REDUCED ACTIVITY OF THE SYMPATHETIC NERVO US-SYSTEM DURING THE CLUSTER PERIOD OF CLUSTER HEADACHE

Cluster headache is a rare, very severe disorder that is clinically we ll 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 syst emic autonomic symptoms are compatible with an altered balance of the sympathetic and parasympathetic nervous system. In this connection, to o, a central etiology is postulated. To evaluate the activation of the sympathetic nervous system, in 12 cluster headache patients we invest igated he plasma catecholamines norepinephrine and epinephrine four ti mes a day (7.00, 12.00, 17.00, 23.00) in the cluster period. In the ce rebrospinal fluid we determined the transmitters norepinephrine, epine phrine, dopamine and the metabolites homovanillic acid (HVA), vanillym andelic 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 significantl y 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 norep inephrine (p < 0.05), HVA (p < 0.01), and 5-HIAA (p < 0.01) were signi ficantly decreased. Plasma norepinephrine was correlated with CSF valu es of HVA and 5-HIAA. The longer the duration of the disease, the lowe r the values of HVA and 5-HIAA in the CSF of fluster headache patients , Moreover, plasma norepinephrine showed a significant correlation wit h the duration, the intensity and the frequency oi: the attacks. The r esults of this study implicate decreased activity of the sympathetic n ervous system with alteration of circadian rhythmicity during the clus ter period. The decreased CSF transmitter values may support the hypot hesis of a centra etiopathogenesis of cluster headache. Moreover, plas ma norepinephrine seems to be involved in triggering and continuing th e attacks. The anatomical region in which this interface of sympatheti c and neurogenic inflammatory processes might be located is the trigem inovascular system.