Abstract
<h3>Objective:</h3> <h3>Introduction:</h3> Vitamin-B12 deficiency-related homocysteinemia is an infrequent cause of stroke. Homocysteinemia is associated with hypercoagulability, increased cholesterol-synthesis, increased oxidative-stress, reduced apolipoprotein-A1 synthesis needed to make protective high-density lipoprotein (HDL), along with cumulative mechanisms that impair endothelial function<sup>1</sup>. We present a case of acute ischemic large vessel stroke in a young patient who was incidentally found to have low Vitamin-B12 related homocysteinemia. <h3>Background:</h3> N/A <h3>Design/Methods:</h3> <h3>Case report:</h3> 33-year-old male presented with acute onset motor-aphasia 30 minutes prior to arrival. Exam was significant for complete motor aphasia, facio-bucco-lingual apraxia and a right nasolabial-fold flattening. CT-head was negative for hemorrhage or acute ischemia and CT angiogram revealed an abrupt cut off of the left M1 segment. Patient received thrombolysis with Tenecteplase (TNK) and was emergently taken for mechanical-thrombectomy. On conventional angiogram, the M1 segment showed restored patency after TNK. Work up for secondary causes of stroke including telemetry, transesophageal echocardiogram, hypercoagulability labs, antinuclear antibody (ANA), and syphilis serology were unremarkable. Vitamin-B12 levels were significantly low at < 148 (normal 213–816pg/ml), folate levels were borderline low at 5.0 (5.4–20ng/ml) and homocysteine was significantly elevated at 35 (5.1–15.4mcmol/l). Patient was treated with dual antiplatelet therapy with aspirin 81mg , clopidogrel 75mg and initiated on B12 and folate supplements. Patient was discharged home with near-complete symptom resolution and occasional word-finding difficulty. <h3>Results:</h3> N/A <h3>Conclusions:</h3> <h3>Discussion:</h3> Vitamin-B12 deficiency increases homocysteine levels which is associated with premature atherosclerosis<sup>2</sup> and is a risk factor for thrombotic events. While vitamin-supplementation can lower homocysteine levels, the benefits as primary-prophylaxis remain uncertain<sup>3</sup>. It is worthwhile to consider vitamin-supplementation with folic-acid (2.5 mg) and B-complex vitamin (50 mg B6 and 1 mg B12) <sup>1</sup> supplements in patients with cryptogenic-strokes who have vitamin-B12 deficiency and homocysteinemia as a plausible cause for stroke. Further studies are needed to understand the pathophysiology of these two entities as risk factors for stroke. <b>Disclosure:</b> Dr. Harish has nothing to disclose. Dr. Rau has nothing to disclose. Dr. Diaz Rojas has nothing to disclose.
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