Dysfunction of either the brainstem or both cerebral hemispheres is necessary for loss of consciousness (LOC) to occur. Syncope, caused by global hypoperfusion of the brain due to a drop in blood pressure or cardiac output, is the most common cause of transient LOC. Seizures may also affect bilateral hemispheres of the brain leading to LOC. One of the challenges in transient LOC is that the underlying causes range from benign (e.g., vasovagal syncope) to extremely dangerous (cardiac arrhythmia). Misdiagnosis is common, particularly mistaking so-called “convulsive syncope,” in which brief myoclonic jerks occur on losing consciousness in the setting of syncope, for seizure activity. Likewise, despite the perception that it is specific for seizure, urinary incontinence occurs frequently irrespective of underlying cause. Careful evaluation and testing guided by the clinical picture is thus important. As patients are by definition unconscious during the event itself, obtaining history from bystanders, family, and first responders is a priority. In rare cases where the patient is able to recall the event, consider mimics such as cataplexy.
Prodromal symptoms preceding LOC may be recalled by the patient or may have been mentioned to witnesses on the scene prior to losing consciousness. Syncope typically has a prodrome of lightheadedness, nausea, diaphoresis, tinnitus, and visual dimming. Chest pain, palpitations, or shortness of breath suggest a cardiac cause. In the rare cases where transient LOC is due to posterior circulation transient ischemic attack (TIA), there may be vertigo or focal neurologic symptoms (e.g., dysarthria, double vision, hemiparesis, or hemisensory loss) preceding the episode. Seizures with a focal onset and secondary generalization may begin with confusion associated with some preservation of consciousness, with focal motor activity, or with an aura.
Commonly described auras are a sense of déjà vu or fear, or visual, auditory, somatic, or olfactory (typically unpleasant) sensations. Seizure onset can also be accompanied by autonomic auras difficult to distinguish from symptoms seen in syncope, such as tachycardia, pallor, diaphoresis, or nausea. Seizures often occur without aura, or the patient may not recall the aura postictally. If convulsive activity is described, one must be careful to distinguish between focal convulsions (e.g., face twitching or arm shaking) before LOC, which strongly suggests seizure, and generalized myoclonic jerks during the period the patient is unconscious, which is nonspecific and, when brief, common in syncope.
The duration of LOC and postictal confusion helps distinguish between seizure and syncope. In syncope, LOC is usually brief (seconds), with rapid recovery once the cause is removed, such as returning to a recumbent position after orthostatic syncope. Seizures may lead to more prolonged LOC as well as a longer period of postictal dysfunction, such as confusion, which may last minutes to hours.
If posterior circulation TIA is suspected, vascular imaging of the head and neck with computed tomography or magnetic resonance angiography should be performed. Absence of high-grade stenosis or occlusion makes this diagnosis extremely unlikely.
Triggers and provoking factors may suggest a specific syncope etiology such as vasovagal, situational (e.g., tussive or micturition), or orthostatic syncope. Vasovagal syncope may be triggered by stress, fear, pain, physical exertion, or prolonged standing. Prior episodes of presyncope, most typically lightheadedness or vision dimming without LOC, provoked by the same triggers should be noted. Very rarely, LOC may be triggered by standing in patients with severe vertebrobasilar or bilateral carotid stenosis.
If seizure is suspected, perform electroencephalogram (EEG) and brain magnetic resonance imaging (MRI). Epileptiform abnormalities on EEG indicate a high probability that seizure is the cause; a normal EEG, however, does not rule out epilepsy and is common in patients with seizures. Brain MRI is performed to look for an obvious seizure focus, such as tumor. If initial testing is unrevealing, EEG should be repeated, and prolonged EEG monitoring considered, both of which increase the yield for finding epileptiform abnormalities.
Cardiogenic syncope is potentially life-threatening; it usually results from either arrhythmia (acquired or from genetic causes such as long QT or Brugada syndrome) or cardiac outflow obstruction (such as aortic stenosis or hypertrophic obstructive cardiomyopathy). Ask about known cardiac disease and family history of early sudden death. Evaluation for suspected cardiac causes of syncope includes electrocardiogram, echocardiography, and potentially long-term cardiac monitoring. When cardiac syncope is suspected, consult cardiology.
Consider psychogenic events in patients with recurrent unexplained episodes of LOC. Suggestive features include recurrent events with variable presentations, prolonged periods of unresponsiveness (often longer than several minutes) with a rapid return to baseline, and eye closure, particularly if forced, throughout the episode (with epileptic seizures the eyes are usually open). Testing to rule out other causes should generally be completed before considering this diagnosis. Continuous video-EEG monitoring in an epilepsy monitoring unit can confirm a diagnosis of psychogenic nonepileptic seizures.