Peripheral nervous system dysfunction is well documented in Sjogrens syndrome (SS), whereas central nervous system involvement is a matter of significant controversy. On the other hand, autonomic nervous system (ANS) dysfunction is not even mentioned in extensive reviews of the disease in classic rheumatology textbooks. Despite isolated reports, attention to such involvement in the rheumatologic literature has only been noted over the last six years, following a controlled prospective study that suggested significant autonomic cardiovascular neuropathy in these patients. Since then, few studies, on relatively small numbers of Sjögrens patients, have yielded conflicting results, including two that claim no abnormality in autonomic nervous system function. A variety of factors may be blamed for these discrepancies, including bias on patient selection but mainly differences in employed methodology, i.e. conventional cardiovascular reflex tests and baroreflex sensitivity vs 24 hour heart rate variability. In any case, besides isolated case reports describing severe autonomic dysfunction, usually manifested by postural hypotension, the majority of studies that indicate the presence of ANS abnormalities in SS, have detected that only by applying objective tests and specific questionnaires. On the other hand, ANS dysfunction, implying defective innervation of exocrine glands, and the presence of muscarinic receptor antibodies have been blamed, partially at least, for the decreased secretory function of exocrine glands in this disease. More importantly, ANS dysfunction has been reported to result in increased mortality in diabetics, post myocardial infarction patients and the elderly. If such a possibility exists for patients with SS, the need for prospective, controlled and long follow up studies on large cohorts is imperative.