Longitudinal Cortical Thickness Research Articles

Effects of electroconvulsive therapy on cortical thickness in depression: a systematic review.

Electroconvulsive therapy (ECT) is one of the most studied and validated available treatments for severe or treatment-resistant depression. However, little is known about the neural mechanisms underlying ECT. This systematic review aims to critically review all structural magnetic resonance imaging studies investigating longitudinal cortical thickness (CT) changes after ECT in patients with unipolar or bipolar depression. We performed a search on PubMed, Medline, and Embase to identify all available studies published before April 20, 2023. A total of 10 studies were included. The investigations showed widespread increases in CT after ECT in depressed patients, involving mainly the temporal, insular, and frontal regions. In five studies, CT increases in a non-overlapping set of brain areas correlated with the clinical efficacy of ECT. The small sample size, heterogeneity in terms of populations, comorbidities, and ECT protocols, and the lack of a control group in some investigations limit the generalisability of the results. Our findings support the idea that ECT can increase CT in patients with unipolar and bipolar depression. It remains unclear whether these changes are related to the clinical response. Future larger studies with longer follow-up are warranted to thoroughly address the potential role of CT as a biomarker of clinical response after ECT.

Cortical growth from infancy to adolescence in preterm and term-born children.

Early life experiences can exert a significant influence on cortical and cognitive development. Very preterm birth exposes infants to several adverse environmental factors during hospital admission, which affect cortical architecture. However, the subsequent consequence of very preterm birth on cortical growth from infancy to adolescence has never been defined; despite knowledge of critical periods during childhood for establishment of cortical networks. Our aims were to: chart typical longitudinal cortical development and sex differences in cortical development from birth to adolescence in healthy term-born children; estimate differences in cortical development between children born at term and very preterm; and estimate differences in cortical development between children with normal and impaired cognition in adolescence. This longitudinal cohort study included children born at term (≥37 weeks' gestation) and very preterm (<30 weeks' gestation) with MRI scans at ages 0, 7 and 13 years (n = 66 term-born participants comprising 34 with one scan, 18 with two scans and 14 with three scans; n = 201 very preterm participants comprising 56 with one scan, 88 with two scans and 57 with three scans). Cognitive assessments were performed at age 13 years. Cortical surface reconstruction and parcellation were performed with state-of-the-art, equivalent MRI analysis pipelines for all time points, resulting in longitudinal cortical volume, surface area and thickness measurements for 62 cortical regions. Developmental trajectories for each region were modelled in term-born children, contrasted between children born at term and very preterm, and contrasted between all children with normal and impaired cognition. In typically developing term-born children, we documented anticipated patterns of rapidly increasing cortical volume, area and thickness in early childhood, followed by more subtle changes in later childhood, with smaller cortical size in females than males. In contrast, children born very preterm exhibited increasingly reduced cortical volumes, relative to term-born children, particularly during ages 0-7 years in temporal cortical regions. This reduction in cortical volume in children born very preterm was largely driven by increasingly reduced cortical thickness rather than area. This resulted in amplified cortical volume and thickness reductions by age 13 years in individuals born very preterm. Alterations in cortical thickness development were found in children with impaired language and memory. This study shows that the neurobiological impact of very preterm birth on cortical growth is amplified from infancy to adolescence. These data further inform the long-lasting impact on cortical development from very preterm birth, providing broader insights into neurodevelopmental consequences of early life experiences.

Baseline long-term potentiation-like cortical plasticity is associated with longitudinal cortical thinning in healthy adults and in adults with bipolar disorder type II.

The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic dysfunction-related loss of synapses are potentially important mechanisms. We used long-term potentiation-like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty-two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography-based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow-up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.

Differential associations of adolescent versus young adult cannabis initiation with longitudinal brain change and behavior.

