Abstracts

Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs) were recently described as an under-recognized EEG phenomenon in critically ill and encephalopathic patients undergoing continuous video-EEG monitoring (CVEEG). SIRPIDs may be elicited in stuporous or comatose patients by various types of alerting stimuli. This is primarily an EEG phenomenon, as only 1 of the initial 33 patients reported had a clinical correlate to their SIRPIDs. Other than this patient, stimulus-induced focal seizures in encephalopathic patients have not been reported in the literature. We describe six encephalopathic patients who displayed stimulus-induced focal clinical seizures during CVEEG. The patients[apos] ages range between 7 and 78. Four patients had prior epilepsy. Admission diagnoses included recurrent seizures (1), status epilepticus (2), hypoglycemia (1), cardiac arrest (1), and sepsis (1). All patients had metabolic derangements or systemic infections, but most had resolved prior to CVEEG. All 6 patients demonstrated evidence of SIRPIDs, with generalized periodic epileptiform discharges (GPEDs) or lateralized periodic epileptiform discharges (PLEDs) being the most common SIRPIDs patterns on EEG, usually with no clinical correlate. All patients also demonstrated reproducible, focal motor seizures on stimulation. These usually involved unilateral face and/or limb rhythmic twitching that lasted at least 30 seconds, often much longer, especially if stimulation continued. With cessation of stimulation, they would gradually cease over seconds to minutes. Five of the 6 patients had clear electrographic changes correlating with their stimulation-induced seizures. Imaging studies in half the patients showed cortical and/or adjacent subcortical white matter lesions, plus deep gray matter involvement. In particular, 3 patients had thalamic abnormalities on MRI. Two patients had subcortical white matter disease without cortical or thalamic involvement. One MRI was normal. We describe 6 encephalopathic patients in whom alerting stimuli repeatedly precipitated focal clinical seizures. This expands and confirms the epileptogenic effect of stimulation/arousal in encephalopathic patients. We hypothesize that SIRPIDs (with or without clinical manifestations) arise when the normal cortical inhibition of thalamo-cortical activity is lost. An alerting stimulus then activates the normal midbrain-thalamo-cortical circuitry, but when combined with a hyperexcitable brain, this culminates in periodic epileptiform discharges or seizures. Focal or heterogeneous brain dysfunction can cause this process to occur unilaterally or focally. A similar but generalized phenomenon has been described in postanoxic myoclonus. Further research is needed to elucidate the pathophysiologic and treatment implications of SIRPIDs and stimulus-induced clinical seizures in encephalopathic patients.