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Objective: Paramagnetic rim lesions (PRLs) are a biomarker of chronic active lesions (CALs), and an important driver of neurological disability in multiple sclerosis (MS). The reason subtending some acute lesions evolvement into CALs is not known. Here we ask whether a relatively lower oxygen content is linked to CALs. Methods: In this prospective cross‐sectional study, 64 people with multiple sclerosis (PwMS), clinically isolated syndrome and radiologically isolated syndrome underwent a 7.0 Tesla (7 T) brain magnetic resonance imaging (MRI). The scanning protocol included a T2‐w fluid‐attenuated inversion recovery (FLAIR), and a single echo gradient echo from which susceptibility‐weighted imaging (SWI) was derived. WM lesions were identified on the T2‐w‐FLAIR whilst PRLs were identified on the SWI sequence. T2‐lesions were classified as PRLs and rimless lesions (PRLs‐). We registered a universal vascular atlas to each subject's T2‐w‐FLAIR and classified each T2‐lesions according to its location into watershed‐ (ws), non‐watershed‐ (nws), and mixed‐lesion (m). Ws‐lesions were defined as lesions that were fully located in a region between the territories of two major arteries. Results: Out of 1,975 T2‐lesions, 88 (4.5%) were PRLs. Ws‐regions had a higher number (p = 0.005) and proportion (p < 0.001) of PRLs‐ compared to nws‐regions. Ws‐PRL‐ were larger compared to nws‐ones (p = 0.009). The number (p = 0.043) and proportion (p < 0.001) of PRLs was higher in ws‐regions compared to nws‐ones. Ws‐PRLs were not significantly larger than nws‐ones (p = 0.195). Interpretation: We propose the novel concept of a link between arterial vascularization and chronic activity in MS by demonstrating a preferential localization of CALs in ws‐territories. [ABSTRACT FROM AUTHOR]

Cerebrovascular disease (CVD) remains a leading cause of death and the leading cause of adult disability in most developed countries. This work summarizes state-of-the-art, and possible future, diagnostic and evaluation approaches in multiple stages of CVD, including (i) visualization of sub-clinical disease processes, (ii) acute stroke theranostics, and (iii) characterization of post-stroke recovery mechanisms. Underlying pathophysiology as it relates to large vessel steno-occlusive disease and the impact of this macrovascular disease on tissue-level viability, hemodynamics (cerebral blood flow, cerebral blood volume, and mean transit time), and metabolism (cerebral metabolic rate of oxygen consumption and pH) are also discussed in the context of emerging neuroimaging protocols with sensitivity to these factors. The overall purpose is to highlight advancements in stroke care and diagnostics and to provide a general overview of emerging research topics that have potential for reducing morbidity in multiple areas of CVD.

Purpose: Axillary lymph nodes (LNs) often present a reservoir for metastatic breast cancer, yet metastatic LN involvement cannot be discerned definitively using diagnostic imaging. This study investigated whether in vivo CEST may discriminate LNs with versus without metastatic involvement. Methods: 3T MRI was performed in patients with breast cancer before clinically‐indicated mastectomy or lumpectomy with LN removal, after which LN metastasic involvement was determined using histological evaluation. Non‐contrast anatomical imaging, as well as B0 and B1 field maps, were acquired in sequence with three‐point CEST‐Dixon (3D turbo‐gradient‐echo; factor = 25; TR/TE1/ΔTE = 851/1.35/1.1 ms; spatial‐resolution = 2.5 × 2.5 × 6 mm; slices = 10; four sinc‐gauss pulses with duty‐cycle = 0.5, total saturation duration = 701.7 ms; B1 = 1.5 μT; saturation offsets = −5.5 to +5.5 ppm; stepsize = 0.2 ppm; scan duration = 6 min 30 s). The mean z‐spectrum from LNs with (n = 20) versus without (n = 22) metastatic involvement were analyzed and a Wilcoxon rank‐sum test (significance: p < 0.05) was applied to evaluate differences in B0, B1, and magnetization transfer ratio (MTR) in differing spectral regions of known proton exchange (nuclear Overhauser effect [NOE], amide, amine, and hydroxyl) between cohorts. Results: No difference in axillary B1 (p = 0.634) or B0 (p = 0.689) was observed between cohorts. Elevated MTR was observed for the NOE (−1.7 ppm; MTR = 0.285 ± 0.075 vs. 0.248 ± 0.039; p = 0.048), amine (+2.5 ppm; MTR = 0.284 ± 0.067 vs. 0.234 ± 0.31; p = 0.005), and hydroxyl (+1 ppm; MTR = 0.394 ± 0.075 vs. 0.329 ± 0.055; p = 0.002) protons in LNs from participants with versus without metastatic involvement. Conclusions: Findings are consistent with a unique metastatic LN microenvironment detectable by CEST‐Dixon and suggest that CEST MRI may have potential for mapping LN metastasis non‐invasively in vivo. [ABSTRACT FROM AUTHOR]