Leveraging ~10 years of prospective longitudinal data on 704 participants, we examined the effects of adolescent versus young adult cannabis initiation on MRI-assessed cortical thickness development and behavior. Data were obtained from the IMAGEN study conducted across eight European sites. We identified IMAGEN participants who reported being cannabis-naïve at baseline and had data available at baseline, 5-year, and 9-year follow-up visits. Cannabis use was assessed with the European School Survey Project on Alcohol and Drugs. T1-weighted MR images were processed through the CIVET pipeline. Cannabis initiation occurring during adolescence (14-19 years) and young adulthood (19-22 years) was associated with differing patterns of longitudinal cortical thickness change. Associations between adolescent cannabis initiation and cortical thickness change were observed primarily in dorso- and ventrolateral portions of the prefrontal cortex. In contrast, cannabis initiation occurring between 19 and 22 years of age was associated with thickness change in temporal and cortical midline areas. Follow-up analysis revealed that longitudinal brain change related to adolescent initiation persisted into young adulthood and partiallymediated the association between adolescent cannabis use and past-month cocaine, ecstasy, and cannabis use at age 22. Extent of cannabis initiation during young adulthood (from 19 to 22 years) had an indirect effect on psychotic symptoms at age 22 through thickness change in temporal areas. Results suggest that developmental timing of cannabis exposure may have a marked effect on neuroanatomical correlates of cannabis use as well as associated behavioral sequelae. Critically, this work provides a foundation for neurodevelopmentally informed models of cannabis exposure in humans.

Predicting cortical thickness with [18F]flortaucipir PET: A longitudinal MRI study

AbstractBackgroundThe association between tau pathology and neurodegeneration (atrophy) in Alzheimer’s disease (AD) is not fully understood. This study aimed to investigate whether tau pathology is associated with concurrent and longitudinal cortical thickness in individuals along the AD continuum.MethodWe included 92 amyloid‐positive cognitively impaired individuals (age 65±7, 48% female, MMSE 23±4) with AD dementia (n = 73) or mild cognitive impairment due to AD (MCI, n = 19) and 61 cognitively normal individuals (CN; age 66±8, 48% female, MMSE 29±1) with subjective cognitive decline (SCD, n = 55, 19 amyloid‐positive) or healthy controls (HC, n = 6, amyloid‐status unknown). All participants underwent dynamic [18F]flortaucipir PET and structural 3T‐MRI at baseline. A subset underwent two‐year follow‐up structural 3T‐MRI (CN: n = 35, time‐interval 24±8 months; AD: n = 26; time‐interval 28±4 months). Parametric [18F]flortaucipir binding potential (BPND) images were generated using receptor parametric mapping (cerebellar gray matter reference region) to quantify tau pathology. Cortical thickness (over time) was measured using Freesurfer (version 6.0.1). Regional associations between [18F]flortaucipir BPND and cortical thickness were assessed using linear mixed models in three commonly used a priori defined regions‐of‐interest, including entorhinal, middle‐and inferior temporal, and neocortical areas. Models were adjusted for age, sex and amyloid status (in case of CN individuals).ResultFor cognitively impaired individuals, higher [18F]flortaucipir BPND (in all three regions) was associated with lower concurrent cortical thickness in the entorhinal cortex [Table‐1&amp;Fig‐1]. Higher middle‐ and inferior temporal and neocortical BPND was associated with cortical thinning over time within the same region (intra‐regionally). Higher middle‐ and inferior temporal BPND additionally showed associations with cortical thinning over time in the neocortex (inter‐regionally). For cognitively normal individuals, we found no associations between [18F]flortaucipir BPND and cortical thickness (over time) [Table‐1&amp;Figure‐1].ConclusionTau pathology is associated with both concurrent and longitudinal atrophy in a region‐specific manner in cognitively impaired individuals (MCI/AD), but not in cognitively normal individuals (HC/SCD). The regional‐specificity of these associations might suggest that there are similarities between tau‐related progression patterns and patterns of neurodegeneration. Taking into account a temporal delay between the development of region‐specific tau pathology and neurodegeneration, this potentially suggests that tau pathology is a (partial) driver of neurodegeneration in AD.

Longitudinal multi-omics alterations response to 8-week risperidone monotherapy: Evidence linking cortical thickness, transcriptomics and epigenetics

