Barbara Jobst MD Peter Williamson MD

bnormal behavior during epileptic seizures was recognized as a brain disorder since antiquity, as noted by the school of Galen (129-216 a.d.) (1). However, it was not until the later parts of the nineteenth century that ictal behavior was anatomically correlated to certain brain regions. Jackson and Gowers established an anatomical-clinical correlation by repeated observation of epileptic seizures in patients with obvious brain lesions, often found on autopsy (2,3). In retrospect the observational skills of clinicians at that time were outstanding. In the absence of advanced technology, descriptions of ictal behavior and the anatomical location thereof were made with much the same accuracy as clinical observations obtained using video-electroencephalographic (EEG) monitoring and magnetic resonance imaging (MRI) techniques (4,5). Their findings are still valid.

As ictal behavior is intermittent, anatomical-clinical correlation is harder to establish than in lesional neurology, where a persistent deficit can be more easily correlated to an obvious brain lesion. With the introduction of EEG by Berger in 1929, it was possible to correlate ictal behavior with areas of abnormal electrical cortical activity. Ajmone-Marsan used the seizure-inducing agent pethylenetetrazol (Metrazol) to induce repeated seizures. He standardized ictal behavior and correlated it to scalp EEG (4).

Penfield, at the Montreal Neurologic Institute, did further pioneering work using direct brain stimulation in patients undergoing electrocorticography under local anesthesia (6). With the help of intraoperative EEG recordings, he was able to localize clinical manifestations to cortical regions. If the patient remained seizure free after surgery, this gave further proof that some of the ictal behavior probably originated in the resected area. Similar experiments were performed by Bancaud and Talairach (Figure 2.1). After initial pioneering work, intracranial EEG recordings were also used outside the operating room during long-term EEG-moni-toring. Multiple centers around the world are now using larger numbers of grid and strip electrodes to localize ictal behavior. Cortical electrical brain mapping gained increasing value to localize ictal behavior and cortical functions. Newer technologies like structural and functional MRI, ictal single photon emission computed tomography (SPECT), and positron emission tomography (PET) are now supplementing previous studies and allow further insights to localize certain behaviors (7-9).

This chapter describes typical epileptic ictal behavior and the anatomical localization thereof. This knowledge

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about brain function has been derived by the following basic principles:

• Ictal behavior was correlated to an obvious brain lesion, which was thought to be the origin of the seizure.

• Ictal behavior was correlated with scalp and intra-cranial EEG findings.

• Stimulation experiments were performed, and stimulation sites were correlated with epileptic behavior that was induced by the stimulation.

• Patients with certain ictal manifestations underwent epilepsy surgery and became seizure free thereafter, which suggests that the ictal behavior originated in the resected area.

All the above methods have their limitations. A large systematic error is introduced by the fact that clinical manifestations may be a result of the propagation of epileptic activity beyond the functional origin and may not originate in the area of the lesion or the resection. Furthermore, seizures originating in certain regions of the brain may remain subclinical, because many areas of the brain are clinically silent. Scalp EEG recordings have been shown to be falsely localizing multiple times (10,11). Thus, the effects of stimulation experiments may not be a complete semiologic match for spontaneous seizure activity. Although our knowledge about the anatomical correlation of seizure activity is greatly enhanced compared to two hundred years ago, there still remains much uncertainty about various ictal behaviors.

In clinical practice, it is crucial to recognize certain behaviors as epileptic and localize them to certain areas of the brain. Misdiagnosis has great implications with respect to the possibilities for surgical treatment. A correct diagnosis of nonepileptic events may protect the patient from significant and unnecessary side effects attributable to antiepileptic medication. Conversely, patients with epileptic seizures may respond to appropriate medical and surgical treatment if the appropriate diagnosis is established. To distinguish nonepileptic events from epileptic seizures it is necessary to recognize certain behaviors and patterns as epileptic, by clinical description and observation. Knowledge of epileptic syndromes and associated seizure types enhances the recognition of epileptic versus nonepileptic events. However, certain behaviors can only ultimately be verified by video-EEG monitoring if the diagnosis is uncertain or the patient does not respond to treatment.

In some patients, even video-EEG monitoring is misleading. For example, frontal lobe seizures originating at the mesial surface may show no electrical abnormalities on scalp EEG. If events are highly stereotypical and brief in duration, the diagnosis of an epileptic seizure should always be considered even if symptoms seem unusual or bizarre. The role of video-EEG monitoring to diagnose the etiology of any type of bizarre episode cannot be overemphasized.

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