Abstract Introduction Pre-operative white matter tract reconstruction of the Meyer’s loop (ML) of the optic radiation using diffusion MRI (tractography) can be used to prevent post-operative visual-field deficit. Due to its complex anatomy, precise reconstruction of the ML is challenging and often underestimated. Previous work has suggested that an innovative tractography technique using oriented priors called MAGNET better approximates reconstruction to reported histological prosections. This proof-of-context study validates the MAGNET methodology in predicting visual-field deficits in patients undergoing TLE surgery. Method Diffusion MRI datasets were used to reconstruct pre-operative ML using MAGNET in five patients. These were overlaid on post-operative T2-MRI series demonstrating the surgically resected area to measure overlap between resection and reconstructed ML. A correlation with post-operative visual-field defects was established. Results There was no evidence of visual field deficit in the cases where there was no overlap between the reconstructed ML and the resected region. In the cases with overlap with reconstructed ML and resection, there was visual deficit found. There was no correlation between proportion of resected ML and visual deficit. Conclusions This pilot demonstrates that MAGNET accurately reconstructs ML in pre-surgical TLE cases compared to standard tractography techniques and can be used to augment neurosurgical planning and resection.

The dorsal hippocampal commissure (DHC) is a white matter tract that provides interhemispheric connections between temporal lobe brain regions. Despite the importance of these regions for learning and memory, there is scant evidence of a role for the DHC in successful memory performance. We used diffusion-weighted magnetic resonance imaging (DW-MRI) and white matter tractography to reconstruct the DHC in both humans (in vivo) and nonhuman primates (ex vivo). Across species, our findings demonstrate a close consistency between the known anatomy and tract reconstructions of the DHC. Anterograde tract-tracer techniques also highlighted the parahippocampal origins of DHC fibers in nonhuman primates. Finally, we derived diffusion tensor MRI metrics from the DHC in a large sample of human subjects to investigate whether interindividual variation in DHC microstructure is predictive of memory performance. The mean diffusivity of the DHC correlated with performance in a standardized recognition memory task, an effect that was not reproduced in a comparison commissure tract-the anterior commissure. These findings highlight a potential role for the DHC in recognition memory, and our tract reconstruction approach has the potential to generate further novel insights into the role of this previously understudied white matter tract in both health and disease.

Sudden unexpected death in epilepsy (SUDEP) in children, although rare, needs critical attention given the tragic nature and devastating consequences for families and caregivers. True incidence is unknown and risk factors are not completely understood, more so in children compared with adults. A focused narrative review of available studies on paediatric SUDEP was undertaken to comprehend its risk factors and to develop strategies to recognise and where possible modify SUDEP risk and ultimately reduce incidence. We reviewed 16 population-based studies from various settings. We found overlapping risk factors from different studies. The prime risk factor is uncontrolled seizures. This review supports the view that children entering adolescence with optimal seizure control could be a key aspect in reducing adult mortality related to SUDEP. Ideally, clinicians would want to be able to predict prospective, individualised SUDEP risk, which is challenging due to a myriad of risk factors and an inherent non-homogeneous paediatric epilepsy population. Nevertheless, an adequate evidence base exists as evidenced by this review to support information giving and communication to support young people with epilepsy and their families in being active partners in recognising and reducing their SUDEP risk. More work particularly in the form of prospective studies and registries are needed to further clarify true incidence which may have been previously underestimated and to update risk factors.

Larger size and higher spatial frequency of grating stimuli have been shown not only to maximally modulate early gamma-band visual cortical responses but also to provoke seizures in photosensitive epilepsy. Occipital brain magnetic field (MEG) oscillatory responses were evoked upon static grating pattern subthreshold stimuli in 12 patients with photosensitive epilepsy and 2 matched control groups, one with epilepsy but no photosensitivity and the other healthy controls. The continuous wavelet transform (CWT) was employed to characterize the time–frequency energy dynamics and phase-locking of the early evoked gamma-band oscillatory responses (eGBR). The photosensitive epilepsy group showed statistically significantly increased phase-locking of the gamma-band responses (eGBR) of the striate visual cortex in the (40–70 Hz) × (25–300 ms) and in the (25–30 Hz) × (300–600 ms) time–frequency windows with respect to the healthy controls. Photosensitive epilepsy seems to be characterized by altered phase synchronization dynamics at a higher frequency range (a-frequency band) compared to healthy controls. Our results indicate that photosensitive epilepsy is driven by the large-scale phase-locking of the underlying striatal visual cortical unit oscillators in specific “photosensitive” frequency components (dynamic phase-attractor theory of epilepsy). Our method could provide a novel diagnostic tool in safely detecting, investigating and assessing response to treatment in photosensitive epilepsy.

