OBJECTIVE: Periodic lateralized epileptiform discharges have been recognized for 33 years; however, little is known about the underlying mechanism causing periodic discharges. The following case provides an opportunity to study PLEDs in a patient with precisely localized subcortical grey matter lesions. METHODS: Routine EEGs and overnight polysomnography were performed on the study patient. Standard 10-20 electrode positions were used, as well as EOG and chin EMG for polysomnography. RESULTS: The study patient was a 39-year-old woman with severe left caudate nucleus atrophy and right hemi-dystonia. She had left ventral-lateral (VL) thalamotomies in 1989 and 1991, pallidotomy in 1992, and centromedian thalamic stimulator implantation in 1997. EEGs prior to surgical intervention demonstrated left hemisphere PLEDs during sleep. Following CM nucleus stimulatory implantation, the patient had overnight polsomnography. EEG during wakefulness and REM sleep was normal. With stages I-IV sleep left hemisphere PLEDs at 1-2 Hz were seen with fronto-temporal predominance. Sleep spindles were present bilaterally. There was no history of seizures, before or after surgery. CONCLUSIONS: The finding of PLEDs confined to synchronized sleep which were not affected by surgical manipulation of the motor basal ganglia circuit suggests a role of the associative basal ganglia circuit in the generation of periodic phenomenon.
OBJECTIVE: Periodic lateralized epileptiform discharges have been recognized for 33 years; however, little is known about the underlying mechanism causing periodic discharges. The following case provides an opportunity to study PLEDs in a patient with precisely localized subcortical grey matter lesions. METHODS: Routine EEGs and overnight polysomnography were performed on the study patient. Standard 10-20 electrode positions were used, as well as EOG and chin EMG for polysomnography. RESULTS: The study patient was a 39-year-old woman with severe left caudate nucleus atrophy and right hemi-dystonia. She had left ventral-lateral (VL) thalamotomies in 1989 and 1991, pallidotomy in 1992, and centromedian thalamic stimulator implantation in 1997. EEGs prior to surgical intervention demonstrated left hemisphere PLEDs during sleep. Following CM nucleus stimulatory implantation, the patient had overnight polsomnography. EEG during wakefulness and REM sleep was normal. With stages I-IV sleep left hemisphere PLEDs at 1-2 Hz were seen with fronto-temporal predominance. Sleep spindles were present bilaterally. There was no history of seizures, before or after surgery. CONCLUSIONS: The finding of PLEDs confined to synchronized sleep which were not affected by surgical manipulation of the motor basal ganglia circuit suggests a role of the associative basal ganglia circuit in the generation of periodic phenomenon.