Because partial seizures can begin anywhere in the cerebral cortex, their manifestations are diverse, and because large portions of the cortex are devoted to primary and secondary interpretation of sensory stimuli, a wide variety of visual, auditory, vestibular, gustatory, and tactile symptoms can be features of epilepsy. Because seizure-related sensory manifestations are so varied, other sensory abnormalities may sometimes be confused with epilepsy. In distinguishing epileptic from nonepileptic sensory symptoms on clinical grounds, a few general principles are important. First, the context of the symptom must be considered. Purely sensory seizures, without other manifestations at least some of the time, are uncommon, so a careful search for other symptoms or signs supportive of epilepsy should be performed. For example, if a single secondarily generalized seizure begins with focal numbness, it is much more likely that the preceding dozens of similar episodes of isolated numbness were actually simple partial seizures. Second, the time course of the patient’s sensory event must be considered. Is it truly paroxysmal? Is the symptom recurrent and unprovoked? How long do the symptoms last? In general, epileptic seizures are unprovoked, paroxysmal, and 1 to 3 minutes in duration. Third, the quality of the sensory experience is relevant. Seizures typically consist of “positive” changes rather than “negative” ones, and this may be helpful in identifying nonepileptic sensory phenomena. For example, visions of swirling colors and shapes are more likely to have an epileptic origin than loss of vision, and localized tingling paresthesias are more likely to be epilepsy than diffuse numbness. Finally, the distribution of the sensory disturbance must be considered and whether it makes anatomic sense. Partial seizures arise from the cerebral cortex, and initial symptoms can therefore often be localized to a fairly discrete brain area. Subsequent evolution of symptoms generally involves adjacent cortex. Thus, visual symptoms typically involve one hemifield. Somatosensory seizures are more likely to involve the face and hand (because these have large areas of representation in the cortex) and should be restricted to one side of the body, at least at onset (insular seizures are an exception⁷).

It is clear that an accurate, detailed description of paroxysmal sensory changes is critical in separating epileptic events from a wide variety of nonepileptic conditions. Important sensory conditions that may be confused with epilepsy are listed in Table 1, and additional testing useful in distinguishing these conditions from epilepsy is listed in Table 2. This chapter describes all of these conditions in further detail and explains how they can best be distinguished from epilepsy.

One of the classic (although not the most common) initial symptoms of seizures originating in the medial temporal lobe is a paroxysmal episode involving an unpleasant odor. Typical descriptions include references to burnt rubber, sulfur, and organic solvents,³⁹ although more commonly the patient is unable to provide a specific analogy. Such “auras” may occur in the absence of other seizure manifestations as an isolated simple partial seizure. However, virtually all such patients experience a complex partial or secondarily generalized seizure at some point, especially if untreated, and this event resolves any diagnostic uncertainty.

Because virtually all abnormalities of the olfactory system result in loss of smell rather than an abnormal sensation of smell, these are not commonly mistaken for epilepsy. The one important exception is psychiatric illness. In such cases, patients will frequently report abnormal smells in association with psychogenic seizures. Although these may superficially resemble the foul odors of temporal lobe epilepsy, more commonly they are described much more precisely and are even reported as pleasant. Thus, a floral scent has been described,³³ as have smells of “perfume,” “food,” and “pure oxygen.” For a more extensive discussion of these seizures, the reader is referred to the section on psychiatric disturbances.

The sudden visual loss that accompanies a vertebrobasilar transient ischemic attack (TIA) is not easily confused with an epileptic seizure. Transient ischemic attacks usually last longer than typical seizures. Both, however, may be associated with vertigo, impaired speech, or altered consciousness. The distinction is discussed more fully in Chapter 275. Recurrent, sometimes stereotyped visual hallucinations may also occur in cases of cerebral amyloid angiopathy²⁰ (see also later discussion).

The complex and sometimes confusing relationship between migraine and epilepsy is also discussed more fully elsewhere (see Chapter 274). Because of its high prevalence, the visual symptoms of migraine represent a common situation in which the sensory symptoms of another disease may be mistaken for epilepsy. The phenomena of the two disorders can be similar, although the classic hemifield scotoma seen in migraine is rare with epilepsy. On the other hand, patients with migraine may see stars, colored lights, or patterns similar to those seen by patients with epileptic seizures arising from the occipital or posterior temporal lobe.

