Neuropsychological and neuroanatomical features of patients with behavioral variant Alzheimer's disease (AD): a comparison to behavioral variant frontotemporal dementia and amnestic AD groups

An understudied non-amnestic variant of Alzheimer's disease (AD), behavioral variant AD (bvAD) is associated with progressive personality, behavior, or executive dysfunction and frontal atrophy. This study characterizes the neuropsychological and neuroanatomical features associated with bvAD by comparing it to behavioral variant frontotemporal dementia (bvFTD), amnestic AD (aAD), and subjects with normal cognition. Subjects included 16 bvAD, 67 bvFTD, and 18 aAD patients, and 26 healthy controls. Compared to bvFTD, bvAD showed more significant visuospatial impairments (Rey Figure copy and recall), more irritability (Neuropsychological Inventory), and equivalent verbal memory (Philadelphia Verbal Learning Test). Compared to aAD, bvAD indicated more executive dysfunction (F-letter fluency) and better visuospatial performance. Neuroimaging analysis found that bvAD showed cortical thinning relative to bvFTD posteriorly in left temporal-occipital regions; bvFTD had cortical thinning relative to bvAD in left inferior frontal cortex. bvAD had cortical thinning relative to aAD in prefrontal and anterior temporal regions. All patient groups had lower volumes than controls in both anterior and posterior hippocampus. However, bvAD patients had higher average volume than aAD patients in posterior hippocampus and higher volume than bvFTD patients in anterior hippocampus after adjustment for age and intracranial volume. Findings demonstrated that underlying pathology mediates disease presentation in bvAD and bvFTD.

Chronic cluster headache: A study of the telencephalic and cerebellar cortical thickness

Purpose Previous studies on brain morphological alterations in chronic cluster headache revealed inconsistent findings. Method The present cross-sectional explorative study determined telencephalic and cerebellar cortex thickness alterations in a relatively wide sample of chronic cluster headache patients (n = 28) comparing them to matched healthy individuals. Results The combination of two highly robust state-of-the-art approaches for thickness estimation (Freesurfer, CERES), strengthened by functional characterization of the identified abnormal regions, revealed four main results: chronic cluster headache patients show 1) cortical thinning in the right middle cingulate cortex, left posterior insula, and anterior cerebellar lobe, regions involved in nociception's sensory and sensory-motor aspects and possibly in autonomic functions; 2) cortical thinning in the left anterior superior temporal sulcus and the left collateral/lingual sulcus, suggesting neuroplastic maladaptation in areas possibly involved in social cognition, which may promote psychiatric comorbidity; 3) abnormal functional connectivity among some of these identified telencephalic areas; 4) the identified telencephalic areas of cortical thinning present robust interaction, as indicated by the functional connectivity results, with the left posterior insula possibly playing a pivotal role. Conclusion The reported results constitute a coherent and robust picture of the chronic cluster headache brain. Our study paves the way for hypothesis-driven studies that might impact our understanding of the pathophysiology of this condition.

A Social Gradient of Cortical Thickness Relative to Age in Adolescence: Relations Among Neighborhood Socioeconomic Disadvantage, Advanced Cortical Thinning, and Depressive Symptoms

Background: Mental and physical health are affected by family and neighborhood socioeconomic status (SES). Accelerated biological aging in the context of lower SES is one mechanism that might contribute to underlying health disparities; few studies, however, have considered neighborhood SES in relation to neural markers of biological aging in adolescents. Methods: In 120 adolescents 13-18 years of age, we examined family and neighborhood SES in relation to biological aging in the brain, indexed by cortical thickness relative to chronological age. We also examined whether advanced cortical thinning relative to age was related to depressive symptoms and explored regions of interest.Results: Neighborhood socioeconomic disadvantage was uniquely associated with advanced cortical thinning in the left hemisphere (=-.20), which was related to more severe depressive symptoms (=-.33). In contrast, family income-to-needs was not significantly associated with cortical thickness age after controlling for relevant covariates. In exploratory, covariate-adjusted analyses of cortical thickness relative to age at the regional level, neighborhood socioeconomic disadvantage was associated with advanced cortical thinning in the left superior frontal gyrus (=-.27), fusiform gyrus (=-.20), and insula (=-.21). Of these regions, only advanced cortical thinning in the left superior frontal gyrus was associated with more severe depressive symptoms (=-.18). Conclusion: Our findings provide evidence for a social gradient of accelerated biological aging at the neural level during adolescence. Adolescents living in less advantaged communities have a thinner left hemisphere cortex than expected given their chronological age. Advanced cortical thinning may increase risk for depression in adolescence.

