Many patients with medically refractory epilepsy now undergo successful surgery based on noninvasive diagnostic information, but intracranial electroencephalography (IEEG) continues to be used as increasingly complex cases are considered surgical candidates. The indications for IEEG and the modalities employed vary across epilepsy surgical centers; each modality has its advantages and limitations. IEEG can be performed in the same intraoperative setting, that is, intraoperative electrocorticography, or through an independent implantation procedure with chronic extraoperative recordings; the latter are not only resource intensive but also carry risk. A lack of understanding of IEEG limitations predisposes to data misinterpretation that can lead to denying surgery when indicated or, worse yet, incorrect resection with adverse outcomes. Given the lack of class 1 or 2 evidence on IEEG, a consensus-based expert recommendation on the diagnostic utility of IEEG is presented, with emphasis on the application of various modalities in specific substrates or locations, taking into account their relative efficacy, safety, ease, and incremental cost-benefit. These recommendations aim to curtail outlying indications that risk the over- or underutilization of IEEG, while retaining substantial flexibility in keeping with most standard practices at epilepsy centers and addressing some of the needs of resource-poor regions around the world.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/epi.13515

Diagnostic utility of invasive EEG for epilepsy surgery: Indications, modalities, and techniques

Focal cortical dysplasia (FCD) is a common cause of pharmacoresistant epilepsy that is amenable to surgical resective treatment. The identification of structural FCD by magnetic resonance imaging (MRI) can contribute to the detection of the epileptogenic zone and improve the outcome of epilepsy surgery. MR epilepsy protocols that include specific T1 and T2 weighted, and fluid-attenuated inversion recovery (FLAIR) sequences give complementary information about the characteristic imaging features of FCD; focal cortical thickening, blurring of the gray-white junction, high FLAIR signal, and gyral anatomical abnormalities. Novel imaging techniques such as magnetic resonance spectroscopy (MRS), magnetization transfer imaging (MTI), and diffusion tensor imaging (DTI) can improve the sensitivity of MR to localize the anatomical lesion. Functional/metabolic techniques such as positron emission tomography (PET), ictal subtraction single photon emission computed tomography (SPECT), functional MRI (fMRI), and magnetic source imaging (MSI) have the potential to visualize the metabolic, vascular, and epileptogenic properties of the FCD lesion, respectively. Identification of eloquent areas of cortex, to assist in the surgical resection plan, can be obtained non-invasively through the use of fMRI and MSI. Although a significant number of FCD lesions remain unidentified using current neuroimaging techniques, future advances should result in the identification of an increasing number of these cortical malformations.

Neuroimaging of focal cortical dysplasia.

The aim of this review is to discuss the existing evidence supporting different processes of visual brain plasticity after early damage, as opposed to damage that occurs during adulthood. There is initial evidence that some of the neuroplastic mechanisms adopted by the brain after early damage to the visual system are unavailable at a later stage. These are, for example, the ability to differentiate functional tissue within a larger dysplastic cortex during its formation, or to develop new thalamo-cortical connections able to bypass the lesion and reach their cortical destination in the occipital cortex. The young brain also uses the same mechanisms available at later stages of development but in a more efficient way. For example, in people with visual field defects of central origin, the anatomical expansion of the extrastriatal visual network is greater after an early lesion than after a later one, which results in more efficient mechanisms of visual exploration of the blind field. A similar mechanism is likely to support some of the differences found in people with blindsight, the phenomenon of unconscious visual perception in the blind field. In particular, compared with people with late lesions, those with early brain damage appear to have stronger subjective awareness of stimuli hitting the blind visual field, reported as a conscious feeling that something is present in the visual field. Expanding our knowledge of these mechanisms could help the development of early therapeutic interventions aimed at supporting and enhancing visual reorganization at a time of greatest potential brain plasticity.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-8749.2010.03710.x

Plasticity of the visual system after early brain damage.

Summary


Purpose: Polymicrogyria (PMG) is recognized as an epileptogenic lesion but few data concerning organization of the epileptogenic zone (EZ) are available.



Methods: We analyzed the distribution of the EZ according to Stereo-EEG (SEEG) with intralesional recordings in four patients evaluated for intractable partial epilepsy associated with focal unilateral PMG, involving the posterior temporal region in two, the perisylvian area in one and the temporoparietal junction in the other. All had ictal scalp EEG, high-resolution structural and functional MRI, fluorodeoxyglucose positron emission tomography (FDG-PET), and SEEG. For each patient, several depth electrodes were implanted both within the PMG and in extralesional areas.



