The history is crucial in suggesting a diagnosis of epilepsy. The value of the interview hinges largely on the availability of an accurate history from both the patient and a witness to the event. In the absence of either of these essential features, the information is usually incomplete or inadequate, and every effort should be made to obtain a complete and detailed account before attempting to formulate a diagnosis.²

The last quarter-century has witnessed a great increase in the number of neurologists sophisticated in the treatment of epilepsy, and such neurologists are now available in many practice groups and academic departments. Many neurologists developed sophisticated monitoring units, to which patients with unexplained paroxysmal events are often referred. It soon became obvious that many of these individuals did not have epileptic seizures, and this led epileptologists and other neurologists to focus on the wide range of disorders presenting for differential diagnosis. More recently this increased awareness and accuracy in diagnosis by referring physicians has led to a reduction in the number of patients with clinically recognizable nonepileptic paroxysmal events who are referred to epilepsy centers.

Nonepileptic seizures present the most common problem in differential diagnosis (see Chapter 282). Increasingly available information and sophistication coupled with ready access to medical literature and the Internet, along with the individual’s ability to learn from previous interviewers and examiners, has led to the appearance of complex accounts of what might be called “pseudoepileptic nonepileptic seizures.” Thus, such patients often provide a history that contains many features of temporal lobe epilepsy or of other specific epileptic disorders. They may have a background of study in a field related to epilepsy, which obviously makes diagnosis difficult. The patients’ social and cultural backgrounds are important determinants not only of the pattern of nonepileptic seizures, but also of their response to treatment. In many settings and localities the majority of patients respond to appropriate psychiatric treatment with remission of the attacks. In other environments with different levels of psychiatric sophistication and social problems, the disorder is much more refractory and the percentage of patients who cannot be relieved of their nonepileptic attacks is higher.⁴³

Anoxic convulsions, or “ischemic convulsions” as they are sometimes termed, continue to present a diagnostic problem. They occur most often as a sequel to syncope and are related usually to the person being kept in an upright or standing position. Sometimes, however, syncope may occur in individuals who are recumbent. The circumstances of the event and the family history will provide clues to the diagnosis.^18,21,29,43 Not only might patients with asthma during an acute attack have cerebral ischemia, but they also might present with tonic episodes, whose mechanism is analogous to that of anoxic convulsions.²⁷ When there is some lateralization, the differential diagnosis is, of course, more difficult. However, lateralization of clinical features is not uncommon and has long been recognized in generalized processes such as idiopathic epilepsy.²⁴ It may be erroneously inferred by the observer, depending on the patient’s position during the attack. It is important to distinguish between persistent or habitual lateralization and less significant and inconstant asymmetries in body and limb postures and movements.

Many individuals with migraine present features that make diagnosis difficult (Chapter 274). Acephalgic migraine occurring in older individuals is often not accompanied by headache, and these patients are not infrequently referred for diagnosis because of the suspicion of intermittent cerebral ischemic attacks or an epileptic etiology. Acephalgic migraine, however, does also occur in younger individuals and children.⁴⁵

The march of the migrainous aura has a time course that frequently is different from that of the recruitment of symptoms in epilepsy, and in a majority of individuals distinguishing between the two is not difficult.^12,38,45 After the migrainous aura, however, the patient may have convulsive seizures, so-called intercalated attacks.^3,47 These are most likely related to spreading depression crossing the central sulcus, but proof of the specific mechanism is lacking. Whether these attacks require treatment with antiepileptic medication is not clear. Patients with a habitual tendency to develop such epileptic manifestations in the course of their migraine attacks eventually may develop seizures, usually temporal in pattern, which no longer occur in relation to clear-cut migrainous events. The mechanism of this form of secondary epileptogenesis is not clear.¹ Confusional migraine may also result in an epileptic seizure occurring during the acute event.^1,19 Here, too, the possibility of eventual development of independent epileptic attacks exists.

Patients with basilar migraine not infrequently present difficult diagnostic problems. It is usually the sequence of symptoms pointing to brainstem involvement, such as diplopia and ataxia, that provides clues to the diagnosis.^9,39,46 Neuro-otologic investigation during an attack documenting the very prominent nystagmus is also helpful.

Patients with basilar migraine also may have epileptic events or in rare instances status epilepticus. Here, too, the account of symptoms preceding the seizure will lead to clarification.¹⁴

The unresponsiveness that is not uncommon during basilar migraine attacks may be interpreted as loss of consciousness; however, the patients generally can be aroused by vigorous stimulation, only to relapse into stupor when stimulation ceases.⁹

In addition to the clinical problems, the recognition that the migraine aura may be manifested by electroencephalographic (EEG) spike discharge (usually over posterior head regions) may lead to diagnostic difficulty.^6,33,44

Migraine is an extraordinarily common disorder, and despite the efforts of the International Migraine Society, there is still considerable disparity in deciding on its prevalence. It seems fairly clear that migraine and epilepsy have different mechanisms but that relationships between the two conditions, at times of a causal nature, exist. An interesting example is the association between benign rolandic epilepsy or benign occipital epilepsy and migraine.¹⁰ Surprisingly, there is no unanimity among pediatric neurologists and epileptologists about the high and probably consistent association of these two disorders. Clarification must await advances in molecular genetics, which, it is hoped, will provide markers for these conditions.

Recent advances in molecular biology have shed some light on the nature of hemiplegic migraine with coma; it is notable that these patients do not have clear epileptic events. The hallucinations that occur as they recover from the coma are similar to those of peduncular hallucinosis.^26,36,50