also referred to as neurocardiogenic or vasodepressor syncope, is common, and results from the activation of a reflex that produces a significant vasodilatory (vasodepressor) and/or bradycardic (cardioinhibitory) response. Typically, it occurs after prolonged standing or sitting and may be reproduced on tilttable testing. Long-term follow-up studies have shown that neurally mediated syncope carries a benign prognosis and a similar survival outcome to those patients with no history of syncope. Several different etiologies can lead to neurally mediated syncope as shown in Table 7.1. Almost all of these etiologies can be diagnosed by a carefully taken history. Classic vasovagal syncope may be considered in this group, and usually occurs in the setting of emotional or orthostatic stress, although it can also have an atypical presentation with no clear triggering events or premonitory signs. A careful history should also diagnose the etiology of several causes of situational syncope (e.g., postprandial, postmicturition, postdefecation, etc.). Syncope due to carotid sinus hypersensitivity occurs in the setting of inadvertent mechanical pressure on the carotid sinus and can
be reproduced by carotid sinus massage. Glossopharyngeal neuralgia may present with syncope associated with painful swallowing.

can cause inadequate cerebral perfusion leading to syncope upon rising from a sitting or supine to an upright position. The most common mechanism of hypotension is the loss of peripheral vascular tone due to the failure of the autonomic nervous system to maintain peripheral vascular resistance. This can occur due to a primary dysfunction of the autonomic nervous system associated with several neurodegenerative conditions (multiple systems atrophy [MSA]) or due to diseases causing secondary autonomic nervous system failure (e.g., diabetes, amyloidosis, etc.). MSA encompasses a group of sporadic progressive neurologic disorders characterized clinically by autonomic dysfunction (i.e., orthostatic hypotension, impotence, urinary retention or incontinence, etc.), parkinsonism, and ataxia in any combination. Medications, alcohol, and drug toxicity should also be considered when evaluating orthostatic hypotension. Volume depletion (e.g., dehydration, hemorrhage, Addison’s disease, etc.) may cause orthostatic syncope.

often present with syncope due to a decrease in cardiac output. This can occur in bradycardia (e.g., sinus arrest, heart block, etc.) or tachycardia (e.g., nonsustained ventricular tachycardia/fibrillation). It is relatively uncommon for supraventricular tachycardias to cause syncope in the absence of other structural heart disease or the Wolff-Parkinson-White’s syndrome (i.e., preexcited atrial fibrillation). Arrhythmic syncope may indicate a risk for sudden death and should be aggressively managed. In patients with congestive heart failure (CHF), syncope is associated with an increased risk for cardiovascular and total mortality.

can cause syncope due to the inability to produce sufficient cardiac output to match demand. Obstructive valvular heart disease and hypertrophic cardiomyopathy are common etiologies. Primary pump failure due to myocardial dysfunction can also lead to syncope; however, associated ventricular arrhythmias are a more common cause. Other less common conditions include atrial myxoma, pericardial tamponade, and acute aortic dissection.

causes of syncope are rare. These include steal syndromes, such as subclavian steal, in which cerebral blood is shunted away from the brain. Obstruction of cerebral blood flow is a rare cause of true syncope. Most carotid artery distribution transient ischemic attacks (TIAs) cause unilateral visual impairment, weakness, or loss of sensation. Posterior circulation TIAs generally manifest as diplopia, vertigo, ataxia, or “drop attacks,” but not loss of consciousness. Rare patients with TIA may have transient loss of consciousness, but isolated syncopal episodes without accompanying neurologic symptoms should generally not be ascribed to a TIA

occurs without any substantial changes in hemodynamics and is often associated with a prior significant psychologic event. Physical causes must be excluded. It and other causes are included in the differential diagnosis of transient loss of consciousness, but are usually distinguished from true syncope.

is a legitimate diagnosis made after a careful history, physical examination, and selected laboratory tests have failed to elucidate a specific etiologic factor. This diagnosis is clinically useful because it is associated with a prognosis that is considerably better than that of patients who have identifiable cardiac or neurologic causes of syncope. Although long-term follow-up studies have shown that patients with syncope and a history of cardiac or neurologic disease have increased long-term mortality, those patients with syncope of unknown causation have a distinctly better prognosis.