No single criterion will absolutely differentiate epilepsy from syncope, but taken as a group and supplemented by the EEG, these criteria usually enable one to distinguish the two conditions.
Cardiovascular structures represented in the insular cortex may give rise to seizures that produce cardiac arrhythmias, leading in turn to syncope. As a rule, seizures arising from the left insula prolong the QT interval and increase sympathetic tone, thereby lowering the threshold for ventricular arrhythmia, whereas those arising from the right insula shorten the QT interval and increase parasympathetic tone, thereby increasing the risk of vagally mediated syncope. Sympathetic storms may arise from the brain in circumstances of generalized injury (e.g., trauma, subarachnoid hemorrhage, infarction, or intracerebral hemorrhages). When severe, this sympathetic hyperactivity can cause acute left ventricular apical ballooning, known as takotsubo cardiomyopathy.
In patients who complain of recurrent faintness or syncope but do not have a spontaneous occurrence while under observation, an attempt to reproduce attacks may prove to be of great assistance in diagnosis. Here it is important to recall that normal persons can faint if made to squat and overbreathe and then to stand erect and hold their breath (especially if the Valsalva maneuver is added). Prolonged standing at attention in the heat often causes even well-conditioned soldiers to faint, as does compression of the chest and abdomen while holding one’s breath, as in the parlor trick of adolescents (“fainting lark”).
When an anxiety state is accompanied by faintness, the pattern of symptoms can often be reproduced by having the subject hyperventilate—that is, breathe rapidly and deeply for 2 to 3 min. This test may also be of therapeutic value, because the underlying anxiety tends to be lessened when the patient learns that the symptoms can be produced and alleviated at will simply by controlling breathing.
Most patients with tussive syncope cannot reproduce an attack by the Valsalva maneuver but can sometimes do so by voluntary coughing, if severe enough. Another useful procedure is to have the patient perform the Valsalva maneuver for more than 10 s (thus trapping blood behind closed valves in the veins) while the pulse and blood pressure are measured (see “Tests for Abnormalities of the Autonomic Nervous System” in Chap. 25).
In each of the aforementioned instances, the crucial point is not whether symptoms are produced but whether they reproduce the exact pattern of symptoms that occurs in the spontaneous attacks.
Other conditions in which the diagnosis is clarified by reproducing the attacks are carotid sinus hypersensitivity (massage of one or the other carotid sinus) and orthostatic hypotension (observations of pulse rate, blood pressure, and symptoms in the recumbent and standing positions or, even better, with the patient on a tilt table).
The measurement of beat-to-beat variation in heart rate is a simple but sensitive means of detecting vagal dysfunction, as described in Chap. 25 but its role in the evaluation of syncope has not been established.
Careful, continuous monitoring of the ECG in the hospital or by using a portable (Holter) recorder may determine whether an arrhythmia is responsible for the syncopal episode. A continuous cardiac loop ECG recorder (which continually records and erases cardiac rhythm) permits prolonged (a month or longer) ambulatory monitoring at reasonable cost. The diagnostic yield from loop recording is modestly greater than that from Holter monitoring (Linzer et al, 1990).
Upright tilting on a tilt table may cause, within seconds, up to 20 or 25 mm Hg drop in systolic blood pressure and 5 to 10 mm Hg in diastolic pressure in normal individuals, usually with only minor symptoms. In response, the heart rate rises 5 to 15 beats per minute.