Linked Life Data

8701243

Source:http://linkedlifedata.com/resource/pubmed/id/8701243

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
1996-9-5
pubmed:abstractText
Cluster headache is a rare, very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Alterations of the hypothalamic-pituitary axis due to chronobiological changes, such as typical temporal pattern of both cluster periods and attacks, point to a central etiopathogenesis. Multiple local and systemic autonomic symptoms are compatible with an altered balance of the sympathetic and parasympathetic nervous system. In this connection, too, a central etiology is postulated. To evaluate the activation of the sympathetic nervous system, in 12 cluster headache patients we investigated the plasma catecholamines norepinephrine and epinephrine four times a day (7.00, 12.00, 17.00, 23.00) in the cluster period. In the cerebrospinal fluid we determined the transmitters norepinephrine, epinephrine, dopamine and the metabolites homovanillic acid (HVA), vanillymandelic acid (VMA) and 5-hydroxyindoleacetic acid (5-HIAA). Values of plasma norepinephrine in the morning (p < 0.01), in the evening (p < 0.01) and the daily mean value (223.8 = 58.3 nmol/ml) were significantly decreased in the cluster headache group in comparison to the control group (328.8 = 53.0 nmol/ml, p < 0.01). The plasma epinephrine showed no significant changes. In the CSF of cluster headache patients norepinephrine (p < 0.05), HVA (p < 0.01), and 5-HIAA (p < 0.01) were significantly decreased. Plasma norepinephrine was correlated with CSF values of HVA and 5-HIAA. The longer the duration of the disease, the lower the values of HVA and 5-HIAA in the CSF of cluster headache patients. Moreover, plasma norepinephrine showed a significant correlation with the duration, the intensity and the frequency of the attacks. The results of this study implicate decreased activity of the sympathetic nervous system with alteration of circadian rhythmicity during the cluster period. The decreased CSF transmitter values may support the hypothesis of a central etiopathogenesis of cluster headache. Moreover, plasma norepinephrine seems to be involved in triggering and continuing the attacks. The anatomical region in which this interface of sympathetic and neurogenic inflammatory processes might be located is the trigemino-vascular system.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0036-7672
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
126
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1054-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
[Reduced sympathetic nervous system activity during the cluster period of cluster-headache].
pubmed:affiliation
Abteilung Neurologie, Universität des Saarlandes, Homburg/Saar, Deutschland.
pubmed:publicationType
Journal Article, English Abstract