Brain communications最新文献

[This corrects the article DOI: 10.1093/braincomms/fcad210.].

Epilepsy is an archetypal brain network disorder characterized by recurrent seizures and associated psychological, cognitive and behavioural sequelae. Progressive brain network dysfunction may contribute to poorer outcomes following treatment, but this has never been tested in humans. In this structural connectomics pilot study, we assess whether there is progressive brain network dysfunction in a cohort of 23 children undergoing repeated multi-shell diffusion tensor imaging as part of their pre-surgical evaluation of focal epilepsy prior to epilepsy surgery. We analyse global and nodal graph metrics and thalamocortical connectivity, comparing the longitudinal changes to a cross-sectional cohort of 57 healthy controls. We identify no robust longitudinal changes in global or nodal network properties over a median of 1.15 years between scans. We also do not identify robust longitudinal changes in thalamic connectivity between scans. On sensitivity analyses, we identify increases in weighted degree at higher scales of brain parcellation and a decrease in the proportion of nodes with a low participation coefficient, suggesting progressive increases in intermodular connections. These findings of no or subtle structural longitudinal brain network changes over a relatively short timeframe indicate that either there are no progressive structural brain network changes over time in epilepsy or the changes appear over longer timescales. Larger studies with longer timeframes between scans may help clarify these findings.

Anti-seizure medications are the primary treatment for epilepsy; yet medication tapering effects have not been investigated in a dose, region and time-dependent manner, despite their potential impact on research and clinical practice. We examined over 3000 h of intracranial EEG recordings in 32 subjects during long-term monitoring, of which 22 underwent concurrent anti-seizure medication tapering. We estimated anti-seizure medication plasma levels based on known pharmaco-kinetics of all the major anti-seizure medication types. We found an overall decrease in the power of delta band (δ) activity around the period of maximum medication withdrawal in most (80%) subjects, independent of their epilepsy type or medication combination. The degree of withdrawal correlated positively with the magnitude of δ power decrease. This dose-dependent effect was evident across all recorded cortical regions during daytime; but not in subcortical regions, or during night time. We found no evidence of a differential effect in seizure onset, spiking, or pathological brain regions. The finding of decreased δ band power during anti-seizure medication tapering agrees with previous literature. Our observed dose-dependent effect indicates that monitoring anti-seizure medication levels in cortical regions may be feasible for applications such as medication reminder systems, or closed-loop anti-seizure medication delivery systems. Anti-seizure medications are also used in other neurological and psychiatric conditions, making our findings relevant to a general neuroscience and neurology audience.

The glymphatic system may play a central role in cognitive impairment associated with Parkinson's disease, but its relationship with regional cortical atrophy is not fully explored. To explore associations among glymphatic dysfunction, regional cortical degeneration and cognitive impairment in Parkinson's disease participants, we evaluated 51 participants with documented Parkinson's disease (28 men; age, 61.65 ± 8.27 years) and 30 age- and sex-matched normal controls (11 men; age, 59.2 ± 5.90 years) who underwent 3.0-T MRI of the brain, including high-resolution T1-weighted imaging and diffusion-tensor imaging along the perivascular space as a surrogate for glymphatic flow. Cortical grey matter volume was segmented automatically based on three-dimensional T1-weighted sequences. Cognitive function was assessed by Mini-Mental State Examination. The relationship between glymphatic dysfunction, cognitive decline and regional cortical degeneration was explored. The participants with Parkinson's disease revealed lower diffusion-tensor imaging along the perivascular space (1.45 ± 0.17 versus 1.64 ± 0.17, P < 0.0001) as compared with normal controls, indicating disturbed glymphatic flow. Glymphatic dysfunction was associated with cognitive scores (r = 0.54, P = 0.003). Diffusion-tensor imaging along the perivascular space values were positively associated with the volume of specific cortical regions (all P-values <0.05) including the temporal pole, posterior orbital gyrus, orbital part of the inferior frontal gyrus, frontal operculum, central operculum and anterior cingulate gyrus. Mediation analysis within the Parkinson's disease participants indicated that the relationship between glymphatic dysfunction and cognitive scores was partially mediated by the integrity of orbital part of the inferior frontal gyrus and anterior cingulate gyrus. Glymphatic dysfunction is associated with cognitive decline in Parkinson's disease, whereas the distribution of regional cortical degeneration may constitute the link between glymphatic dysfunction and cognitive impairment.

