Corpus callosotomy in pediatric patients with non-lesional epileptic encephalopathy with electrical status epilepticus during sleep.

Epileptic encephalopathy with electrical status epilepticus during sleep (ESES) is often refractory to medical treatment and leads to poor cognitive outcomes. Corpus callosotomy may be an effective treatment option for drug-resistant ESES with no focal etiology. We retrospectively identified three patients who underwent corpus callosotomy for drug-resistant ESES in our institution. Electroencephalography (EEG) findings and cognitive functions were evaluated before surgery, at 3 months, 6 months, 1 year, and 2 years after surgery. Age at surgery was 6 years 10 months, 7 years 9 months, and 8 years 4 months, respectively. Period between the diagnosis of ESES and surgery ranged from 7 to 25 months. All patients had no obvious structural abnormalities and presented with cognitive decline despite multiple antiseizure medications and steroid therapies. One patient showed complete resolution of ESES and an improvement of intelligence quotient after surgery. Epileptiform EEG was lateralized to one hemisphere after surgery and spike wave index (SWI) was decreased with moderate improvement in development and seizures in the other 2 patients. SWI re-exacerbated from 6 months after surgery, but without subsequent developmental regression in these 2 patients. Corpus callosotomy may become an important treatment option for drug-resistant ESES in patients with no structural abnormalities.

Single-Institutional Experience of Chronic Intracranial Electroencephalography Based on the Combined Usage of Subdural and Depth Electrodes.

Implantation of subdural electrodes on the brain surface is still widely performed as one of the "gold standard methods" for the presurgical evaluation of epilepsy. Stereotactic insertion of depth electrodes to the brain can be added to detect brain activities in deep-seated lesions to which surface electrodes are insensitive. This study tried to clarify the efficacy and limitations of combined implantation of subdural and depth electrodes in intractable epilepsy patients. Fifty-three patients with drug-resistant epilepsy underwent combined implantation of subdural and depth electrodes for long-term intracranial electroencephalography (iEEG) before epilepsy surgery. The detectability of early ictal iEEG change (EIIC) were compared between the subdural and depth electrodes. We also examined clinical factors including resection of MRI lesion and EIIC with seizure freedom. Detectability of EIIC showed no significant difference between subdural and depth electrodes. However, the additional depth electrode was useful for detecting EIIC from apparently deep locations, such as the insula and mesial temporal structures, but not in detecting EIIC in patients with ulegyria (glial scar). Total removal of MRI lesion was associated with seizure freedom. Depth electrodes should be carefully used after consideration of the suspected etiology to avoid injudicious usage.

Surgical Management of Deep Brain Stimulator Infection without Electrode Removal: Report of Two Cases.

Objective Stimulation of the subthalamic nucleus by implanted electrodes (deep brain stimulation [DBS]) is performed to suppress symptoms of Parkinson's disease. However, postoperative wound dehiscence and infection can require removal of the implanted electrode leads. This report describes treatment of intractable unilateral wound infection in two patients without removing the DBS device. Methods First, components of the DBS system were removed except for the electrode lead and thorough debridement of the infected wound was conducted. Second, the edges of the bone defect left by removal of DBS components were smoothed to eliminate dead space. Subsequently, the electrode lead was covered by using a pericranial-frontalis-muscle flap or a bi-pedicled-scalp flap with good blood supply. Closed intrawound continuous negative pressure and irrigation treatment was conducted for 1 week after the surgery, and then the drain was removed. Results We treated two patients with wound infection after implantation of DBS electrodes. Case 1 developed a cutaneous fistula and Case 2 had wound dehiscence. After treatment by the method described above, complete wound healing was achieved in both patients. Conclusion DBS is always associated with a risk of infection or exposure of components and treatment can be very difficult. We successfully managed intractable wound infection while leaving the electrode lead in situ, so that it was subsequently possible to continue DBS for Parkinson's disease.

Is intracranial electroencephalography useful for planning resective surgery in intractable epilepsy with ulegyria?

