Beyond dependably identifying artifacts in the EEG recording, one of the main challenges for the electroencephalographer is to differentiate between normal patterns that simulate seizures and true epileptic or interictal discharges. These paroxysmal but ostensibly normal patterns appear mostly during sleep, each with a highly characteristic morphology. These include small sharp spikes, “14 and 6” polyspike activity, lambda and posterior occipital mu rhythm, and occipital sharp transients. These are pictured in most standard textbooks on the subject of EEG and discussed in Chap 2.
Several methods of long-term EEG monitoring are now in common use and are of particular value in the investigation of patients with surgically removable epileptogenic foci and of nonepileptic spells. The most common of these makes use of telemetry systems, in which the patient is attached to the EEG machine by cable or radio transmitter without unduly limiting freedom of movement. The telemetry system is joined to an audiovisual recording system, making it possible to record seizure phenomena (even at night, under dim or infrared light) and to synchronize them with the EEG abnormalities. An alternative is the use of a small digital recording device that is attached to a miniature EEG machine worn by the patient at home and at work (“ambulatory EEG”). The patient is instructed to push a button if he experiences an “event,” which can later be correlated with EEG activity.
Cerebral imaging has come to play a major role in the diagnosis of seizures. CT is able to demonstrate many of the typical underlying causes of seizures in adults but MRI is more sensitive for the detection of small structural abnormalities underlying epilepsy including tumor, stroke and traumatic lesions. Furthermore, more subtle abnormalities such as medial temporal sclerosis, heterotopias and other disorders of neuronal migration, and small glial scars can be clearly visualized with MRI. Advances in MRI field strength and techniques such as thin slice acquisition, continue to expose structural lesions in what were previously called cryptogenic cases and some of these lesions may be surgically remediable.
After a seizure, particularly one with a focal component, MRI sometimes discloses subtle focal cortical swelling and signal change in the FLAIR (fluid-attenuated inversion recovery) and diffusion-weighted sequences, or, if a contrast agent is administered, an ill-defined cortical blush may be visible. These changes are transient and are the effect of, rather than cause of, seizure and are thought to reflect disruption of the blood–brain barrier and metabolic changes in the cortex. There is an approximate relationship between the duration of seizure activity and the intensity and extent of these changes but they rarely persist for more than a day or two. Likewise, angiography or perfusion imaging performed soon after a seizure may show a focal area of enhanced blood flow or elevated blood volume. Less-well understood is the findings on MRI of increased T2 signal or restricted diffusion in the hippocampi and posterior thalamus after a prolonged seizure or status epilepticus. There are also imaging changes in the white matter, particularly the splenium of the corpus callosum that may occur soon after the withdrawal of certain antiepileptic medications as discussed in the later section on the use of these drugs and by Gürtler and colleagues.
The CSF after a seizure occasionally contains a small number of white blood cells (most often in the range of 10/mm3) in about 5 percent of patients. In a series of 309 individuals, Tumani and colleagues found up to 24 white blood cells but the median was far lower. A slight increase in protein is also possible. Like the imaging abnormalities these findings may lead to spurious conclusions about the presence of an active intracranial lesion, particularly if polymorphonuclear leukocytes predominate; a larger pleocytosis should always be construed as a sign of inflammatory or infectious disease.