Anthropometric Adiposity and Systemic Inflammatory Markers and Response in Neurological Disease: An Exploratory Study of Cerebrovascular Ischaemic Events Associated to Carotid Atheromatous Processes

Abstract

This exploratory study examined whether anthropometric adiposity and systemic inflammatory response represent convergent or partially distinct biological dimensions in neurological disease, and whether these characteristics differ according to cerebrovascular ischemic-event status. A retrospective observational analysis included 32 clinical monitoring observations from adults evaluated in a neurology department. Anthropometric indicators comprised body mass index (BMI), mid-upper arm circumference (MUAC), waist circumference, and waist-to-height ratio (WHtR). Inflammatory markers included erythrocyte sedimentation rate (ESR), leukocyte, neutrophil, lymphocyte counts, and neutrophil-to-lymphocyte ratio (NLR). Spearman correlations, Benjamini–Hochberg false-discovery-rate correction, Kruskal–Wallis and Mann–Whitney tests, Cliff’s delta, and sensitivity analyses for extreme NLR values were applied. As results, excess body weight was common: 50.0% of observations were overweight and 37.5% obese. NLR was markedly right-skewed (median 3.20; IQR 2.35–4.57). None of the 20 anthropometric–inflammatory correlations remained significant after false-discovery-rate correction. BMI–NLR (ρ=-0.285, p=0.135) and waist circumference–NLR (ρ=-0.350, p=0.063) associations were inverse and nonsignificant. In contrast, strong within-domain correlations were observed, including BMI–WHtR (ρ=0.860) and leukocyte–neutrophil counts (ρ=0.901). Inflammatory markers did not differ significantly across BMI categories. Fourteen observations were classified as cerebrovascular ischemic events; neither anthropometric measures nor NLR significantly differentiated these from other neurological diseases. Sensitivity analyses excluding extreme NLR values did not materially change the findings. In conclusion, anthropometric adiposity and systemic inflammatory response showed strong internal but limited cross-domain coherence. In this small neurological cohort, NLR was not a direct surrogate of adiposity or an isolated discriminator of cerebrovascular ischemic events. These findings support multidimensional, context-dependent interpretation of adiposity and inflammation in neurological disease.