Results: In three patients, the PMG displayed high-frequency spiking activity. However, interictal and ictal recordings demonstrated a large epileptogenic network, which was more widespread than the PMG, including the mesial temporal structures in two. In another patient, interictal spiking and seizure onset site were located within the hippocampus and outside of the PMG, although it was rapidly involved during seizure spread. Overall, EZ was considered to be larger than the PMG in all patients although hypometabolic areas detected by PET were concordant with EZ. Three patients underwent extensive surgery including the PMG and are seizure free with a follow-up >2 years.



Discussion: Although intralesional recordings demonstrated intrinsic epileptogenicity in PMG, our data provide evidence that unilateral focal PMG belongs to a large epileptogenic network extending beyond the MRI lesion. SEEG may be helpful for planning surgery with favorable outcome, providing large resections are feasible, even in apparently focal PMG.

Intralesional recordings and epileptogenic zone in focal polymicrogyria.

Summary


Purpose: Surgical resection of single, dominant, epileptogenic lesions in patients with tuberous sclerosis complex (TSC) is now accepted as an effective therapy. However, patients with symptomatic tubers in eloquent cortex are sometimes not offered surgery because of the concern for postoperative neurologic morbidity. In this study, we examine our results in children undergoing surgery for resection of tubers and associated seizure foci in rolandic and perirolandic cortex.



Methods:  Between 1998 and 2008, 52 pediatric patients (mean age 4 years) with TSC underwent epilepsy surgery at the NYU Comprehensive Epilepsy Center. Fifteen of these patients underwent multistage surgery for invasive mapping of seizure foci and surrounding functional cortex followed by resection of tubers/seizure foci in or near rolandic cortex. Data were retrospectively collected and neurologic outcomes were tabulated.



Results:  Postoperatively, four patients (27%) had either new hemiparesis or worsening of a preexisting hemiparesis. However, all patients were back to their neurologic baselines at 3-month follow-up, yielding no permanent postoperative deficits. The modified Engel outcome was class I in nine patients (60%), class II in three patients (20%), class III in two patients (13%), and class IV in one patient (7%) after 40 months mean follow-up.



Discussion:  Surgical resection of tubers and associated epileptogenic foci in rolandic and perirolandic cortex in children with TSC is feasible, with low neurologic morbidity, and yields good seizure control. These results suggest that tubers and perituberal epileptogenic foci can be safely resected even in eloquent regions because of reorganization of functional cortex or because these lesions contain no neurologic function.

Do tubers contain function? Resection of epileptogenic foci in perirolandic cortex in children with tuberous sclerosis complex.

Background: The evaluation for epilepsy surgery of patients with malformations of cortical development (MCDs) in areas of clinically important cerebral function is a challenge because of the unpredictable localization of critical sensory, motor, and cognitive function. Magnetoencephalography (MEG) source localization of evoked fields can address whether functional reorganization of primary sensory modalities exists in MCDs. Methods: Consecutive patients with MRI- demonstrated rolandic and calcarine cortex MCDs were identified who had a 148- channel whole- head MEG study to identify the localization of primary somatosensory and visual cortices. Reorganization was considered when localization contrasted that expected upon general anatomic or homuncular rules and was defined against controls. Results: Twelve patients (n = 12) were studied. Six had focal cortical dysplasia, two had polymicrogyria and schizencephaly, and four had isolated polymicrogyria. In the patients with cortical dysplasias, the somatosensory cortices were identified outside the rolandic area. In the two patients with polymicrogyria and schizencephaly, the somatosensory cortices remained in the rolandic areas as long as the anatomy was not distorted by the presence of the schizencephalic cleft. In the patients with isolated polymicrogyria, the somatosensory cortex was mapped without evidence of reorganization. Conclusion: In patients with epileptic MCDs involving rolandic and calcarine regions, cortical function may be reorganized if the MCDs are due to an abnormal neuronal or glial proliferation (i.e., cortical dysplasia) but may not be in MCDs caused by abnormal cortical organization (i.e., polymicrogyria).

Cortical reorganization in malformations of cortical development: A magnetoencephalographic study

Although not approved by the US Food and Drug Administration for the treatment of status epilepticus (SE), valproic acid (VPA) is an emerging option for this purpose. The authors reviewed 63 patients (30 men) with SE treated with IV VPA (average dose, 31.5 mg/kg). Analysis of demographic, clinical, and treatment information indicated an overall efficacy of 63.3% and favorable tolerance of rapid administration.

Uab Epilepsy

Papers

Cortical reorganization in malformations of cortical development: A magnetoencephalographic study

Efficacy of rapid IV administration of valproic acid for status epilepticus