Background: Dementia can be caused by numerous different diseases that present variable clinical courses and reveal multiple patterns of brain atrophy, making its accurate early diagnosis by conventional examinative means challenging. Although highly accurate and powerful, magnetic resonance imaging (MRI) currently plays only a supportive role in dementia diagnosis, largely due to the enormous volume and diversity of data it generates. AI-based software solutions/algorithms that can perform automated segmentation and volumetry analyses of MRI data are being increasingly used to address this issue. Numerous commercial and non-commercial software solutions for automated brain segmentation and volumetry exist, with FreeSurfer being the most frequently used.Objectives: This Review is an account of the current situation regarding the application of automated brain segmentation and volumetry to dementia diagnosis.Methods: We performed a PubMed search for “FreeSurfer AND Dementia” and obtained 493 results. Based on these search results, we conducted an in-depth source analysis to identify additional publications, software tools, and methods. Studies were analyzed for design, patient collective, and for statistical evaluation (mathematical methods, correlations).Results: In the studies identified, the main diseases and cohorts represented were Alzheimer’s disease (n = 276), mild cognitive impairment (n = 157), frontotemporal dementia (n = 34), Parkinson’s disease (n = 29), dementia with Lewy bodies (n = 20), and healthy controls (n = 356). The findings and methods of a selection of the studies identified were summarized and discussed.Conclusion: Our evaluation showed that, while a large number of studies and software solutions are available, many diseases are underrepresented in terms of their incidence. There is therefore plenty of scope for targeted research.

Acute sleep deprivation is known to impair vigilance performance and alter brain physiology. This study investigates structural, physiological and cognitive effects of one night of sleep deprivation (SD) and subsequent recovery. Thirty healthy participants underwent (18M/12F, mean age 28.0 ± 4.7 years, range 20-38) a multimodal assessment including 7T MRI, plasma biomarker analysis, and Psychomotor Vigilance Task (PVT) testing at three time points: baseline, after 24 h of SD, and following a 72-h recovery period. Our results demonstrate that SD induced a significant increase in total perivascular space (PVS) volume (from 6711.5 mm³ to 7475.3 mm³; p < 0.001), a marker of impaired glymphatic function, which completely normalized after recovery. These macrostructural changes were accompanied by reversible microstructural alterations, including decreased T1 relaxation times and shifts in quantitative susceptibility mapping (QSM) in multiple brain regions, indicative of dynamic fluid shifts. Systemically, SD led to an increase in pro-inflammatory markers, notably MMP-9 (from 52.3 pg/mL to 69.2 pg/mL; p < 0.05), and changes in multiple peripheral biomarkers. Behaviorally, participants exhibited significantly more attentional lapses (slowest 10 % RT: 386.4 ms-410 ms; p < 0.05), which were also reversed upon recovery. In conclusion, a single night of SD triggers a cascade of interconnected and fully reversible physiological changes, likely initiated by transient glymphatic disruption. Healthy individuals are able to recover mostly from one night of SD, suggesting that adverse effects of SD, when not in a chronic state, can potentially be reversed.

Early and late. In the early subacute phase, infarct edema occurs, which can lead to compression of healthy brain tissue and a midline shift. In the late phase, this edema regresses. Discussion An older definition describes an acute stroke as the first 24 h after symptom onset, a subacute stroke as the phase between day 1 and day 5, and a stroke older than 5 days as chronic [2]. Another definition describes an early hyperacute phase (0-6 h), a late hyperacute phase (6-24 h), an acute phase (1-7 days), as subacute phase (1-3 weeks) and a chronic phase (> 3 weeks) [3]. If you look through the definition, statements [4, 5] and guidelines [6-8], you won't get any wiser. In order to create clear definitions in these papers, mixed terms such as "acute stroke < 6 hours" or "acute stroke < 4.5 hours" are often used. The question is also who should set and name these times in the interdisciplinary competition. In our opinion, it's actually quite clear: only the imaging. Due to the individual compensation possibilities for different collaterals and anatomical variants of the patients, one cannot and should not set a fixed time for the stages of the stroke. For example, a recent prospective study found a Diffusion-Weighted Imaging (DWI)-Fluid-Attenuated Inversion Recovery (FLAIR) mismatch in 52.6% of patients between 4.5 and 10 h after symptom onset [9]. This indicates that an active or acute infarction process is ongoing at this time, and under certain circumstances, a thrombectomy might still be considered appropriate. For this reason, the nomenclature of the phase of a stroke should be strictly based on imaging to accelerate interventions and simplify interdisciplinary

Purpose: High-resolution multislice CT (HR-MSCT) and cone beam CT (CBCT) are commonly used for preoperative temporal bone imaging, with HR-MSCT often preferred due to its shorter scan duration and lower susceptibility to motion artifacts. However, recent advancements in accelerated flat panel CT (Acc-FPCT) available with the latest generation angiography systems have addressed traditional limitations of CBCT by significantly decreasing scan time. This cadaver-based study evaluates the diagnostic performance and radiation dose of Acc-FPCT compared to HR-MSCT in preoperative temporal bone imaging. Methods: Six different Acc-FPCT protocols were acquired on five whole-head cadaveric specimens (ten temporal bones). Three neuroradiologists experienced in temporal bone imaging assessed the image quality of Acc-FPCT protocols in comparison to that of HR-MSCT for the visualization of 31 landmarks of middle and inner ear using a 5-point Likert scale. We also compared radiation dose parameters (CT dose index and dose length product) among the protocols. Results: Two high-Resolution Acc-FPCT protocols were found to be superior to HR-MSCT by all raters (p < 0.001). There were no significant differences between the two HR-FPCT protocols (p = 0.25). The remaining Acc-FPCT protocols were rated significantly inferior to HR-MSCT. The inter-rater reliability was excellent (ICC (2,k) = 0.925; CI [0.92–0.93]). The dose length product was significantly lower in all Acc-FPCT protocols compared to HR-MSCT. Conclusion: The results of our cadaver-based study highlight the utility of certain Acc-FPCT protocols as a viable alternative to HR-MSCT in preoperative temporal bone imaging, improving the visualization of critical anatomical landmarks without increasing radiation exposure.

Objective: In patients with non-lesional epilepsy, MR imaging detects no structural or functional abnormalities. The aim of this study was to determine whether subtle local reductions or increases in brain volume, undetectable to the human eye, can indicate an epileptic focus directly or indirectly. To address this, we performed brain volumetry using 7T MRI. Methods: We evaluated 7T MRI in patients with non-lesional epilepsy as part of a retrospective study and a healthy control cohort from another prospective study. FastSurfer segmentations were performed using T1 MPRAGE. Additionally, we also performed volumetry of the hippocampal subfields, the thalamic nuclei and the brainstem. We created a control group matched for age and gender distribution. Results: 7T segmentation as described above was possible in 14 patients with epilepsy and 27 participants of a control cohort. We detected a significant volume loss in the ipsilateral central lateral nucleus of thalamus, as well as a significant increase in the presubiculum body and the ipsilateral and contralateral entorhinal and medial orbitofrontal cortices. Conclusion: High-resolution 7T MRI-based volumetric analysis in patients with non-lesional epilepsy revealed significant atrophy in brain regions commonly implicated in epileptogenesis. These structures exhibited strong sensitivity and specificity, highlighting the potential of volumetry as a diagnostic tool in the absence of visible lesions. Validation in larger, independent cohorts is required to confirm these findings and assess clinical applicability.

Is microcatheter-associated plastic debris the primary cause of non-ischemic cerebral enhancing (NICE) lesions in endovascular procedures?