Low-frequency bilateral hypothalamic stimulation for treatment of drug-resistant aggressiveness in a young man with mental retardation.

Stereotactic bilateral electrode implantation in the medial portion of the posterior hypothalamus was performed on a 22-year-old male with drug-resistant aggressiveness. To localize the targets during implantation, microrecording was performed, and the clinical and electroencephalographic responses to intraoperative stimulation were monitored. The patient had an improved response to low-frequency stimulation that was sustained 18 months later at a follow-up examination.

Skin erosion over implants in deep brain stimulation patients.

We analyzed factors associated with skin erosion in 55 patients treated with deep brain stimulation (Kinetra or Soletra) for Parkinson's (PD) or other diseases. Nine of 55 patients developed erosion, all of whom were PD patients who had been fitted with a Kinetra device (r = 0.9292; p < 0.005). Erosions may be due to an increased pressure over the skin resulting from the larger size and weight of the Kinetra device. Alternatively, erosions in patients with the Kinetra device and bilateral leads may arise from the larger size of the 2 extension wires into the same subcutaneous tunnel and from the larger size of the 2 close parieto-occipital connections on the same cranial side. In PD patients, erosions were not related to age, immobility or PD severity. Specific studies examining the role of the skin of PD patients in erosion development and the use of smaller stimulation systems may help minimize the erosion rate.

Voltage sources in mesial temporal lobe epilepsy recorded with foramen ovale electrodes.

OBJECTIVE: We introduce a monopole model to examine the sources of ictal and interictal activity in mesial temporal lobe epilepsy (MTLE) recorded using foramen ovale electrodes (FOE). METHODS: Classical electrostatic theory was applied to derive mathematical expressions. Interictal and ictal activity was acquired using FOE and scalp video-electroencephalography (v-EEG) during awake and sleep states. A total of 2057 interictal spikes and 712 ictal spikes were analyzed. Thirty-five seizures from several consecutive episodes were examined. MRI and clinical data were correlated with voltage source localization. RESULTS: Patients (20) were grouped according to the spatial distribution of voltage sources of interictal activity. Voltage sources were located over 3.4 and 21.6mm in the anterior-to-posterior axis of mesiotemporal structures and separated no more than 7 mm from this axis. In most patients (16), sources were restricted to 11.1+/-1.5mm, whereas other patients (4) exhibited a wider distribution (29.6-43.5mm). Sources of ictal and interictal activity partially overlapped, with ictal sources exhibiting a posterior localization at 20-40 mm. Both interictal and ictal sources were anterior to MRI atrophy. No difference between awake and sleep states were found, neither correlation between source scattering and history of epilepsy. CONCLUSIONS: Voltage source analysis applied to FOE suggests that, in most MTLE patients, interictal activity emerges from very restricted areas. Some patients, however, exhibited sources which are distributed all along the mesiotemporal structures. Our data suggest an anterior-to-posterior alignment of the irritative, ictal and atrophic zones. SIGNIFICANCE: The voltage source model applied to FOE can help to map the extension of the irritative and ictal areas in mesiotemporal structures.

First true initial ictal SPECT in partial epilepsy verified by electroencephalography.

Drug-resistant epilepsy can sometimes be treated by surgery. In these cases, an accurate identification of the epileptogenic area must be addressed before resection. Ictal SPECT is one of the presurgical evaluations that can be performed, but usually, the increase in the regional cerebral perfusion observed is produced by diffusion of ictal activity. Here we describe a patient studied with v-EEG and foramen ovale electrodes that suffered a seizure after intravenous infusion of etomidate. The sequence of etomidate administration, followed by radiotracer and seizure was good enough for us to suspect that a true initial ictal SPECT was observed. We have implemented a kinetic model with four compartments, previously described (Andersen 1989), in order to estimate the fraction of hydrophilic radiotracer in the brain during the pre-ictal and ictal periods. This model has shown that the fraction of hydrophilic radiotracer during the seizure into the brain would be between 18.9% and 42.3% of total infused. We show the first true initial ictal SPECT demonstrated by bioelectrical recordings of the brain activity, obtained by a correct succession of events and compatible with theoretical data obtained from the kinetic model.