Association of Admission Serum Homocysteine with Discharge Neurocognitive Dysfunction after Acute Cerebrovascular Disease in a High-Altitude Setting.

Discharge-phase neurocognitive abnormalities may affect rehabilitation participation, self-management, and discharge safety after acute cerebrovascular disease, but early clinically accessible correlates remain incompletely defined. We examined the association between admission serum homocysteine and clinically adjudicated discharge neurocognitive dysfunction in a high-altitude clinical setting. This single-center retrospective cohort included 227 adults admitted for acute ischemic stroke, intracerebral hemorrhage, or transient ischemic attack. The first available serum homocysteine measurement within 24 h of hospital arrival was analyzed continuously and by cohort-derived tertiles. The primary outcome was neurocognitive dysfunction documented within 24-48 h before discharge and adjudicated independently by two reviewers blinded to homocysteine levels; standardized cognitive instruments were not systematically available. Logistic regression was sequentially adjusted for demographic, renal, neurological, neuroimaging, and cerebrovascular phenotype-related factors. Among 227 patients, 98 (43.2%) had discharge neurocognitive dysfunction. Admission homocysteine was higher in patients with dysfunction than in those without dysfunction (18.3 ± 6.2 vs. 12.4 ± 4.7 µmol/L, P < 0.001), and dysfunction prevalence increased from 22.4% in T1 to 38.5% in T2 and 69.9% in T3 (P for trend < 0.001). In the primary fully adjusted model, each 1 µmol/L increase in homocysteine was associated with higher odds of dysfunction (OR 1.14, 95% CI 1.07-1.21, P < 0.001), and T3 versus T1 remained associated with the outcome (OR 4.36, 95% CI 2.00-9.51, P < 0.001). Estimates were similar in prespecified sensitivity analyses, including exclusion of delirium or positive confusion assessment method for the intensive care unit (CAM-ICU) screening and restriction to acute ischemic stroke. Higher admission homocysteine was associated with discharge-phase neurocognitive dysfunction, supporting prospective evaluation of homocysteine as a potential marker of short-term neurocognitive vulnerability rather than a validated predictor of persistent post-stroke cognitive impairment.