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INTRODUCTION

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Epilepsy has often been described as the great imitator with protean paroxysmal manifestations from sudden arousals out of sleep, to confusional states, to stiffening only when the individual arises and turns to one side and not the other. However, each of the behaviors listed previously (and many, many others) can be equally well explained in many individuals by nonepileptic mechanisms. According to the International League Against Epilepsy, imitators of epileptic seizures are defined not by the presentation but by the absence of abnormal and excessive neuronal discharges. The International League Against Epilepsy (ILAE) subdivides nonepileptic events into physiological disturbances with a nonepileptic mechanism such as syncope, sleep disorders, paroxysmal movements, transient global amnesia, and migraine as well as nonepileptic events of psychogenic origin (which may occur in the same patient with documented epileptic seizures).1

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There is an expression in medicine that "all that wheezes is not asthma." Yet many parents and primary care physicians still assume that all paroxysmal events are epileptic in origin. This becomes even more problematic in high-risk individuals such as developmentally delayed toddlers with nocturnal arousals, academically challenged children who "zone out," or adolescents with syncope. It often comes as a shock to many observers that so many individuals admitted to an epilepsy-monitoring unit (EMU), even those with undisputed epilepsy, have a nonepileptic basis for the event in question. A recent series of 223 children referred to a specialized epilepsy center in Denmark found that 39% did not have epilepsy.2 Even in a selected group from the Danish study where the referring physician was certain about the diagnosis of seizure disorder, fully 35% did not have epilepsy. It has also been demonstrated that there were occasional children diagnosed with medically refractory epilepsy who had a nonepileptic basis for their entire clinical syndrome.

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The value of electroencephalographic (EEG) is indisputable, but nonspecific abnormalities or unrelated epileptiform features like rolandic spikes may be wrongly interpreted to explain confusional episodes, headaches, or attention deficit disorder. A positive response to clinical trials or antiepileptic medication may not always provide a definitive answer to the challenge of the etiology of paroxysmal behavior such as aggression, headache, or movement disorders. Certainly there are many antiepileptic drugs such as lamotrigine, carbamazepine, and oxcarbazepine that are used (off-label) for mood stabilization, and topiramate and valproate have been approved for migraine prophylaxis. While it has long been recognized that carbamazepine can induce tics, there are recent reports demonstrating the value of topiramate and levetiracetam for controlling symptoms of Tourette syndrome.

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It is difficult to organize the imitators of epilepsy into a pathophysiologically based or clinically relevant schema. One could choose syndromes that occur primarily in sleep versus waking, disorders of early childhood or older childhood into adolescence, or paroxysmal disorders with presenting symptoms such as unusual movements or altered awareness, respiratory abnormalities, perceptual changes, or sudden behavioral alterations. This chapter will review the major imitators of ...

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