Reported cases of syncope caused directly by laughter are rare. The common scenario described in a few reports involved episodes of fortuitous laughter, sometimes followed by a short prodrome of lightheadedness, facial flushing, and dizziness, followed by an episode of definite syncope. There were no seizure-like movements, automatisms, or bladder or bowel incontinence. After the syncopal episodes that were seconds in length, the patients regained consciousness, and at that point were fully oriented. These episodes could recur in a similar situation with such laughter. Many of these patients subsequently underwent full syncope workups, without elucidating a primary cardiac or neurologic cause. In this review of laughter-induced syncope, we describe a patient of ours who fit these descriptions. This phenomenon is likely a subtype of benign Valsalva-related syncope, with autonomic reflex arcs coming into play that ultimately results in global cerebral hypoperfusion. Besides the Valsalva produced by a great fit of laughter, laughter itself has its own neuroendocrine and vasculature effects that may play a role.
Mechanism of laughter-induced syncope
Laughter is produced in response to a subjective humorous stimulus that activates pseudobulbar cortical and limbic circuits, by spasmodic contraction of the diaphragm and various other thoracic muscles, along with respiratory changes. This contraction of thoracic muscles produces an acute increase in intra-abdominal pressure, in effect, a Valsalva maneuver. However, it should be noted that coughing and laughter have a staccato pattern, as opposed to the continuous Valsalva in forced micturition or defecation. The increased intra-abdominal pressure that accompanies the Valsalva reduces venous return to the heart. In addition, the isometric muscular contraction in prolonged, intense laughter causes vascular dilatation for increased muscular perfusion, further reducing venous return.5 Decreases in venous return led to decreased cardiac output by the Frank-Starling principle. Decreased cardiac output activates various neural reflex arcs downstream by several mechanisms, though all intimately related.
One such mechanism is a baroceptor reflex arc. Baroceptors in the aortic arch and carotid arteries recognize the reduced cardiac output and trigger increased sympathetic tone to maintain blood pressure, and thus adequate cerebral perfusion. In addition to maintaining blood pressure, the increased sympathetic tone stimulates increased contractility of the left ventricle, which causes an additional neural reflex arc to come into play. Vigorous left ventricular contraction then activates stretch mechanoreceptors that are located in the left ventricular wall and trabeculae and conduct to vagal afferent type C fibers. Activation of these mechanoreceptors increases parasympathetic activity and decreases sympathetic activity, as occurs in the Bezold-Jarisch reflex, which is hallmarked by the triad of hypotension, bradycardia, and vasodilation. It has been hypothesized that the parasympathetic mechanoreceptor response overrides the sympathetic baroceptor response,6 causing the paradoxical bradycardia and hypotension that ultimately results in cerebral hypoperfusion and syncope.
In addition to these neural reflex-mediated effects, there may be other direct cardiovascular effects of laughter.3 The response to a humorous situation may also directly cause an acute decrease in cortisol levels,3,7 and renin and vasopressin levels, which also decreases blood pressure. Miller et al8 demonstrated an increase in measurements of brachial artery flow-mediated vasodilation in 19 of 20 healthy volunteers exposed to a humorous movie segment, with a total vasodilation increase of 22% during laughter, which they hypothesized to be mediated by local nitric oxide release. Thus, there seem to be several components, with neural reflexes and neuroendocrine effects involved in the pathway of laughter leading to syncope.3 On one additional note, laughter-induced syncope may be confused with cataplexy, which is a loss of postural tone with strong emotional stimulus and is seen in epilepsy. However, cataplexy is related to the actual emotion, whereas laughter syncope is related to the physical act of laughing.
Laughter-induced syncope is similar to other causes of vasovagal syncopes, such as cough, micturition, defecation, and Valsalva-induced syncope. There is an increase in intrathoracic pressure that causes an exaggerated response of the autonomic nervous system. Increased parasympathetic stimulation coupled with decreased sympathetic tone results in a decrease in heart rate, blood pressure, and cardiac output, which in turn causes global hypoperfusion and a transient decrease in cerebral hypoperfusion. Symptoms usually improve in a matter of seconds. Vagally mediated syncope is a benign diagnosis. Most patients have decreased symptoms over time. This may be associated with pharmacologic treatment or improved recognition of prodromal symptoms and lifestyle modifications.
Conservative treatment of vagally mediated syncope involves recognition of prodromal and maneuvers to abort attacks. Avoidance of precipitating factors, such as prolonged standing, rapid postural changes, and excessive alcohol intake, should be emphasized. Liberalization of salt and fluid intake coupled with compression stockings also decreases events. Discontinuation of vasodilators also may decrease episodes of syncope. Pharmacologic treatment of vagally mediated syncope primarily involves the initiation of beta-blockers. Their primary effect is in the reduction of myocardial contractility, which prevents the stimulation of the C fibers in the heart and the Bezold-Jarisch–type reflex that occurs. Beta-blockers also may decrease circulating catecholamines that are found in patients who develop syncope.4 Laughter-induced syncope or vagally mediated syncope is a benign disorder. Conservative therapy, including patient education, discontinuation of potentially offending medications, and treatment with beta-blockers, is the preferred initial therapeutic intervention.