Antipsychotic treatment-related alterations of cortical thickness (CT) and clinical symptoms have been previously corroborated, but less is known about whether the changes are driven by gene expression and epigenetic modifications. Utilizing a prospective design, we recruited 42 treatment-naive first-episode schizophrenia patients (FESP) and 38 healthy controls. Patients were scanned by TI weighted imaging before and after 8-week risperidone monotherapy. CT estimation was automatically performed with the FreeSurfer software package. Participants' peripheral blood genomic DNA methylation (DNAm) status, quantified by using Infinium® Human Methylation 450K BeadChip, was examined in parallel with T1 scanning. In total, CT measures from 118 subjects and genomic DNAm status from 114 subjects were finally collected. Partial least squares (PLS) regression was used to detect the spatial associations between longitudinal CT variations after treatment and cortical transcriptomic data acquired from the Allen Human Brain Atlas. Canonical correlation analysis (CCA) was then performed to identify multivariate associations between DNAm of PLS1 genes and patients' clinical improvement. We detected the significant PLS1 component (2,098 genes) related to longitudinal alterations of CT, and the PLS1 genes were significantly enriched in neurobiological processes, and dopaminergic- and cancer-related pathways. Combining Laplacian score and CCA analysis, we further linked DNAm of 33 representative genes from the 2,098 PLS1 genes with patients' reduction rate of clinical symptoms. This study firstly revealed that changes of CT and clinical behaviors after treatment may be transcriptionally and epigenetically underlied. We define a "three-step" roadmap which represents a vital step toward the exploration of treatment- and treatment response-related biomarkers on the basis of multiple omics rather than a single omics type as a strategy for advancing precise care.

Cortical Thickness Changes After Computerized Working Memory Training in Patients With Mild Cognitive Impairment.

BackgroundAdaptive computerized working memory (WM) training has shown favorable effects on cerebral cortical thickness as compared to non-adaptive training in healthy individuals. However, knowledge of WM training-related morphological changes in mild cognitive impairment (MCI) is limited.ObjectiveThe primary objective of this double-blind randomized study was to investigate differences in longitudinal cortical thickness trajectories after adaptive and non-adaptive WM training in patients with MCI. We also investigated the genotype effects on cortical thickness trajectories after WM training combining these two training groups using longitudinal structural magnetic resonance imaging (MRI) analysis in Freesurfer.MethodMagnetic resonance imaging acquisition at 1.5 T were performed at baseline, and after four- and 16-weeks post training. A total of 81 individuals with MCI accepted invitations to undergo 25 training sessions over 5 weeks. Longitudinal Linear Mixed effect models investigated the effect of adaptive vs. non-adaptive WM training. The LME model was fitted for each location (vertex). On all statistical analyzes, a threshold was applied to yield an expected false discovery rate (FDR) of 5%. A secondary LME model investigated the effects of LMX1A and APOE-ε4 on cortical thickness trajectories after WM training.ResultsA total of 62 participants/patients completed the 25 training sessions. Structural MRI showed no group difference between the two training regimes in our MCI patients, contrary to previous reports in cognitively healthy adults. No significant structural cortical changes were found after training, regardless of training type, across all participants. However, LMX1A-AA carriers displayed increased cortical thickness trajectories or lack of decrease in two regions post-training compared to those with LMX1A-GG/GA. No training or training type effects were found in relation to the APOE-ε4 gene variants.ConclusionThe MCI patients in our study, did not have improved cortical thickness after WM training with either adaptive or non-adaptive training. These results were derived from a heterogeneous population of MCI participants. The lack of changes in the cortical thickness trajectory after WM training may also suggest the lack of atrophy during this follow-up period. Our promising results of increased cortical thickness trajectory, suggesting greater neuroplasticity, in those with LMX1A-AA genotype need to be validated in future trials.

The maturation and cognitive relevance of structural brain network organization from early infancy to childhood

The interactions of brain regions with other regions at the network level likely provide the infrastructure necessary for cognitive processes to develop. Specifically, it has been theorized that in infancy brain networks become more modular, or segregated, to support early cognitive specialization, before integration across networks increases to support the emergence of higher-order cognition. The present study examined the maturation of structural covariance networks (SCNs) derived from longitudinal cortical thickness data collected between infancy and childhood (0–6 years). We assessed modularity as a measure of network segregation and global efficiency as a measure of network integration. At the group level, we observed trajectories of increasing modularity and decreasing global efficiency between early infancy and six years. We further examined subject-based maturational coupling networks (sbMCNs) in a subset of this cohort with cognitive outcome data at 8–10 years, which allowed us to relate the network organization of longitudinal cortical thickness maturation to cognitive outcomes in middle childhood. We found that lower global efficiency of sbMCNs throughout early development (across the first year) related to greater motor learning at 8–10 years. Together, these results provide novel evidence characterizing the maturation of brain network segregation and integration across the first six years of life, and suggest that specific trajectories of brain network maturation contribute to later cognitive outcomes.

