Loss of consciousness following cough was first described in 1876 as “laryngeal vertigo” Since then, several hundred cases of what is now most commonly termed cough syncope have been reported, often in association with various medical conditions. Some early authors assumed this entity to be a form of epilepsy, but by the mid-20th century, general consensus reflected that post-tussive syncope was a consequence of markedly elevated intrathoracic pressures induced by coughing. A typical profile of the cough syncope patient emerging from the literature is that of a middle-aged, large-framed or overweight male with obstructive airways disease. Presumably, such an individual would be more likely to generate the extremely high intrathoracic pressures associated with cough-induced fainting. The precise mechanism of cough syncope remains a matter of debate. Theories proposed include various consequences of the marked elevation of intrathoracic pressures induced by coughing: diminished cardiac output causing decreased systemic blood pressure and, consequently, cerebral hypoperfusion; increased cerebrospinal fluid (CSF) pressure causing increased extravascular pressure around cranial vessels, resulting in diminished brain perfusion; or, a cerebral concussion-like effect from a rapid rise in CSF pressure. More recent mechanistic studies suggest a neurally mediated reflex vasodepressor-bradycardia response to cough. Since loss of consciousness is a direct and immediate result of cough, elimination of cough will eliminate the resultant syncopal episodes. Thus, the approach to the patient with cough syncope requires thorough evaluation and treatment of potential underlying causes of cough, as summarized in several recently published cough management guidelines.