OBJECTIVE: Intractable epilepsy patients with ulegyria could be candidates for resective surgery. Complete resection of ulegyria in the epileptogenic hemisphere is associated with favorable seizure outcome, although the risk of postoperative functional deficits is higher. The authors evaluated the extent of resection and postsurgical outcomes in epilepsy patients with ulegyria who underwent intracranial electroencephalography (iEEG) monitoring prior to resection to clarify the efficacy of iEEG-guided partial resection of ulegyria. METHODS: Ten consecutive epilepsy patients with ulegyria (7 males and 3 females, age range at surgery 7-34 years) underwent iEEG prior to resective surgery between 2011 and 2017 with a minimum follow-up of 12 months (range 12-72 months). The diagnosis of ulegyria was based on the typical pattern of cortical atrophy especially at the bottom of the sulcus on MRI. An iEEG study was indicated after comprehensive preoperative evaluations, including high-field MRI, long-term video-EEG, magnetoencephalography, and FDG-PET. The resection planning was based on iEEG analysis. Total lesionectomy was not always performed, as preservation of cortical function was prioritized. RESULTS: Ulegyria was seen in the occipital and/or parietal lobe in 9 patients and bilaterally in 5 patients. Ictal EEG onset involved the temporal neocortex in 6 patients. Intracranial electrodes were implanted unilaterally in all except 1 patient with bilateral lesions. The extent of MRI lesion was covered by the electrodes. Seizure onset zones (SOZs) and irritative zones (IZs) were identified in all patients. SOZs and IZs were completely resected in 8 patients but were only partially removed in the remaining 2 patients because the eloquent cortices and the epileptogenic zones overlapped. Ulegyria of the epileptogenic side was totally resected in 1 patient. Seizure freedom was achieved in 4 patients, including 3 after partial lesionectomy. Extended resection of the temporal neocortex was performed in 4 patients, although postoperative seizure freedom was achieved only in 1 of these patients. Visual field deficit was seen in 4 patients. Three of 5 patients with bilateral lesions achieved seizure freedom after unilateral resective surgery. CONCLUSIONS: Intracranial EEG-guided partial lesionectomy provides a reasonable chance of postoperative seizure freedom with a lower risk of functional deficits. Patients with bilateral ulegyria should not be excluded from consideration as surgical candidates.

Effects of fluid percussion injury on the neuronal activity in the hippocampal CA1 area and the dentate gyrus of the rat.

The effect of fluid percussion injury (FPI) on the propagation of neuronal activity in the rat hippocampus was investigated by using optical and extracellular recording techniques. Under anesthesia with pentobarbital sodium, a moderate impact (1.5-2.0 atm) was applied to the parietal cerebral cortex of the left hemisphere at -3 mm (i.e. caudal) from bregma, 3.5 mm lateral from the sagittal suture. Systemic oxygenation remained normal during the anesthesia. The rats recovered fully from anesthesia within 30-60 min, and their subsequent behavior, such as feeding and grooming, was normal. After a survival period of 1 week from the FPI or sham-operation, neuronal activities were recorded from the hippocampal CA1 region and the dentate gyrus (DG) in either coronal or horizontal brain slice preparations. In sham-operated rats, there was no significant difference in the neuronal activity between contralateral and ipsilateral hippocampal CA1 areas and DG. In coronal slices (-5.6(-)-6.4 mm from bregma), moderate impact (1.5-2.0 atm) markedly depressed the neuronal activity of the ipsilateral (impact side) CA1 region and of the DG directly under the cerebral cortex that received the impact. In horizontal slices, on the other hand, the neuronal activity was markedly enhanced in the ipsilateral hippocampal CA1 region and the DG adjacent the temporal lobe of the cerebral cortex. Field potentials were recorded from the dentate granule cell layer and the hippocampal CA1 pyramidal cell layer in either coronal or horizontal slice. Moderate impact strongly depressed the field potential in the ipsilateral CA1 region and DG directly under the injured cerebral cortex. In horizontal slices, the field potential was followed by multiple population spikes in ipsilateral hippocampal CA1 and the DG neurons. Bicuculline (15 microM) increased the number of spikes of the field potential even after the brain injury. These results suggest that FPI depresses the neuronal activity in the ipsilateral hippocampus directly under the injured parietal cortex, while it enhances the neuronal activity of the ipsilateral hippocampus adjacent to the temporal cortex. The facilitation of neuronal activity following FPI is not due to disinhibition resulting from depression of GABAergic interneuron activity.

Hyperexcitability of hippocampal CA1 neurons after fluid percussion injury of the rat cerebral cortex.

Effects of fluid percussion injury (FPI) of the parietal cerebral cortex on the neuronal activity in the temporal region of the rat hippocampal CA1 area were investigated by using optical and extracellular recording techniques. Application of moderate impact (1.5-2.0 atm) to the parietal cerebral cortex enhanced the optical signal of the neuronal activity in the ipsilateral hippocampal CA1 area. The field potential evoked by the Schaffer collaterals had multiple population spikes in the ipsilateral hippocampal CA1 pyramidal cell layer. Bicuculline (15 microM) increased the amplitude and the number of population spikes of the field potential even after the brain injury. These results suggest that FPI produces hyperexcitability of hippocampal CA1 neurons, probably by increasing the activity of the Schaffer collaterals of hippocampal CA3 neurons.