Probable REM sleep behavior disorder is associated with longitudinal cortical thinning in Parkinson\u2019s disease

REM sleep behavior disorder (RBD) has a poor prognostic implication in both motor and non-motor functions in Parkinson’s disease (PD) patients. However, to the best of our knowledge no study to date investigated the longitudinal cerebral changes underlying RBD symptoms in PD. We performed the longitudinal study to investigate the association between probable RBD and cortical and subcortical changes in early, de novo PD patients. We studied 78 participants from the Parkinson’s Progression Marker Initiative who underwent structural MRI at baseline and after 2 years. The presence of probable RBD (pRBD) was evaluated using the RBD screening questionnaire. We compared the cross-sectional and longitudinal cortical thickness and subcortical volume changes, between PD patients with and without pRBD. At baseline, we found bilateral inferior temporal cortex thinning in the PD-pRBD group compared with the PD-noRBD group. Longitudinally, the PD-pRBD group revealed a significant increase in the rate of thinning in the left insula compared with the PD-noRBD group, and the increased thinning correlated with decreased cognitive performance. In subcortical volume analyses, the presence of pRBD was linked with volume decrease over time in the left caudate nucleus, pallidum and amygdala. The volume changes in the left caudate nucleus revealed correlations with global cognition. These results support the idea that RBD is an important marker of rapid progression in PD motor and non-motor symptoms and suggest that the atrophy in the left insula and caudate nucleus might be the underlying neurobiological mechanisms of the poorer prognosis in PD patients with RBD.

Differential association between tau pathology and longitudinal cortical atrophy in subtypes of Alzheimer’s disease

AbstractBackgroundTau neurofibrillary tangle pathology and cortical atrophy progress at different rates when investigated cross‐sectionally or retrospectively (LaPoint 2017). However, convergence of the two over time remains unclear, especially in the subtypes of AD, which could inform about the underlying neural mechanisms. Here, we studied the association between tau pathology with positron emission tomography (PET) and cortical atrophy with retrospective and prospective structural magnetic resonance imaging (sMRI) in Alzheimer’s disease (AD) dementia. We identified subtypes using both modalities to compare their temporal evolution.MethodsWe identified 383 participants from the ADNI database, which comprised of 30 Aβ+ AD dementia patients, 54 Aβ+ prodromal AD patients, 99 Aβ+ preclinical AD and 200 Aβ‐ healthy individuals (HC). All subjects had tau PET (AV‐1451) and concurrent sMRI (T1‐weighted). Additionally, retrospective and prospective sMRI were available. Preliminarily, we analyzed data from the AD dementia group. Tau PET and longitudinal sMRI were preprocessed to generate regional measures (Desikan 2006) of partial volume corrected standardized uptake value ratio (SUVR) (Greve 2016) and cortical volume, thickness respectively. AD subtypes were characterized by regional volumes and tau SUVR as in a previous study (Byun 2015). Four subtypes were identified: typical AD (TAD), limbic predominant (LP), hippocampal sparing (HS) and minimal atrophy (MA). We investigated the association between tau SUVR and longitudinal cortical thickness in AD dementia and the four subtypes.ResultsIn the preliminary analysis, we observed a significant negative association between tau SUVR and longitudinal cortical thickness (baseline and prospectively) in the entorhinal cortex. Significant association between tau SUVR and cortical thickness was also observed in temporal and parietal areas prospectively. Additionally, subtypes identified based on tau PET and sMRI did not always coincide at baseline, but prospective tracking was indicative of potential convergence between the two (Figure 1).ConclusionThe association of increased tau PET binding with prospective cortical thinning suggests that including prospective imaging is critical to track disease progression. Preliminary evidence suggests that the convergence between tau pathology and cortical atrophy could occur at different rates in different subtypes. Learning subtype‐specific trajectory would be valuable for the design of disease‐slowing/modifying clinical trials.

Longitudinal cortical thinning progression differs across multiple sclerosis phenotypes and is clinically relevant: A multicentre study

