Electrical cortical stimulation is widely performed and is the gold standard for functional mapping in intractable epilepsy patients; however, a standard protocol has not yet been established. With respect to stimulation methods, two techniques can be applied: monopolar and bipolar stimulation. We compared the threshold to induce clinical symptoms between these two stimulation techniques. Twenty patients with intractable epilepsy who underwent electrical cortical stimulation for functional mapping were retrospectively investigated. We evaluated the stimulation intensity thresholds required to induce motor, sensory, and language symptoms. A total of 114 electrodes in 20 patients were used to investigate motor, sensory, and language symptoms. The thresholds required to induce motor (median value, bipolar: 4 mA, monopolar: 5 mA, p < 0.05) and language symptoms (bipolar: 8 mA, monopolar: 10 mA, p < 0.0005) were significantly higher for monopolar stimulation than those for bipolar stimulation. However, for sensory symptoms, no significant differences were found in the required thresholds between monopolar and bipolar stimulation (bipolar: 4 mA, monopolar: 4 mA, p = 0.474). Bipolar cortical stimulation required lower intensities to produce clinical motor and language symptoms and thus would be safe and suitable for screening of the eloquent area in functional mapping.
Intraoperative electrocorticography (iECoG) is widely performed to identify irritative zones in the cortex during brain surgery; however, several limitations (e.g., short recording times and the effects of general anesthesia) reduce its effectiveness. The present study aimed to evaluate the utility of iECoG for localizing epileptogenic zones. We compared the results of iECoG and chronic electrocorticography (cECoG) in 25 patients with refractory epilepsy. Subdural electrodes were implanted with iECoG under general anesthesia (2% sevoflurane). cECoG recordings were performed for 3-14 days. The distribution of iECoG spikes was compared with cECoG spike, seizure onset zone, and resection areas. The concordance patterns of each distribution were classified into four patterns: Group 1:
Impaired reperfusion in ischemic brain disease is a condition that we are increasingly confronted with owing to recent advances in reperfusion therapy. In the present study, rat models of reperfusion were investigated to determine the causes of acute seizures using magnetic resonance imaging (MRI) and histopathological specimens. Rat models of bilateral common carotid artery ligation followed by reperfusion and complete occlusion were created. We compared the incidence of seizures, mortality within 24 h, MRI, and magnetic resonance spectroscopy (MRS) to evaluate ischemic or hemorrhagic changes and metabolites in the brain parenchyma. In addition, the histopathological specimens were compared with those observed on MRI. In multivariate analysis, the predictive factors of mortality were seizure (odds ratios (OR), 106.572), reperfusion or occlusion (OR, 0.056), and the apparent diffusion coefficient value of the striatum (OR, 0.396). The predictive factors of a convulsive seizure were reperfusion or occlusion (OR, 0.007) and the number of round-shaped hyposignals (RHS) on susceptibility-weighted imaging (SWI) (OR, 2.072). The incidence of convulsive seizures was significantly correlated with the number of RHS in the reperfusion model. RHS on SWI was confirmed pathologically as microbleeds in the extravasation of the brain parenchyma and was distributed around the hippocampus and cingulum bundle. MRS analysis showed that the N-acetyl aspartate level was significantly lower in the reperfusion group than in the occlusion group. In the reperfusion model, RHS on SWI was a risk factor for convulsive seizures. The location of the RHS also influenced the incidence of convulsive seizures.
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