Any decrease in cerebral perfusion may result in syncope. Various etiologies may include neurally mediated syncope, orthostasis, cardiac arrhythmias, or cardiac outflow obstructions.

Vasovagal faints, carotid sinus hypersensitivity, and situational faints all are examples of neurally mediated syncope, resulting from inappropriate bradycardia and hypotension. Pressure on hypersensitive carotid sinus baroreceptors increases vagal tone, causing hypotension or bradycardia, or both, thereby leading to cerebral hypoperfusion. Situational faints may occur with physical pain, receipt of frightening news, defecation, micturition, or cough; these typically occur in healthy individuals with normal blood pressure and frequently consistent triggers.

Orthostasis may also cause syncope, due to either autonomic dysfunction or decreased blood volume due to dehydration or blood loss. Autonomic dysfunction may be seen with neurodegenerative disorders, such as Shy-Drager syndrome, Parkinson disease, or postural orthostatic syndrome. Alternatively, systemic diseases such as diabetes, alcoholism, or amyloidosis may cause an autonomic neuropathy that results in orthostasis. In addition, medications that cause peripheral vasodilatation (e.g., nitroglycerin, beta blockers) may cause a relative decrease in blood volume.

Finally, cardiac disease may also contribute to syncope, through either arrhythmias or decreased cardiac output. Bradyarrhythmias, such as atrial fibrillation with slowed ventricular response, atrioventricular block, and long QTc syndrome, and tachyarrhythmias, such as supraventricular tachycardia, ventricular tachycardia, or torsades de pointes, may decrease cardiac output and thereby decrease cerebral perfusion episodically. Conversely, a more persistent decrease in cardiac output may be seen with obstructive cardiac disease, such as hypertrophic obstructive cardiomyopathy or aortic stenosis, and may also be seen with low ejection fraction from prior myocardial infarctions.

If clinical features alone do not help differentiate between syncope and seizures, an EEG and simultaneous EKG during the event may help clarify the diagnosis. Numerous EEG studies of syncope have revealed the following sequence: initial alpha depression, followed by low-voltage fast activity, generalized high-amplitude theta, and then delta slowing occurring concomitantly with the loss of consciousness. In general, a period of 10 seconds elapses before high-voltage delta waves appear. If the loss of consciousness is prolonged (>15 seconds), the EEG may demonstrate electrocerebral flattening. The patient may experience myoclonic jerks, with no corresponding epileptiform discharges (4,8). After the event, the EEG demonstrates recovery to the normal background rhythms. Conversely, epileptic loss of consciousness may reveal epileptiform discharges consistent with the seizure type, either focal or generalized.

The symptomatology of the hysterical attack has been well known since the work of Briquet (12) and Charcot (13). Briquet’s approach to this problem has proved to be a more solid foundation for modern theories than the work of Charcot, which is beset with iatrogenic artifacts.

Other concepts were essentially based on psychodynamic mechanisms such as dissociation (14) and conversion (15, 16, 17 and 18). The concept of Kretschmer with emphasis on “hyponoic” and “hypobulic” mechanisms warrants particular attention (19,20).

Hysterical seizures are associated with loss of impulse, usually in stressful situations. These attacks used to be attributed solely (and by definition) to females; this clearly has been proved to be untrue, although female adolescents and young adults are most often affected.

The term pseudoseizures denotes a conglomeration of non-cerebral or nonepileptic attacks. It was introduced by Liske and Forster, who were aware of the fact that many, but not all, of the patients had psychogenic (hysterical) attacks (21). Unfortunately, this term is not conducive to a differentiation of the nonepileptic attacks with certain distinctive features.

The term pseudoseizures has been more or less equated with psychogenic attacks. This may have been the result of a search for a euphemistic term since older terms such as hysterical or psychogenic attacks have been thought to have a derogatory connotation. Interestingly, the term pseudoseizures has been fading since 1990, while the term psychogenic seizures once again is being used more frequently.

By definition, nonepileptic seizures (NES) connote paroxysmal events that behaviorally or symptomatically mimic epileptic seizures but are not associated with concomitant epileptiform activity on EEG. Presumably, these events are secondary to a psychologic mechanism, with conversion disorder often being cited. The incidence of NES is variable and estimated between 0.91 and 3.03/100,000 in the general population (22,23). Correct diagnosis is often delayed in these patients, leading to increased risk for iatrogenic complications of anticonvulsant use, delayed referral to psychiatric treatment, and potential exposure to unnecessary emergency therapies, including intubation and CNS-suppressant medications. Furthermore, earlier diagnosis of NES is associated with improved outcomes and better NES event control. Nonetheless, the differentiation between these entities is often difficult based on historical features alone and is best diagnosed with video-EEG monitoring. Complicating the discrimination between NES and epileptic seizures is their common co-occurrence.

Numerous researchers have attempted to find a diagnostic test that may easily differentiate between NES and epileptic seizures. Excellent reviews by Cragar and colleagues, as well as by Reuber, provide a summary of differentiating features based on demographic variables, medical history, and seizure semiology (24,25). Of note, patients with NES are more likely to be women, and have a prior history of psychiatric treatment and a prior history of abuse or sexual abuse; however, men with NES frequently have a history of work-related problems or posttraumatic stress disorder. NES patients are typically older at the onset of the events and had been treated with fewer anticonvulsants than patients with epilepsy. With regard to seizure semiology, NES patients had greater variability in behaviors during the events, greater frequency of pelvic thrusting and eye closure during the event. Reuber also cited commonly held beliefs that NES events often manifest with gradual onset, excessive limb movements, often asynchronous and asymmetric, with possible opisthotonus, side-to-side head shaking, crying, resistance to eye opening, preservation of pupillary light responses, and purposeful movements (25). Interestingly, there were no significant differences between patients with NES or epileptic seizures with regards to age, years of education, seizure frequency, or family history of epilepsy or psychiatric disorders. Similarly, there were no significant differences between these groups regarding presence of urinary incontinence or tongue biting during the ictus. Epileptic seizures were typically of shorter duration, more commonly associated with injuries during the event, more frequently occurred during sleep, and were associated with postictal confusion.

More recent studies have similarly looked for historical and event behaviors that may predict whether the events represent NES or epileptic seizures. Benbadis established that patients evaluated in an epilepsy clinic for refractory seizures were more likely to exhibit NES if they had a history of fibromyalgia or chronic pain or had experienced a typical event in the waiting or examining room (26). Opherk and Hirsch found that during staring spells, patients with NES had no change in heart rate, while patients with complex partial seizures had a marked tachycardia; a similar pattern was seen comparing generalized tonic-clonic seizures with nonepileptic convulsive seizures (27). Oliva and colleagues noted a low sensitivity (8%) but high specificity (100%) for epileptic seizures when both oral lacerations and urinary incontinence were observed during inpatient video-EEG monitoring compared to their occurrence in NES events (28). Postictally, whispering responses, partial motor responses to commands, and shallow, irregular, rapid breathing are more commonly seen with NES events (29,30). For a summary of these features, see Table 31-2.