Pathophysiology of white fingers in workers using hand-held vibrating tools.

The pathogenic events and the localization of the primary lesion in white fingers among persons using hand-held vibrating tools are still unclarified. A "vibration disease" has been proposed to be due to damage to the limbic system and other brain structures which causes autonomic dysfunction. Current common opinion regards the pathogenesis of white fingers to be a result of longterm exposure to various physical and psychological environmental stressors, but the relative importance of one stressor or other is unknown. Observations indicating a chronic autonomic disturbance include changes in cardiac functions, excessive hearing loss in persons with VWF, and reduced toe skin temperature also in the absence of acute cold or vibration exposure. Sympathetic hyperactivity alone has long been postulated to account for vibration-induced white fingers, but damage to vaso-regulatory structures and functions in the finger skin now also seems to be involved. An abnormal level of sympathetic efferents is likely to be important for producing the symptoms in white fingers. Recent findings, however, indicate that the pathogenesis also involves changes in alpha-adrenergic receptor mechanisms as well as endothelial damage with deficient function of endothelial-derived relaxing factor. The role of vessel lumen reduction due to organic changes and an increase in whole blood viscosity remains unclarified. The understanding of the influence of confounders such as cold exposure, smoking habits and variations in individual susceptibility is also lacking. In particular, the physiological complexity of the response to cold is so great and the interaction between various vaso-regulatory mechanisms so intricate that only a multifactorial etiology and pathogenesis is likely for Raynaud's phenomenon in persons using hand-held vibrating tools. A model is suggested for the manifestation of abnormally strong vasoconstriction and white fingers as a result of a narrowing of the gap between the individual symptom threshold and the level of sympathetic activity.