The remainder of the evening was without incident. After the episode he denied nausea, diaphoresis or otherwise feeling sick and proceeded to eat when his entrée was served. No seizure-like activity or incontinence was witnessed. Prior to losing consciousness, he described feeling short of breath and noted that his surroundings were becoming dark. To everyone's surprise, he then fell forward resting his head on the table and remained unresponsive for a few seconds before regaining consciousness. " in decrescendo until he was out of breath. While waiting for the meals to be served, a guest had told a very amusing joke and the patient began to laugh heartily, "Ha, ha, ha, ha. He informed the physician of an incident that occurred one evening as he entertained his colleagues in a fine restaurant. He mentioned that he had recently been very busy with overtime work, which had left him exhausted. We present the case of a 56-year-old man who suffered from syncope secondary to intense laughter.Ī 56-year-old, moderately obese (body mass index of 35) man with a past medical history of sleep apnea, hypertension and hyperlipidemia presented to his primary care physician for routine health maintenance. To the best of the authors' knowledge, only five cases of laugh syncope among adults have been reported in the literature (Table (Table2). Aside from laughter-induced syncope, this mechanism is also thought to account for syncope secondary to coughing, sneezing and other Valsalva-related activities. It is hypothesized that increased ventricular contraction in response to reduced venous return stimulates the left ventricle mechanoreceptors to a degree that is able to override the baroreceptor reflex and cause an inappropriate increase in parasympathetic tone.
However, in neurally mediated syncopes, there is acute and inappropriate hypotension and bradycardia exacerbating the reduction in cerebral perfusion, resulting in a transient loss of consciousness. The resulting increase in sympathetic tone maintains blood pressure for adequate cerebral perfusion. In one of the most well-known reflex arcs, reduced cardiac output leads to decreased stimulation of carotid sinus and aortic arch baroreceptors, as well as mechanoreceptors in the left ventricle wall. Normally the body is able to compensate for these changes through cerebral vascular autoregulation and autonomic reflexes. It has also been proposed that strenuous laughter might produce isometric muscle contraction resulting in acute vascular dilatation, thereby exacerbating the reduction in venous return. The associated increase in intrathoracic pressure reduces venous return resulting in decreased cardiac output and a transient reduction in cerebral perfusion. Intense laughter causes repetitive forced expirations in a staccato pattern with a Valsalva-type effect. It is a sub-type of the situational syncopes hypothesized to be the result of a neurally mediated reflex triggered by increased intrathoracic pressure. Laughter-induced or gelastic (derived from the Greek word for laughter, 'gelos') syncope is extremely rare. Vasodilators (nitrates, calcium channel blockers, angiotensin-converting enzyme inhibitors), phenothiazines, antidepressants (tricyclic agents, monoamine oxidase inhibitors), central nervous system depressants (barbiturates), drugs associated with torsades de pointes (quinidine, procainamide, disopyramide, amiodarone, sotalol, flecainide), diuretics, digitalis, insulin, marijuana, alcohol, cocaine
Panic disorder, conversion reaction, hysteria Transient ischemic attack, subclavian steal syndrome, Takayasu disease, seizure Vasovagal, situational (micturition, laughter, tussive, defecation, postprandial, sneeze, swallow), orthostatic syncope, carotid sinus syncope Aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, aortic dissection, myocardial infarction, left atrial myxoma, cardiac tamponade, atrioventricular block, sick sinus syndrome, tachyarrhythmia, bradyarrhythmia
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