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Tuesday, 26 November 2013

Cluster Headache - The Risk factors and Causes

Cluster Headache
Cluster Headache also known as suicide headache, is defined as an uncommon distinctive neurovascular syndrome occurring in either episodic or chronic patterns of that occur periodically over a long period of time. The diseases affects over 0.1% of the population, occurring at 45-to 60-day intervals with one to three headaches a day lasting 45 min to 2 h(a), if untreated it, can cause increased frequency of the attacks.
Risk factors 
1. Gene
In the review of only genetic studies with limited sample sizes have been performed, but results have indicated an association with the HCRTR2 gene, which is involved in the regulation of chronobiological rhythms(c). Other suggested that cluster headache has an autosomal dominant gene with a penetrance of 0.30 to 0.34 in males and 0.17 to 0.21 in females. The gene is present in 3% to 4% of males and 7% to 10% of females with cluster headache(f)

2. Gender
Men are at higher risk than women in development of cluster headache(d)

3. Family history
In the study of California Medical Clinic For Headache, found that three generations of cluster headache were found in 7/24 kindreds (29.17%). Parental cluster headache was found in 19 of the 24 probands (79.17%); in 14/19 (73.68%), transmission was from father to proband. fifty percent of cluster probands also had migraine headaches, and almost 50% had a family history of migraine. Similarly, of the larger population of 300 cluster patients, approximately 45% had a positive family history of migraine. f 1652 relatives of all cluster patients, 3.45% had cluster headache (thirteen times the expected frequency of cluster headache in the general population) and 17.55% had migraine headaches(g)

4. Age
Cluster headache is commonly considered to be a young-male disorder, but middle-aged and elderly women may also be affected. The characteristics of the pain and its manner of occurrence were similar in our cases to those reported in the young-male population(e)

IV. Causes
1. Chronic headache
Paitent who have chronic headache may see their diseases evolved into chronic cluster headache with a milder chronic headache in-between the severe cluster headache attacks as a result of trigeminal nerve root compression(3)

2. Parasympathetic pathway
Some researchers suggested that the internal carotid artery (ICA) with proximal pial and orbital-periorbital branches, as well as external carotid vessels adjacent to the orbital region, are involved in the autonomic symptoms of an attack of cluster headache. Dilation of the intracranial ICA due to activation of this parasympathetic pathway may aggravate pain (10)

3. Post-traumatic headache (PTH) 
In the study conducted by The National Hospital for Neurology and Neurosurgery, researchers suggested that a better understanding of the association between head trauma and CH may provide important insights into both the pathophysiology of CH and the mechanisms by which traumatic head injury predisposes patients to developing headaches(11)

4. Arrhythmias
Arrhythmias is defined as a condition of of the heart rate (pulse) or heart rhythm, such as beating too fast (tachycardia), too slow (bradycardia), or irregularly

5. Sleep disorder
sleep disorders may themselves trigger headache attacks and can be symptoms of other underlying pathologies(13)

6. Serotonin
a type of neurotransmitter, passes messages between nerve cells, low serotonin levels in the brain may increase the risk of the process of constriction of the blood vessels as it alters levels of dopamine and stress hormones, and may be part of a complex cellular membrane trafficking dysfunction involving not only the serotonin transporter but also other transporters and ion channels of which trigger a migraine (14)

7. Block sodium channel
In the study of "Cluster headache with Brugada electrocardiogram pattern" conducted by University of Fukui, recommended therapies without sodium channel blocking effect were failed in a 40-year-old male with CH whose ECG shows Brugada ECG pattern, clonazepam and codein phosphate, which are exceptional treatments for CH, were effective for severe unilateral orbital pain(15)

8. Posterior hypothalamus
In a study conducted by University Hospital Central de Asturias, researchers suggested that theefficacy of DBS in very refractory CCH with a slightly modified hypothalamic target conceived to avoid the lateral ventricle wall so as to extend the stimulated brain area and to decrease the morbidity of potential haemorrhagic complications(16)

9. Histamine  
Some researchers suggested that histamine may be associated to the in the pathogenesis of cluster headache , but other study found that there are no association with histamine, in a double-blind crossover trial of a combined histamine H1 and H2 antagonist treatment(17)

10. Granulomatous pituitary
some studies suggested that the association between cluster headache and granulomatous enlargement of the pituitary gland.(30)

V. What trigger cluster headaches
1.  Smoking, alcohol consumption, and head trauma
many researchers believe that  smoking, alcohol consumption, and head trauma triger the onset of cluster headache but accoring to the study conducted by Karolinska University Hospital Huddinge, suggested that formerly described demographic relationships in CH regarding cigarette smoking, alcohol consumption, and head trauma were also seen in our CH patients and their nonaffected relatives. These findings might represent a gene environment interaction in affected CH patients or it could be personality-lifestyle-related phenomena or a combination of these mechanisms(19)
2. Other triggering factors
Beside the causes above, out of 126/179 replies, other factors triggering migraine attack include too much work (under the stress category 54/64), reflected sunlight (under the light category 35/44), too little sleep (under the sleep category 19/24), red wine (under the alcohol category 20/22), passive smoking (under the smoke category 11/11), menstruation (under the menstruation or break from the pill category 12/14) and perfume (under the fumes/heavy scents category 12/15). Hormones, light and stress were reported to cause at least 50 % of MA attacks in 62%, 47% and 42% of participants, respectively. No participants reported alcohol to be the trigger of 50% or more of their attacks. In the groups of participants with "light", "fumes/heavy scents", "smoke" or "physical effort" as triggers, nearly all patients reported that an exposure time to the trigger of less than 3 hours (90-100% of patients) was necessary to trigger an attack and a latency to onset of attack of less than 3 hours (90-100% of patients) in the study conducted by University of Copenhagen and Glostrup Hospital, Denmark J. (20)

3. Medication-overuse headache (MOH)
In the study of Ghent University Hospital, Dr. Paemeleire K and the team suggested that a personal or familial history of migraine appears to be strongly associated with the development of MOH in CH, at least with the phenotype of background headache(21)

4. Coccaine
Cluster headache usually appeared 1 to 2 hours after cocaine consumption, though it disappeared 5 to 10 minutes after again inhaling the drug(22)

5. Nitric oxide pathway
Some researchers suggested that Nitric oxide (NO) may participate in the mechanisms underlying vascular headaches, but in the study of conducted by University of Pavia, data of the study do not support the presence of a basal hyperactivity of the L-arginine-NO pathway in CH patients. Increased NO production may be of importance in the mechanisms leading to CH attacks, but other factors are likely to render CH patients hyperresponsive to NO, and ultimately to cause the occurrence of pain and associated features(26) 
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