Multiple sclerosis is an inflammatory demyelinating condition of the central nervous system affecting approximately 1 million people in the USA. Although standard structural MRI techniques are now the main imaging modality for multiple sclerosis diagnosis and management, they are yet to provide information regarding the metabolic profile of the disease. Ultra-high field 7T MRI systems have provided gains in signal-to-noise ratio (SNR) and spatial resolution for structural MRI as well as larger chemical shifts leading to improvements in specialized imaging sequences, such as nuclear Overhauser effect (NOE) imaging, that can evaluate macromolecular metabolite composition. In this work, NOE images were acquired on a cohort of multiple sclerosis and healthy control subjects to spatially map differences in their lipid metabolites as a result of NOE effects. NOE image data were acquired on a total of 25 subjects {15 multiple sclerosis subjects [10 females, 5 males (21-70 years)] and 10 healthy controls [5 females, 5 males (23-71 years)]} on a 7T MRI system with a frequency offset range of -5 to 5 ppm. A five-pool Lorentzian line fitting model was utilized to fit and quantitatively compare direct saturation (DS), magnetization transfer (MT), amide proton transfer (APT), amine, and relayed NOE (rNOE) and used as a comparison to conventional T₁ maps. Grey and white matter tissues were segmented using the T₁ maps, while the lesion tissue was segmented manually. Correlations between disease duration and lesion load were performed to investigate any existing relationship to image contrast. The primary findings of this work include statistically significant decreases in the rNOE pool for the normal-appearing white matter (NAWM) (11.4% decrease) and normal-appearing grey matter (NAGM) (10.6% decrease) in multiple sclerosis subjects compared to healthy controls. Additionally, a significant decrease in the amine pool was also observed for NAWM (15.3% decrease) in multiple sclerosis subjects compared to healthy controls. Changes in multiple sclerosis lesion contrast were also observed for several pools (DS, amine, and rNOE). Decreases in both the rNOE and amine pools suggest that in multiple sclerosis, there are diffuse decreases in mobile lipids, such as those found in neuronal cell bodies, as well as a decrease in proteins with amine groups. Furthermore, these measurable contrast changes were not detected in the corresponding T₁ maps. NOE imaging can provide complementary metabolic information to conventional MRI methods. Future studies will focus on utilizing this technique for longitudinal tracking of disease progression and investigating similar demyelinating diseases.

This scientific commentary refers to 'Retinal microstructure and microvasculature in association with brain amyloid burden', by Egle et al. (https://doi.org/10.1093/braincomms/fcaf013).

Transcranial direct current stimulation shows promise as a non-invasive therapeutic method for patients with focal drug-resistant epilepsy. However, there is considerable variability in individual responses to transcranial direct current stimulation, and the factors influencing treatment effectiveness in targeted regions are not well understood. We aimed to assess how the extent and depth of the epileptogenic zone and associated networks impact patient responses to transcranial direct current stimulation therapy. We conducted a retrospective analysis of stereoelectroencephalography data from 23 patients participating in a personalized multichannel transcranial direct current stimulation protocol. We evaluated the extent and depth of the epileptogenic zone network, propagation zone network, and the combined network of the entire epileptogenic and propagation zones, correlating these factors with clinical response measured by the reduction in seizure frequency following repeated transcranial direct current stimulation sessions. Among the patients, 10 (43.5%) were classified as responders (R), experiencing a significant (>50%) decrease in seizure frequency, while 13 were non-responders, showing minimal improvement or increased seizure frequency. Importantly, we found a significant positive correlation between the extent of the epileptogenic zone network and changes in seizure frequency. A smaller epileptogenic zone network extent was associated with better transcranial direct current stimulation efficacy, with responders demonstrating a significantly smaller epileptogenic and propagation zones compared with non-responders. Additionally, non-responders tended to have a significantly deeper epileptogenic zone network compared with responders. Our results highlight the significant impact of the extent and depth of the epileptogenic zone network on transcranial direct current stimulation efficacy in patients with refractory focal epilepsy. Responders typically exhibited a smaller and shallower epileptogenic zone network compared with non-responders. These findings suggest that utilizing individualized epileptogenic zone network characteristics could help refine patient selection for personalized transcranial direct current stimulation protocols, potentially improving therapeutic outcomes.

Cortical amyloid burden is associated with neuronal and vascular abnormalities. The retina shares significant structural and physiological similarities with the brain. This study assessed the association of retinal microstructural and microvascular signs with cortical amyloid burden in the prospective Atherosclerosis Risk in Communities-Positron Emission Tomography study. One hundred and twenty-four participants without a diagnosis of dementia underwent florbetapir PET (2011-13) and optical coherence tomography and optical coherence tomography angiography imaging (2017-19). Retinal nerve fibre thickness, total macular thickness and the ganglion cell-inner plexiform layer thickness were derived from the optical coherence tomography scan. Vessel density and the foveal avascular zone were measured on the 3 × 3 mm² optical coherence tomography angiography scan. Amyloid burden, defined by global cortical standardized uptake value ratio, was treated as a dichotomous (standardized uptake value ratio > 1.2) and continuous outcome measure in logistic and robust linear regression models, respectively. Only lower intermediate capillary plexus vessel density [β (95% confidence interval) = -0.05 (-0.12, -0.01)] was significantly associated with increased continuous amyloid standardized uptake value ratio but not elevated dichotomous amyloid burden independently of demographic, genetic and vascular risk factors. No other retinal measure showed a significant association. Microvascular signs may accompany greater amyloid burden in late life in individuals without dementia.