Background: Longitudinal evolution of cortical thickness (CTh) in different MS phenotypes has been rarely studied. Aim: To investigate the regional pattern and 1-year progression of cortical thinning in relapsing-remitting (RR) and progressive (P) MS. Methods: 3T high-resolution T1-weighted magnetic resonance imaging (MRI) was obtained from 86 patients (75 RRMS, 11 PMS) and 34 healthy controls (HC) at three European sites at baseline and 1-year follow-up. Using FreeSurfer, baseline CTh between-group differences, longitudinal CTh changes and their correlations with clinical and MRI variables were assessed. Results: Baseline frontal, parietal and sensorimotor atrophy was found in MS versus HC. Such pattern was driven by RRMS, while PMS showed additional parietal, insular and sensorimotor cortical atrophy versus RRMS. At 1-year versus baseline, additional frontal and temporal cortical thinning was detected in RRMS patients, while a widespread CTh reduction was found in PMS patients (significant at time-by-group interaction vs RRMS). In MS, baseline fronto-parietal atrophy correlated with more severe disability and higher lesion volume. Baseline inferior parietal CTh decrease and 1-year temporal cortical thinning correlated with more severe disability. Conclusion: Parieto-temporal baseline CTh abnormalities and thinning pattern over time characterized the main MS clinical phenotypes and were associated with 1-year disability worsening.

Longitudinal ComBat: A method for harmonizing longitudinal multi-scanner imaging data

While aggregation of neuroimaging datasets from multiple sites and scanners can yield increased statistical power, it also presents challenges due to systematic scanner effects. This unwanted technical variability can introduce noise and bias into estimation of biological variability of interest. We propose a method for harmonizing longitudinal multi-scanner imaging data based on ComBat, a method originally developed for genomics and later adapted to cross-sectional neuroimaging data. Using longitudinal cortical thickness measurements from 663 participants in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) study, we demonstrate the presence of additive and multiplicative scanner effects in various brain regions. We compare estimates of the association between diagnosis and change in cortical thickness over time using three versions of the ADNI data: unharmonized data, data harmonized using cross-sectional ComBat, and data harmonized using longitudinal ComBat. In simulation studies, we show that longitudinal ComBat is more powerful for detecting longitudinal change than cross-sectional ComBat and controls the type I error rate better than unharmonized data with scanner included as a covariate. The proposed method would be useful for other types of longitudinal data requiring harmonization, such as genomic data, or neuroimaging studies of neurodevelopment, psychiatric disorders, or other neurological diseases.

Longitudinal Cortical Thickness Changes in Bipolar Disorder and the Relationship to Genetic Risk, Mania, and Lithium Use

BackgroundBipolar disorder (BD) is a highly heritable psychiatric disorder characterized by episodes of manic and depressed mood states and associated with cortical brain abnormalities. Although the course of BD is often progressive, longitudinal brain imaging studies are scarce. It remains unknown whether brain abnormalities are static traits of BD or result from pathological changes over time. Moreover, the genetic effect on implicated brain regions remains unknown. MethodsPatients with BD and healthy control (HC) subjects underwent structural magnetic resonance imaging at baseline (123 patients, 83 HC subjects) and after 6 years (90 patients, 61 HC subjects). Cortical thickness maps were generated using FreeSurfer. Using linear mixed effects models, we compared longitudinal changes in cortical thickness between patients with BD and HC subjects across the whole brain. We related our findings to genetic risk for BD and tested for effects of demographic and clinical variables. ResultsPatients showed abnormal cortical thinning of temporal cortices and thickness increases in visual/somatosensory brain areas. Thickness increases were related to genetic risk and lithium use. Patients who experienced hypomanic or manic episodes between time points showed abnormal thinning in inferior frontal cortices. Cortical changes did not differ between diagnostic BD subtypes I and II. ConclusionsIn the largest longitudinal BD study to date, we detected abnormal cortical changes with high anatomical resolution. We delineated regional effects of clinical symptoms, genetic factors, and medication that may explain progressive brain changes in BD. Our study yields important insights into disease mechanisms and suggests that neuroprogression plays a role in BD.

