The significance of periodic lateralized epileptiform discharges in EEG: An electrographic, clinical and pathological study

Abstract

Periodic lateralized epileptiform discharges (PLEDs) were recorded in 33 subjects. In their most typical form the PLEDs consisted of sharp wave discharges repeating periodically or quasi-periodically at rates generally close to 1/sec and separated by intervals of apparent quiescence. Twenty-nine of 33 patients experienced epileptic seizures consisting of epilepsia partialis continua in seven cases, reiterative, sporadic or isolated focal motor seizures in eighteen cases and continuous psychical seizures in four cases. Four subjects did not present detectable clinical signs of seizure activity. All patients with PLEDs exhibited other symptoms and signs of impaired neurological and mental function, motor and sensory deficits, visual field defects and alterations of symbolic functions. The etiology of the lesion(s) or disorders was: cerebral infarct(s) in thirteen cases, recent infarct or chronic focal seizure disorder in seven cases, chronic focal seizure disorder in three cases, space-occupying lesion (metastases and glioblastomas) in eight cases, pneumococcal meningitis in one case and post-vaccinal encephalomyelitis in one case. Twenty-four subjects suffered from uremia, alterations of fluid, electrolyte and acid-base balance, impairment of liver function (18 cases) and/or had histories of previous epileptic seizures (7 cases) and chronic alcoholism (12 cases). The role played in these focal seizure disorders by local anoxia, systemic metabolic derangements, alcohol withdrawal and pre-existing convulsive disorders is discussed. Most of the cases ran fairly benign courses with recovery in a few days to several weeks. In six of twelve patients who expired, autopsy was obtained. Correlation of the electrographic, clinical and pathological findings suggested that the central cortex implicated in the seizure discharge was generally the farthest from the anatomical lesion. Maximal increase of cerebral excitability peripheral to the bulk of the edema and of the metabolic derangement surrounding the lesion may account for this discrepancy. Between the site of lesion and general neurologic and electrographic abnormalities better correlation was found.