Cortical Thinning of Motor and Non-Motor Brain Regions Enables Diagnosis of Amyotrophic Lateral Sclerosis and Supports Distinction between Upper- and Lower-Motoneuron Phenotypes

Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder clinically characterized by muscle atrophy and progressive paralysis. In addition to the classical ALS affecting both the upper and lower motoneurons (UMN and LMN), other subtypes with the predominant (or even exclusive) affection of the UMN or LMN have been identified. This work sought to detect specific patterns of cortical brain atrophy in the UMN and LMN phenotypes to distinguish these two forms from the healthy state. Methods: Using high-resolution structural MRI and cortical thickness analysis, 38 patients with a diagnosis of ALS and predominance of either the UMN (n = 20) or the LMN (n = 18) phenotype were investigated. Results: Significant cortical thinning in the temporal lobe was found in both the ALS groups. Additionally, UMN patients displayed a significant thinning of the cortical thickness in the pre- and postcentral gyrus, as well as the paracentral lobule. By applying multivariate analyses based on the cortical thicknesses of 34 brain regions, ALS patients with either a predominant UMN or LMN phenotype were distinguished from healthy controls with an accuracy of 94% and UMN from LMN patients with an accuracy of 75%. Conclusions: These findings support previous hypothesis that neural degeneration in ALS is not confined to the sole motor regions. In addition, the amount of cortical thinning in the temporal lobe helps to distinguish ALS patients from healthy controls, that is, to support or discourage the diagnosis of ALS, while the cortical thickness of the precentral gyrus specifically helps to distinguish the UMN from the LMN phenotype.

Cortical Thinning and Sleep Slow Wave Activity Reductions Mediate Age-Related Improvements in Cognition During Mid-Late Adolescence

Study Objectives Gains in cognitive test performance that occur during adolescence are associated with brain maturation. Cortical thinning and reduced sleep slow wave activity (SWA) are markers of such developmental changes. Here we investigate whether they mediate age-related improvements in cognition. Methods 109 adolescents aged 15-19y (49 males) underwent magnetic resonance imaging, polysomnography (PSG) and a battery of cognitive tasks within a 2-month time window. Cognitive tasks assessed non-verbal intelligence, sustained attention, speed of processing and working memory and executive function. To minimize the effect of sleep history on SWA and cognitive performance, PSG and test batteries were administered only after at least 8 nights of 9-h time-in-bed (TIB) sleep opportunity. Results Age-related improvements in speed of processing (r = 0.33, p = 0.001) and non-verbal intelligence (r = 0.24, p = 0.01) domains were observed. These cognitive changes were associated with reduced cortical thickness, particularly in bilateral temporoparietal regions (rs = -0.21 to -0.45, ps < 0.05), as well as SWA (r = -0.35, p < 0.001). Serial mediation models found that ROIs in the middle/superior temporal cortices, together with SWA mediated the age-related improvement observed on cognition. Conclusions During adolescence, age-related improvements in cognition are mediated by reductions in cortical thickness and sleep slow wave activity.

Bayesian Causal Network Modeling Suggests Adolescent Cannabis Use Promotes Accelerated Prefrontal Cortical Thinning

While there is substantial evidence that cannabis use is associated with differences in brain structure and function, most of this evidence is correlational in nature. This is particularly true regarding the association of adolescent cannabis use on human brain development, which cannot be tested in an experimental approach. Bayesian causal network (BCN) modeling attempts to identify probable causal associations in correlational data by using the conditional probabilities among a set of interrelated variables to estimate directional associations between those variables. The current report builds on a recent analysis conducted by Albaugh et al. (2021) that found an association between neurodevelopment and cannabis use in the IMAGEN study of adolescent brain development. Here, we employ BCN modeling on the same sample to provide evidence that the associations found previously are driven by cannabis use affecting neurodevelopment and not, for example, by a pre-existing neurodevelopmental trajectory that also promotes cannabis use. Structural MRI was acquired at ages 14 and 19, from which average cortical thickness was derived for a region of interest in the dorsal prefrontal cortex identified by Albaugh et al. as differing in adolescents who initiated cannabis use between ages 14 and 19. Adolescents were all cannabis naïve at age 14 and 46% had used cannabis at least once by age 19. We tested multiple learning algorithms with a variety of different parameters to build BCNs that would describe the relationship between cortical thickness and cannabis use. All BCN models strongly suggested a directional relationship from cannabis use between the ages of 14 and 19 to accelerated cortical thinning during that same period. Acknowledging that BCN modeling cannot prove a causal relationship between adolescent cannabis use and accelerated cortical thinning, these results are consistent with a body of preclinical and human research suggesting that adolescent cannabis use adversely affects brain development.

An Unusual Presentation of a Child with Scurvy: A Case Report

Nutritional deficiency is very common in pediatric patients, especially in developing countries. A 4-year-old Maldivian boy presented with pain in major joints of lower limbs since two months and was unable to stand and walk since one month. There was no history of fever or fall. The growth was average with mild pallor. There was no joint swelling. Xray knee joint showed epiphyseal separation, cortical thinning suggesting a radiological diagnosis of Scurvy and after Vit C supplementation the child showed clinical and radiological improvement in two weeks. So, a high index of suspicion is required for early diagnosis and treatment.