Progressive Cortical Thinning in Patients With Focal Epilepsy

It is controversial whether epilepsy is a static or progressive disease. Evidence of progressive gray matter loss in epilepsy would support early diagnosis, rapid treatment, and early referral for surgical interventions. To demonstrate progressive cortical thinning in patients with focal epilepsy distinct from cortical thinning associated with normal aging. A case-control neuroimaging study was conducted from August 3, 2004, to January 26, 2016, among 190 patients with focal epilepsy at a tertiary epilepsy referral center (epilepsy data) and 3 independent comparison cohorts matched for age and sex (healthy volunteer data; n = 141). Two or more high-resolution T1-weighted magnetic resonance imaging scans at least 6 months apart (mean [SD] interval, 2.5 [1.6] years). Global and vertexwise rate of progressive cortical thinning. A total of 190 people with focal epilepsy (99 women and 91 men; mean [SD] age, 36 [11] years; 396 magnetic resonance imaging scans) were compared with 141 healthy volunteers (76 women and 65 men; mean [SD] age, 35 [17] years; 282 magnetic resonance imaging scans). Widespread highly significant progressive cortical thinning exceeding normal aging effects, mainly involving the bilateral temporal lobes, medial parietal and occipital cortices, pericentral gyri, and opercula, was seen in 146 individuals with epilepsy (76.8%; 95% CI, 58%-95%). The mean (SD) annualized rate of global cortical thinning in patients with epilepsy was twice the rate of age-associated thinning observed in healthy volunteers (0.024 [0.061] vs 0.011 [0.029] mm/y; P = .01). Progression was most pronounced in adults older than 55 years and during the first 5 years after the onset of seizures. Areas of accelerated cortical thinning were detected in patients with early onset of epilepsy and in patients with hippocampal sclerosis. Accelerated thinning was not associated with seizure frequency, history of generalized seizures, or antiepileptic drug load and did not differ between patients with or without ongoing seizures. Progressive atrophy in temporal (n = 101) and frontal (n = 28) lobe epilepsy was most pronounced ipsilaterally to the epileptic focus but also affected a widespread area extending beyond the focus and commonly affected the contralateral hemisphere. For patients with temporal lobe epilepsy, accelerated cortical thinning was observed within areas structurally connected with the ipsilateral hippocampus. Widespread progressive cortical thinning exceeding that seen with normal aging may occur in patients with focal epilepsy. These findings appear to highlight the need to develop epilepsy disease-modifying treatments to disrupt or slow ongoing atrophy. Longitudinal cortical thickness measurements may have the potential to serve as biomarkers for such studies.

Abstract P3-03-20: Which biopsy is preferred to stage the axilla under ultrasound guidance in early breast cancer patients: Fine-needle aspiration cytology or core needle biopsy?

Abstract Background: Preoperative axillary ultrasound (AUS) offers the potential to identify clinically axillary negative patients with axillary lymph node (ALN) metastasis directly to axillary lymph node dissection (ALND) with avoid of unnecessary sentinel lymph node biopsy (SLNB) except Z0011 candidates. Which biopsy should be preferred is pendent with lack of enough prospective studies. The purpose of our study was to compare the accuracy of ultrasound guided fine-needle aspiration cytology (FNAC) and core needle biopsy (CNB) for the designated ALN prospectively. Methods: Consecutive patients with histologically confirmed breast cancer from April, 2010 to December, 2014 were preliminary screened for our study. All the candidate patients were prospectively assessed by ipsilateral AUS before initial treatment regardless of clinical ALN status.Abnormal lymph nodes were characterized by round shape with uniform or eccentric thickening, focal bulging or irregularity of the cortex displacement, obliteration of the hilum; or total loss of recognizable lymph node architecture. If suspicious ALN was identified, both ultrasound-guided FNAC and CNB were performed for the same designated ALN.The diameter in longitudinal section, transverse section and maximum cortical thickness of the target node was recorded. When more than one abnormal lymph node was present, the most abnormal-appearing node was sampled. The target tissue for biopsy was hypoechoic thickened cortex. Patients with a positive FNAC/CNB underwent ALND, and those with a negative FNAC and CNB biopsy or without suspicious ALN by AUS underwent SLNB. The paired parameters of FNAC and CNB were compared using McNemar's exact test. Results: 705 consecutive patients were screened and 558 patients (561 axillae) underwent AUS evaluation with confirmed ALN pathological results.145 patients (146 axillae) with both FNAC and CNB were finally enrolled. Final histopathological results showed that 83.6% (122/146) were node positive (5 micro-metastases were considered negative). Sensitivity of FNAC and CNB was 67.2% (82/122) and 91.8% (112/122). Overall accuracy of FNAC and CNB was 72.6% (106/146) and 93.2% (136/146). Negative predictive value (NPV) of FNAC and CNB was 37.5% (24/64) and 70.6% (24/34). There was significant difference in sensitivity, overall accuracy and NPV between FNAC and CNB (p&amp;lt;0.001). 80.6% (29/36) FNAC negative and CNB positive patients have ALN cortical thickness of 3.3-7.2 mm. Conclusion: CNB is more sensitive and accurate than FNAC to stage the axilla under ultrasound guidance in operable breast cancer patients, especially in patients with ALN cortical thickness of 3.3-7.2 mm. Citation Format: Zhou M, Qiu J, Chen J, Hu Y, Deng Y, Zheng S. Which biopsy is preferred to stage the axilla under ultrasound guidance in early breast cancer patients: Fine-needle aspiration cytology or core needle biopsy? [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-03-20.

