CLINICAL HISTORY:  54 year old man with a history of epilepsy, now with prolonged generalized tonic/clonic seizures.
MEDICATIONS:  Dilantin, Depakote, Keppra, Phenobarbital.
REASON FOR STUDY:  Status Epilepticus
INTRODUCTION:  Continuous digital video long-term EEG was performed at bedside using the standard 10-20 electrode placement system with additional anterior temporal and single-lead EKG electrodes.  The patient was recorded in wakefulness and sleep.  No activating procedures were performed.  Continuous spike detection software as well as alarm and nurses' notes were used to review the EEG.
DESCRIPTION OF THE RECORD:  The record opens to a diffusely slow background with a frequency of 2 to 4 Hz and an amplitude of 20 to 40 microvolts.  There is frontocentral beta seen.  No abnormal sleep architecture is seen.  No activating procedures are performed.
ABNORMAL DISCHARGES:
Focal sharp waves/PLEDS at FP1 at 1 to 2 Hz with an amplitude of 20 to 70 microvolts seen almost continuously throughout the recording, although by the last 24 hours the frequency had diminished and they were only seen in some spurts with inter bursts of more than 10 seconds.  The morphology at the end of the recording was a lot more blunt and of lower amplitude.
Generalized slow waves.
SEIZURES:  During the recording, the patient would have, at the FP1 electrode, rhythmic discharges that would increase in frequency and decrease in amplitude, and then suddenly stop multiple times per hour for the first 10 hours.  Suddenly they subsided and stopped, and for the rest of the recording none were seen.  During the ones that occurred at the beginning of the recording, no clear clinical correlation was noted.
IMPRESSION:  Abnormal EEG due to:
Seizures from the left prefrontal region which subsided after the first 10 hours, and none were seen for the last 50 hours of recording.
Focal sharp waves/PLEDS seen in the left prefrontal region.
Generalized slow waves.
CLINICAL CORRELATION:  This EEG reveals evidence of acute structural dysfunction and irritability arising from the left prefrontal region which has a high correlation with an acute structural lesion in that region.  In addition, there is evidence of seizures arising from the same region for the first 10 hours of the recording and none seen in the next 50 hours.  There is also evidence of diffuse cerebral dysfunction, which is nonspecific in regard to etiology and is likely due, at least in part, to medication effect.  These changes were noted to the primary team during the recording.