Background: National survey data exploring the patient experience with lipedema are lacking. Methods: We conducted national surveys from 2016 to 2022 of women with lipedema as well as female controls. Surveys collected information on symptomatology, pain, and therapies. We performed logistic regression comparing symptoms among those with lipedema versus controls adjusting for age and BMI. Results: A total of 707 women with lipedema and 216 controls completed the surveys. Those with lipedema had a mean age of 48.6 years and mean BMI of 40.9 kg/m2. Lipedema symptom onset occurred frequently at puberty (48.0%) or pregnancy (41.2%). Compared to controls, women with lipedema were more likely to report leg swelling in heat (odds ratio [OR], 66.82; 95% CI, 33.04–135.12; p < 0.0001), easy bruising (OR, 26.23; 95% CI, 15.58–44.17; p < 0.0001), altered gait (OR, 15.54; 95% CI, 7.58–31.96; p < 0.0001), flu-like symptoms (OR, 12.99; 95% CI, 4.27–39.49; p < 0.0001), joint hypermobility (OR, 12.88; 95% CI, 6.68–24.81; p < 0.0001), cool skin (OR, 12.21; 95% CI, 5.20–28.69; p < 0.0001), varicose veins (OR, 11.29; 95% CI, 6.71–18.99; p < 0.0001), and fatigue (OR, 9.59; 95% CI, 6.10–15.09; p < 0.0001). Additionally, 70.3% had upper arm involvement, 21.2% reported foot swelling, and 16.6% reported foot pain. Most (52.2%) reported no symptom improvement with diet or exercise. Common therapies used included compression therapy (45.0%), gastric bypass (15.7%), and lower-extremity liposuction (14.0%). Conclusion: In a large, national, symptom survey, women with lipedema reported excess pain, swelling, and fat in the legs along with numerous symptoms beyond those classically described. Symptom responses to common therapies remain understudied. [ABSTRACT FROM AUTHOR]

Background and Purpose: Choroid plexus (ChP) hyperemia has been observed in patients with intracranial vasculopathy and to reduce following successful surgical revascularization. This observation may be attributable to impaired vascular reserve of the ChP or other factors, such as the ChP responding to circulating markers of stress. We extend this work to test the hypothesis that vascular reserve of the ChP is unrelated to intracranial vasculopathy. Methods: We performed hypercapnic reactivity (blood oxygenation level‐dependent; echo time = 35 ms; spatial resolution = 3.5 × 3.5 × 3.5 mm, repetition time = 2000 ms) and catheter angiography assessments of ChP reserve capacity and vascular patency in moyamoya patients (n = 53) with and without prior surgical revascularization. Time regression analyses quantified maximum cerebrovascular reactivity and reactivity delay time in ChP and cortical flow territories of major intracranial vessels with steno‐occlusion graded as <70%, 70%‐99%, and occlusion using Warfarin‐Aspirin‐Symptomatic‐Intracranial‐Disease stenosis grading criteria. Analysis of variance (significance: two‐sided Bonferroni‐corrected p <.05) was applied to evaluate cortical and ChP reactivity, after accounting for end‐tidal carbon dioxide change, for differing vasculopathy categories. Results: In patients without prior revascularization, arterial vasculopathy was associated with reduced cortical reactivity and lengthened reactivity delay (p ≤.01), as expected. Regardless of surgical history, the ChP reactivity metrics were not significantly related to the degree of proximal stenosis, consistent with ChP reactivity being largely preserved in this population. Conclusions: Findings are consistent with ChP reactivity in moyamoya not being dependent on observed vasculopathy. Future work may investigate the extent to which ChP hyperemia in chronic ischemia reflects circulating markers of glial or ischemic stress. [ABSTRACT FROM AUTHOR]

Impulsivity is a behavioral trait that is elevated in many neuropsychiatric disorders. Parkinson's disease (PD) patients can exhibit a specific pattern of reward-seeking impulsive-compulsive behaviors (ICBs), as well as more subtle changes to generalized trait impulsivity. Prior studies in healthy controls (HCs) suggest that trait impulsivity is regulated by D2/3 autoreceptors in mesocorticolimbic circuits. While altered D2/3 binding is noted in ICB+ PD patients, there is limited prior assessment of the trait impulsivity-D2/3 relationship in PD, and no prior direct comparison with patterns in HCs. We examined 54 PD (36 M; 18F) and 31 sex- and agematched HC (21 M; 10 F) subjects using [18F]fallypride, a high-affinity D2/3 receptor ligand, to measure striatal and extrastriatal D2/3 nondisplaceable binding potential (BPND). Subcortical and cortical assessment exclusively used ROI or exploratory-voxelwise methods, respectively. All completed the Barratt Impulsiveness Scale, a measure of trait impulsivity. Subcortical ROI analyses indicated a negative relationship between trait impulsivity and D2/3 BPND in the ventral striatum and amygdala of HCs but not in PD. By contrast, voxelwise methods demonstrated a positive trait impulsivity-D2/3 BPND correlation in ventral frontal olfactocentric-paralimbic cortex of subjects with PD but not HCs. Subscale analysis also highlighted different aspects of impulsivity, with significant interactions between group and motor impulsivity in the ventral striatum, and attentional impulsivity in the amygdala and frontal paralimbic cortex. These results suggest that dopamine functioning in distinct regions of the mesocorticolimbic circuit influence aspects of impulsivity, with the relative importance of regional dopamine functions shifting in the neuropharmacological context of PD. [ABSTRACT FROM AUTHOR]