PNES can occur at any age; reported patients have ranged from 4 to 77 years (3). Three quarters are women (3).

The clinical manifestations of PNES can closely resemble those of epileptic seizures. Emergency room personnel, epilepsy monitoring unit staff, and even epilepsy experts have been fooled (12). Some motor manifestations such as pelvic thrusting or asynchronous movements have been reported to differentiate, but may not, because these can occur both with PNES and with epileptic, particularly frontal lobe seizures. Injury (21, 22, 23) and urine or fecal incontinence (21,23,24) can occur both with epileptic seizures and with PNES. Patients may be insensitive to pain testing, including standard clinical tests such as conjunctival stimulation (25). PNES patients may present in pseudoepileptic status and allow themselves to be intubated (16,26,27). PNES episodes may sometimes, but not always be longer than epileptic seizures (21,28, 29, 30). Some manifestations are more useful, however. Eyes and mouth are generally open during epileptic seizures, and often closed with PNES (31,32). Eyelids may flutter during PNES (25,30). Weeping can occur with PNES, and is unusual with epilepsy (33,34). PNES episodes do not occur during EEG-documented sleep (35,36).

The heart rate may not increase as much with PNES. A 30% increase has been suggested to differentiate between PNES and complex partial or generalized tonic-clonic seizures (37). Prolactin levels, if obtained within 15 to 30 minutes after the end of an episode, may increase severalfold with generalized tonic-clonic or complex partial seizures, and should not with PNES. However, both falsepositive and false-negative results can occur (3). Episode induction during video-EEG monitoring can be very helpful, if a clinically typical episode is induced, but should be done carefully, and while maintaining respect for the dignity of the patient (24,38).

The most useful test is an ictal video-EEG. Careful video-EEG analysis usually can determine the etiology of the episode (3). Interictal EEGs are less useful; some individuals with no history of epilepsy have true interictal epileptiform discharges (3). Also, normal variant patterns are frequently mistaken to be epileptiform discharges, so the EEG needs to be evaluated carefully, and by an experienced reader (3).

It would be interesting to know if specific conversion symptoms would be more likely to have specific etiologies, but little is known about this in the case of PNES. Broadly, psychogenic nonepileptic seizures can present with prominent motor activity or with prominent changes in affect, or both (21,39). Presumably, a patient could have a psychogenic nonepileptic seizure with purely sensory symptoms, but this is not the subject of comment in the PNES literature. Motor manifestations can vary: Shaking may be of greater amplitude in some patients, lesser amplitude in others, and still others may fall to the ground (40). One study found that patients with prominent motor components to their PNES were less likely to achieve seizure control (41). Similarly, a second study found that patients without rigidity or shaking, ictal incontinence, or tongue biting, no episodes of PNES status, and without admissions to intensive care units had better outcomes (42). However, another study reported that patients with prominent affectual components and less prominent motor components to their episodes might be more disturbed emotionally (43). Such a finding suggested that PNES episodes might be more likely to persist in these patients, although the study was not designed to assess that question. Therefore, the clinical manifestations of PNES may or may not help in determining prognosis. On the other hand, if patients who are more emotionally disturbed nonetheless subsequently are more likely to improve, interesting questions could be raised regarding the relationships among the underlying etiology of a patient’s PNES, the clinical manifestations, and the capacity of the patient for emotional improvement.

The psychological causes for PNES vary; a great many have been described in the literature (Table 12.1) (3,44, 45, 46). It is likely that the etiologies underlying other “conversion reactions” similarly vary.

First, episodes can occur due to a disturbance in the patient’s interactions with others, or in others’ interactions with the patient. These include patients with inadequate personalities, adjustment reactions, family conflicts, or who have been victims of sexual or physical abuse. It also includes circumstances in which other people have reinforced a patient’s PNES behaviors and in which patients have difficulties managing anger or hostility.

Second, episodes can be due to intrinsic emotional problems or to internalized conflicts. These etiologies include affective disorders, panic attacks, anxiety, obsessive-compulsive disorders, conversion/somatization disorders, dissociative/depersonalization disorders, and posttraumatic stress disorders. Patients may, for internal reasons, misinterpret, or overinterpret occurrences in the environment. These include patients in whom simple partial seizures may occur, but elaborate into PNES (53).

Third, patients may be psychotic or schizophrenic.

Fourth, they may have personality disorders. This group includes patients with borderline, histrionic, narcissistic, antisocial, passive-aggressive, avoidant, and passive-dependent personality. Etiologies such as malingering, factitious disorder, and substance abuse can be included in this group.

Fifth, cognitive difficulties may be present or there may be a history of head trauma (54,55). At least some studies
report an increased likelihood of MRI or EEG abnormalities in patients with PNES (49,50,56, 57, 58, 59). It also is worth pointing out that there are data demonstrating that somatization disorder may have a genetic component. Patients with PNES do not necessarily fulfill the criteria for somatization disorder. However, these findings point out that behaviors of this type can have an “organic” basis.