Systemic (lactic) acidosis is a common result of convulsive seizures, and it is not unusual for the serum pH to reach levels near or below 7 if taken immediately after a convulsion. Of more practical value is the fact that almost all generalized convulsions produce a rise in serum creatine kinase activity that persists for hours, a finding that could be used to greater advantage in emergency departments to assist in distinguishing seizures from fainting. Of course, extensive muscle injury from a fall or prolonged compression during a period of unconsciousness can produce the same abnormality.
Concentrations of serum prolactin, like those of other hypothalamic hormones, rise for 10 to 20 min after all types of generalized seizures, including complex partial types, but not in absence or myoclonic types. An elevation may help differentiate a psychogenic seizure from a genuine one; however, serum prolactin may also be slightly elevated after a syncopal episode (Fisher et al). There is also a postictal rise in ACTH and serum cortisol, but these changes have a longer latency and briefer duration. If elevations in these hormonal levels are used as diagnostic tests, one must have information about normal baseline levels, diurnal variations, and the effects of concurrent medications. Changes in body temperature, which are said to sometimes precede a seizure, may reflect hypothalamic changes but are far less consistent and difficult to use in clinical work.
In most autopsied cases of primary generalized epilepsy of the genetic variety, the CNS is grossly and microscopically normal. Not surprisingly, there are also no visible lesions in the seizure states complicating drug intoxication and withdrawal, transient hyperand hyponatremia, and hyperand hypoglycemia, which presumably represent derangements at the cellular level.
In contrast, symptomatic epilepsies have definable lesions. MRI, which has been used as a surrogate for pathology, has improved matters by exposing some cortical heterotopias that had been previously difficult to detect, and to highlight the frequency of gliosis in the medial temporal lobes. Other lesions include zones of neuronal loss and gliosis (scars) or other lesions such as heterotopia, dysgenic cortex, hamartoma, vascular malformation, porencephaly, and tumor. Vascular malformations, hamartomas, ganglioneuromas and related dysembryoplastic neuroectodermal tumors (DNET), which are important causes of drug resistant epilepsy, and low-grade astrocytomas were less frequent; again, in a small number, no abnormalities could be found. Certainly the focal epilepsies are associated with the highest incidence of structural abnormalities, although in certain cases no morphologic change is visible.
It has not been possible to determine which component of the lesion is responsible for the seizures. Gliosis, fibrosis, vascularization, and meningocerebral cicatrix have all been incriminated, but they are found in nonepileptic foci as well. The Scheibels’ Golgi studies of neurons from epileptic foci in the temporal lobe showed distortions of dendrites, loss of dendritic spines, and disorientation of neurons near the scars, but these findings have dubious status because they were not usually compared with similar nonepileptic lesions. Once a gliotic focus of whatever cause becomes epileptogenic, it may remain so throughout the patient’s lifetime.