Convulsive seizures are quite uncommon in the acute or evolving phases of an arterial stroke. The ischemic convulsive phenomena of a “limb-shaking TIA” and a burst of generalized clonic motor activity during basilar artery occlusion have been mentioned earlier, but are uncommon and are not truly epileptic phenomena. Embolic infarcts involving the cortex become epileptogenic in fewer than 10 percent of cases and only after an interval of several months or longer. It has been stated in texts that thrombotic infarcts involving the cortex are almost never convulsive at their onset. Lacunar infarction, being deep and not involving the cortical surface, of course, does not produce convulsions.
In contrast, cortical venous thrombosis with underlying ischemia and infarction acts as a highly epileptogenic lesion (see Chap. 33). The same is true for hypertensive encephalopathy [including the above mentioned posterior reversible encephalopathy (PRES) and eclampsia] and thrombotic thrombocytopenic purpura (TTP), which has a strong tendency to cause nonconvulsive status epilepticus. The rupture of a saccular aneurysm is sometimes marked by one or two generalized convulsions that are not epileptic in nature and are probably predicated on the arrest of cerebral circulation. Cerebral hemorrhages, spontaneous or traumatic, that extend near the cortex, also may present with seizures acutely or become sources of recurrent focal seizures as a delayed consequence.
The use of anticonvulsants as prophylaxis for seizures after a typical cortical stroke of embolic or thrombotic type or nontraumatic cerebral hemorrhage is not necessary. The rate of such seizures has been estimated to be 3 percent or less in the first year. This subject is addressed further in Chap. 33.
It is not uncommon for severe concussion to be attended by brief convulsive movements (see Chap. 34). The appearance is in most cases of clonic twitching but may include a momentary tonic phase. Rarely, a prolonged clonic convulsion occurs. The nature of this event, whether originating in the reticular formation as a component of concussion, or from some disruption of cortical activity, is not clear. Almost invariably in our experience, the EEG recorded hours or a day later is normal, and imaging studies are likewise normal or show a small contusion. There is little to guide one in treatment of these patients; we tend to give a course of antiepileptic medications for several weeks but it is not established if this is the correct approach. Aside from penetrating brain trauma, the risk of delayed seizures is low. Further details on this subject, particularly seizures that occur as a late effect of traumatic brain injury can be found in Chap. 34.
Here one contends with two scenarios: the woman with epilepsy who becomes pregnant and the woman who has her first seizure during pregnancy. According to the extensive EURAP study, about two-thirds of epileptic women who become pregnant have no change in seizure frequency or severity (the majority remain seizure free); the remainder are evenly split between those in whom the frequency increases and in an equal number, it lessens. A systematic review has indicated that almost 90 percent of women who were seizure-free for a year before becoming pregnant, have no seizures during pregnancy.