Other unusual causes of visual hallucinations that can occasionally be confused with epilepsy include withdrawal from alcohol or sedative drugs and psychiatric disease. In both, the images are typically well formed, but their variability and long duration (hours to days rather than minutes) usually distinguish them from epilepsy, even in the absence of other clinical information. Hallucinations occurring exclusively during the transitions between sleep and wakefulness (hypnic hallucinations) are often visual. These can be associated with narcolepsy, but also occur sporadically in otherwise normal individuals and can be precipitated by sleep deprivation.²

Peduncular hallucinations, a more unusual cause of paroxysmal visual symptoms, were first described by Lhermitte.³² These typically occur in the evening and may last for hours. They are quite vivid and well formed; examples include
a brightly colored parrot⁹ or other animals.^1,32,41 Affected patients may have alterations in consciousness, adding to the confusion with seizures. Associated symptoms such as cranial nerve palsies, hemiplegia, hemianesthesia, or ataxia are seen in many patients. Hypomania and increased tone occur often,⁴¹ which may also help to distinguish peduncular hallucinations from seizures. The condition results from infarction of the thalamus or the pars reticulata of the substantia nigra.⁹

As with olfactory disturbances, most seizures that affect hearing and balance manifest the “positive” features of auditory hallucinations or distortions and vertigo. Therefore, it is these symptoms that are most often mistaken for epilepsy. Auditory hallucinations are common in schizophrenia (see Chapter 287) and also occur occasionally in acute withdrawal states from alcohol and other sedative drugs. In both cases, the variability of the hallucinations in any single patient and the particular clinical setting usually make the distinction from epilepsy fairly easy. Auditory hallucinations are rare in vascular disease. These may be transient, and the absence of psychiatric disease can lead to confusion with epilepsy. Auditory hallucinations, including musical hallucinations, can occur with hearing loss, drug intoxication, or drug withdrawal.¹⁴

Episodes of dizziness and, in particular, paroxysmal vertigo are more likely to be confused with epilepsy. Dizziness is a very common complaint, especially in the elderly, and although only a small fraction of cases may be confused with epilepsy, this still represents a substantial number. The causes of vertigo are quite diverse and may involve either central or peripheral vestibular mechanisms. Peripheral vertigo can result from cupulolithiasis, head trauma, acceleration injuries, and middle ear infections and typically lasts seconds to minutes. Central vertigo can be caused by drugs, cerebrovascular disease, tumors, and multiple sclerosis and typically lasts several days,¹⁷ and therefore these would not typically be confused with epilepsy. The most common disorder is benign positional vertigo, which is usually idiopathic, the result of head trauma, or related to a viral infection.⁵ Unlike vertigo associated with seizures, paroxysmal nonepileptic vertigo is rarely unprovoked. The diagnosis is made when positional changes (including Hallpike and Barany maneuvers) elicit the patient’s typical symptoms with accompanying nystagmus. Paroxysmal vertigo is also usually of longer duration than vertiginous symptoms seen with epilepsy.

Benign paroxysmal vertigo of childhood is characterized by sudden, brief episodes of vertigo and nystagmus. It was first described by Basser.⁶ The syndrome occurs most often in children, usually beginning after 4 years of age, but occasionally before age 1 year; it typically resolves by age 10 years. Episodes last from 20 seconds to 3 minutes and may be accompanied by nausea, vomiting, or headache. The child may stumble or fall because of disequilibrium and, not surprisingly, becomes frightened or confused, features that may further suggest a complex partial seizure. The typical frequency is one to five spells per month.¹³ Results of audiologic, otologic, and neurologic examinations are normal. Findings of caloric/rotatory tests may be normal¹³ or abnormal.¹² The electroencephalogram (EEG) is uniformly normal. Nystagmus occurs during the actual episodes and, if observed, helps in the distinction from seizures. Benign paroxysmal vertigo is associated with migraine^13,15,26 and may perhaps be a variant of basilar migraine. The disorder most likely results from a transient disturbance in the vertebrobasilar circulation that produces central vestibular dysfunction.¹⁶