Logistic regression error-in-covariate models for longitudinal high-dimensional covariates.

We consider a logistic regression model for a binary response where part of its covariates are subject-specific random intercepts and slopes from a large number of longitudinal covariates. These random effect covariates must be estimated from the observed data, and therefore, the model essentially involves errors in covariates. Because of high dimension and high correlation of the random effects, we employ longitudinal principal component analysis to reduce the total number of random effects to some manageable number of random effects. To deal with errors in covariates, we extend the conditional-score equation approach to this moderate dimensional logistic regression model with random effect covariates. To reliably solve the conditional-score equations in moderate/high dimension, we apply a majorization on the first derivative of the conditional-score functions and a penalized estimation by the smoothly clipped absolute deviation. The method was evaluated through a set of simulation studies and applied to a data set with longitudinal cortical thickness of 68 regions of interest to identify biomarkers that are related to dementia transition.

Social Responsiveness Scale (SRS) in Relation to Longitudinal Cortical Thickness Changes in Autism Spectrum Disorder.

The relationship between brain development and clinical heterogeneity in autism (ASD) is unknown. This study examines the Social Responsiveness Scale (SRS) in relation to the longitudinal development of cortical thickness. Participants (N = 91 ASD, N = 56 TDC; 3-39years at first scan) were scanned up to three times over a 7-year period. Mixed-effects models examined cortical thickness in relation to SRS score. ASD participants with higher SRS scores showed regionally increased age-related cortical thinning. Regional thickness differences and reduced age-related cortical thinning were found in predominantly right lateralized regions in ASD with decreasing SRS scores over time. Our findings emphasize the importance of examining clinical phenotypes in brain-based studies of ASD.

Longitudinal Cortical Thickness Changes in Early Parkinson’s Disease Patients with Impulsive Compulsive Behaviors (P3.070)

Longitudinal Cortical Thickness Changes in Early Parkinson’s Disease Patients with Impulsive Compulsive Behaviors (P3.070)

MULTI-TASK SPARSE SCREENING FOR PREDICTING FUTURE CLINICAL SCORES USING LONGITUDINAL CORTICAL THICKNESS MEASURES.

Cortical thickness estimation performed in-vivo via magnetic resonance imaging (MRI) is an effective measure of brain atrophy in preclinical individuals at high risk for Alzheimer's disease (AD). However, the high dimensionality of individual cortical thickness data coupled with small population samples make it challenging to perform cortical thickness feature selection for AD diagnosis and prognosis. Thus far, there are very few methods that can accurately predict future clinical scores using longitudinal cortical thickness measures. In this paper, we propose an unsupervised dictionary learning algorithm, termed Multi-task Sparse Screening (MSS) that produces improved results over previous methods within this problem domain. Specifically, we formulate and solve a multi-task problem using extracted top-p significant features from the Alzheimer's Disease Neuroimaging Initiative (ADNI) longitudinal data. Empirical studies on publicly available longitudinal data from ADNI dataset (N = 2797) demonstrate improved correlation coefficients and root mean square errors, when compared to other algorithms.

Rostral anterior cingulate cortex is a structural correlate of repetitive TMS treatment response in depression

BackgroundRepetitive transcranial magnetic stimulation (rTMS) is an effective treatment for medication-refractory major depression, yet the mechanisms of action for this intervention are poorly understood. Here we investigate cerebral cortex thickness as a possible biomarker of rTMS treatment response. MethodsLongitudinal change in cortical thickness is evaluated relative to clinical outcomes across 48 participants in 2 cohorts undergoing left dorsolateral prefrontal cortex rTMS as a treatment for depression. ResultsOur results reveal changes in thickness in a region of the left rostral anterior cingulate cortex that correlate with clinical response, with this region becoming thicker in patients who respond favorably to rTMS and thinner in patients with a less favorable response. Moreover, the baseline cortical thickness in this region correlates with rTMS treatment response – those patients with thinner cortex before treatment tended to have the most clinical improvement. ConclusionsThis study is the first analysis of longitudinal cortical thickness change with rTMS as a treatment for depression with similar results across two cohorts. These results support further investigation into the use of structural MRI as a possible biomarker of rTMS treatment response.