosomal dominant gene may be involved, but the alleles sensitive calcium channel activity or nitric oxide is still not identified. Vasodilation and carotid artery ophthalmic artery and increased sensitivity to vasodilator stimuli can be triggered by trigeminal parasympathetic reflex .

       Abnormal variation in heart rate and an increase in nocturnal lipolysis during the attack and during remission strengthen the theory of autonomic function abnormalities with increased function of the parasympathetic and sympathetic function decline. The attack often begins during sleep, which involves disruption of circadian rhythms. Increased incidence of sleep apnea in patients with cluster headache showed periods of reduced oxygenation in vital tissue that can trigger an attack.

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