Neurology International

Background: Acute ischemic stroke (AIS) is a major cause of mortality. Despite substantial advances in stroke diagnosis, investigation, and therapeutic management, the need for improved prognostic assessment remains an important clinical challenge. This study aimed to evaluate the role of combining magnetic resonance imaging (MRI)-derived and blood biomarkers in predicting functional outcomes in AIS at 3 months. Methods: A retrospective observational cohort study used data from Prince Mohd bin Naser Hospital in Saudi Arabia to integrate clinical variables and MRI-derived and blood biomarkers from adult patients with AIS. Results: The primary outcome, 3-month functional status, was assessed by the modified Rankin Scale (mRS) (good outcome: mRS < 3; poor outcome: mRS ≥ 3). The corrected analytical cohort included 100 patients. Among the 100 patients (median age: 61 years; male: 75.0%), 67 and 33 had good and poor 3-month outcomes, respectively. Compared with the good outcome group, the poor outcome group had significantly higher National Institutes of Health Stroke Scale (NIHSS) score at admission, which was the strongest discriminator between the two groups, and a trend toward a lower lesion’s mean apparent diffusion coefficient (ADC) that did not reach statistical significance. Multivariable analysis showed the best predictive performance (area under the curve (AUC): 0.934; cross-validated AUC: 0.906) with the base model consisting of admission NIHSS, lesion’s mean ADC, neutrophil percentage, and red cell distribution width; this cross-validated performance was not statistically distinguishable from a comparator model using NIHSS alone (CV-AUC: 0.898). Correlation analyses showed weak-to-moderate relationships between MRI-derived and blood biomarkers, with no correlations remaining significant after false discovery rate correction. Conclusions: Admission NIHSS score was the most powerful and consistent predictor of the 3-month outcome, while the incremental value of the multimarker model over NIHSS alone requires confirmation in larger, externally validated cohorts.

Descending pain modulation is a major determinant of pain processing across physiological and pathological conditions. Although descending pain modulation has long been recognized as bidirectional, capable of both inhibiting and facilitating nociceptive transmission, recent advances now allow it to be examined with far greater anatomical, cellular, neurochemical, and functional precision. Circuit tracing, optogenetic and chemogenetic manipulation, molecular profiling, connectomics, and human neuroimaging have expanded classical brainstem models, revealing a modulatory network in which inhibitory and facilitatory influences are dynamically recruited according to physiological and pathological state. In this narrative review, we revisit descending pain modulation across acute, inflammatory, neuropathic, and nociplastic pain states. We discuss canonical pathways, including the periaqueductal gray–rostral ventromedial medulla axis and locus coeruleus–spinal noradrenergic projections, together with the established dorsal reticular nucleus system and more recently identified descending circuits. We examine how circuit organization, neurochemical diversity, and local and long-range network interactions shape modulatory output across pain conditions. Attention is given to state-dependent plasticity and to the progressive reorganization of descending systems during pain chronification. In this context, reduced inhibitory flexibility and enhanced facilitatory bias emerge as recurrent, but not uniform, features of chronic pain. We also consider how human experimental paradigms, pharmacological approaches, and neuroimaging findings can be interpreted in light of these mechanistic advances, while acknowledging the limits of translating circuit-specific animal findings into integrated human measures. By framing descending pain modulation as a distributed and dynamically reconfigurable network rather than as a unitary analgesic system, this review highlights its relevance to pain phenotyping, treatment stratification, and mechanism-informed therapeutic strategies.

Background: Unlike acute basilar artery occlusion, non-acute vertebrobasilar occlusion has limited evidence for intervention and requires individualized risk assessment. Case Presentation: A 62-year-old woman developed progressive vertigo, diplopia, dysarthria, and gait ataxia over ten days. Dual antiplatelet therapy was started after posterior circulation ischemia was suspected, but symptoms continued to progress. MRI showed acute to subacute left cerebellar infarction, and CTA showed absent antegrade basilar opacification with collateral distal filling. DSA showed distal left vertebral artery occlusion, retrograde basilar filling through posterior communicating artery collaterals, and hypoplastic right vertebral artery. Endovascular recanalization was performed after multidisciplinary review and informed consent. Intraluminal crossing, stepwise angioplasty, and stent reconstruction restored antegrade basilar flow without angiographic complications. NIHSS improved from 5 to 2 at discharge, and mRS was 1 at 30 days. No follow-up vascular imaging was available. Conclusions: This case illustrates technical feasibility in selected non-acute vertebrobasilar occlusion, but does not establish medical treatment failure, causal recovery, generalizable safety, or long-term durability.