This case demonstrated to me the difficulties in distinguishing non-epileptic seizures with prolonged focal motor activity from EPC, as well as the potential hazards of misdiagnosis.
Several features helped distinguish this case from true EPC. The appearance of the movements suggested a potential psychogenic origin. Movements varied between episodes, on one occasion with flexion-extension movements at the metacarpophalangeal joints and at other times with flexion-extension movements at the wrist.
A psychogenic mechanism was further supported by the transient abolition of movements when the face or contralateral extremity was engaged in an effortful task. This probably occurred because of the patient's inability to co-ordinate simultaneous movements on a functional basis. A similar finding has emerged in studies of posthypnotic suggestion. Task interference occurs when subjects receive a posthypnotic suggestion to search for one number and are asked to search for another number in a series of digits.10 Thus, although posthypnotic suggestion and conversion symptoms are executed without conscious awareness, they tap the same attentional networks that are used to execute conscious tasks. Although inhibition or activation of movements related to EPC may occur with voluntary motor tasks or sensory stimulation of the affected limb,11,12 this patient and two others I have seen demonstrated abolition of activity when they performed tasks using other parts of the body. Eliciting and abolishing typical episodes with normal saline and suggestion provide very strong support for the diagnosis of non-epileptic seizures.
Most patients with EPC demonstrate varying degrees of peri-ictal muscle weakness. This patient had no paresis immediately before, during or between episodes.1,2,12-14 Furthermore, his calm demeanor - he appeared undisturbed by the events - also suggested non-epileptic seizure, although this was a less definitive sign.
The failure to see hyperperfusion on ictal SPECT scan also suggests non-epileptic seizure. Although the sensitivity of ictal SPECT scanning in EPC is unknown, several reports suggest that SPECT scanning is sensitive and can reveal hyperperfusion even in the absence of EEG changes.15,16
Our patient had no demonstrable etiology for EPC despite vigorous blood testing and neuroimaging. Although the number of idiopathic cases of EPC is unknown, most reports of EPC describe readily identified causes such as metabolic,17 inflammatory,18 infectious,19-21 vascular,2 neoplastic13 and other structural22 etiologies. Although one of my patients had a history of seizures, the other two showed no evidence of neurological or metabolic disturbance.
A number of features demonstrated in this case were not helpful in distinguishing non-epileptic seizure from EPC. For example, the arrhythmic movements did not prove their functional nature, since EPC movements are often arrhythmic.2 The failure to demonstrate episodes during sleep does not exclude EPC since it can diminish or stop during sleep.2 A previous psychiatric history was also not helpful since psychiatric disturbances, including depression23-26 and anxiety,27,28 are common in epilepsy.29 Finally, the failure of these episodes to respond to antiepileptic drugs did not exclude EPC, since the response to antiepileptic drugs, including intravenous benzodiazepines, is often poor in EPC.2
Other techniques can help distinguish EPC from non-epileptic seizure. Supplemental scalp electrodes near the sensory-motor strip may enhance the identification of changes on EEG during the episodes. Other electrophysiological techniques, including demonstration of giant somatosensory evoked potentials30,31 and isolated spikes preceding myoclonic jerks on back-averaged EEG,4,31 can also help to diagnose EPC.
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