Is neuroimaging necessary to evaluate syncope?
WHEN TO PURSUE ADDITIONAL TESTING
Routine use of additional testing is costly; tests should be ordered on the basis of their potential diagnostic and prognostic value. Additional evaluation should follow a stepwise approach and can include targeted blood work, autonomic nerve evaluation, tilt-table testing, transthoracic echocardiography, stress testing, electrocardiographic monitoring, and electrophysiologic testing.1
Syncope is rarely a manifestation of neurologic disease, yet 11% to 58% of patients with a first episode of uncomplicated syncope undergo extensive neuroimaging with magnetic resonance imaging, computed tomography, electroencephalography (EEG), and carotid ultrasonography.4 Evidence suggests that routine neurologic testing is of limited value given its low diagnostic yield and high cost.
Epilepsy is the most common neurologic cause of loss of consciousness but is estimated to account for less than 5% of patients with syncope.5 A thorough and thoughtful neurologic history and examination is often enough to distinguish between syncope, convulsive syncope, epileptic convulsions, and pseudosyncope.
In syncope, the loss of consciousness usually occurs 30 seconds to several minutes after standing. It presents with or without a prodrome (warmth, palpitations, and diaphoresis) and can be relieved with supine positioning. True loss of consciousness usually lasts less than a minute and is accompanied by loss of postural tone, with little or no fatigue in the recovery period.6
Conversely, in convulsive syncope, the prodrome can include pallor and diaphoresis. Loss of consciousness lasts about 30 seconds but is accompanied by fixed gaze, upward eye deviation, nuchal rigidity, tonic spasms, myoclonic jerks, tonic-clonic convulsions, and oral automatisms.6
Pseudosyncope is characterized by a prodrome of lightheadedness, shortness of breath, chest pain, and tingling sensations, followed by episodes of apparent loss of consciousness that last longer than several minutes and occur multiple times a day. During these episodes, patients purposefully try to avoid trauma when they lose consciousness, and almost always keep their eyes closed, in contrast to syncopal episodes, when the eyes are open and glassy.7
ROLE OF ELECTROENCEPHALOGRAPHY
If the diagnosis remains unclear after the history and neurologic examination, EEG is recommended (class IIa, ie, reasonable, can be useful) during tilt-table testing, as it can help differentiate syncope, pseudosyncope, and epilepsy.1
In an epileptic convulsion, EEG shows epileptiform discharges, whereas in syncope, it shows diffuse brainwave slowing with delta waves and a flatline pattern. In pseudosyncope and psychogenic nonepileptic seizures, EEG shows normal activity.8
Routine EEG is not recommended if there are no specific neurologic signs of epilepsy or if the history and neurologic examination indicate syncope or pseudosyncope.1
Structural brain disease does not typically present with transient global cerebral hypoperfusion resulting in syncope, so magnetic resonance imaging and computed tomography have a low diagnostic yield. Studies have revealed that for the 11% to 58% of patients who undergo neuroimaging, it establishes a diagnosis in only 0.2% to 1%.9 For this reason and in view of their high cost, these imaging tests should not be routinely ordered in the evaluation of syncope.4,10 Similarly, carotid artery imaging should not be routinely ordered if there is no focal neurologic finding suggesting unilateral ischemia.10
CASE CONTINUED
In our 40-year-old patient, the history suggests dehydration, as she recently started taking a diuretic. Thus, laboratory testing is reasonable.
Loss of bladder control is often interpreted as a red flag for neurologic disease, but syncope can often present with urinary incontinence. Urinary incontinence may also occur in epileptic seizure and in nonepileptic events such as syncope. A pooled analysis by Brigo et al11 determined that urinary incontinence had no value in distinguishing between epilepsy and syncope. Therefore, this physical finding should not incline the clinician to one diagnosis or the other.
Given our patient’s presentation, findings on physical examination, and absence of focal neurologic deficits, she should not undergo neuroimaging for syncope evaluation. The more likely cause of her syncope is orthostatic intolerance (orthostatic hypotension or vasovagal syncope) in the setting of intravascular volume depletion, likely secondary to diuretic use. Obtaining orthostatic vital signs is mandatory, and this confirms the diagnosis.