IntroductionSurgery for refractory temporal lobe epilepsy can cause postoperative visual field defects (VFD). This study aimed to predict personalised risk of VFDs for patients undergoing selective transsylvian amygdalohippocampectomy.MethodsPreoperative reconstruction of the optic radiations (OR) using diffusion tensor-based tractography was completed on two patients. The ‘average resection model’ uses a template from postoperative structural scans of five patient scans to predict an average resection in the patient. The OR tractography was compared with the resection margins to determine fibre involvement. The ‘multiple individual comparison model’ compared individual postoperative scans with the preoperative tractography to determine risk of VFD.ResultsIn Patient 1 the average resection overlapped the OR, so an average resection would be expected to produce a VFD. In 3/5 postoperative scans the resection intersected with the OR, indicating that 60% of prior resections would have caused a defect. In Patient 2 no overlap between resection and OR was found in either model. Perimetry confirmed VFD in patient 1 but not in patient 2.DiscussionThis pilot study demonstrates that the risk of postoperative VFDs can be predicted. The two models provide qualitatively different form of quantitative risk which could inform the discussion between patient and clinician.

Objective: Juvenile myoclonic epilepsy (JME) is a common idiopathic (genetic) generalized epilepsy (ICE) syndrome characterized by impairments in executive and cognitive control, affecting independent living and psychosocial functioning. There is a growing consensus that JME is associated with abnormal function of diffuse brain networks, typically affecting frontal and fronto-thalamic areas.Methods: Using diffusion MRI and a graph theoretical analysis, we examined bivariate (network-based statistic) and multivariate (global and local) properties of structural brain networks in patients with JME (N = 34) and matched controls. Neuropsychological assessment was performed in a subgroup of 14 patients.Results: Neuropsychometry revealed impaired visual memory and naming in JME patients despite a normal full scale IQ (mean = 98.6). Both JME patients and controls exhibited a small world topology in their white matter networks, with no significant differences in the global multivariate network properties between the groups. The network-based statistic approach identified one subnetwork of hyperconnectivity in the JME group, involving primary motor, parietal and subcortical regions. Finally, there was a significant positive correlation in structural connectivity with cognitive task performance.Conclusions: Our findings suggest that structural changes in JME patients are distributed at a network level, beyond the frontal lobes. The identified subnetwork includes key structures in spike wave generation, along with primary motor areas, which may contribute to myoclonic jerks. We conclude that analyzing the affected subnetworks may provide new insights into understanding seizure generation, as well as the cognitive deficits observed in JME patients. (C) 2014 The Authors. Published by Elsevier Inc.

### Learning Point for Clinicians Voltage gated potassium channel (VGKC) encephalitis is a recently recognized autoimmune condition with antibodies against components of the VGKC protein complex. Clinical phenotype can vary, but patients typically present with a limbic encephalitis involving amnesia, seizures, psychiatric disturbance and occasionally faciobrachial dystonic seizures. A 66-year-old man presented following a generalized tonic-clonic seizure and a 1 month history of paroxysmal episodes with autonomic and sensory symptoms. Magnetic resonance imaging (MRI) found right medial temporal lobe swelling and high signal. Cardiac telemetry found supra-ventricular tachycardia and prolonged pauses during the paroxysmal episodes. Voltage gated potassium channel (VGKC) antibodies were positive. Immunomodulatory treatment lead to resolution of symptoms, MRI and cardiac abnormalities. This case highlights a recently recognized and treatable cause of late onset epilepsy and cardiac arrhythmia—typical presentations to primary care or the acute medical take. In our patient, an incorrect initial diagnosis of brain tumour and unnecessary permanent pacemaker (PPM) were avoided after a unifying diagnosis of VGKC limbic encephalopathy was made and treated. A 66-year-old man presented …

The EEG/MEG signal is generated primarily by the summation of the post-synaptic potentials of cortical principal cells. At a microcircuit level, these glutamatergic principal cells are reciprocally connected to GABAergic interneurons and cortical oscillations are thought to be dependent on the balance of excitation and inhibition between these cell types. To investigate the dependence of movement-related cortical oscillations on excitation-inhibition balance, we pharmacologically manipulated the GABA system using tiagabine, which blocks GABA Transporter 1(GAT-1), the GABA uptake transporter and increases endogenous GABA activity. In a blinded, placebo-controlled, crossover design, in 15 healthy participants we administered either 15mg of tiagabine or a placebo. We recorded whole-head magnetoencephalograms, while the participants performed a movement task, prior to, one hour post, three hour post and five hour post tiagabine ingestion. Using time-frequency analysis of beamformer source reconstructions, we quantified the baseline level of beta activity (15-30Hz), the post-movement beta rebound (PMBR), beta event-related desynchronisation (beta-ERD) and movement-related gamma synchronisation (MRGS) (60-90Hz). Our results demonstrated that tiagabine, and hence elevated endogenous GABA levels causes, an elevation of baseline beta power, enhanced beta-ERD and reduced PMBR, but no modulation of MRGS. Comparing our results to recent literature (Hall et al., 2011) we suggest that beta-ERD may be a GABAA receptor mediated process while PMBR may be GABAB receptor mediated.