Hypertension and Neurovascular Compression of the Left Lateral Medulla oblongata in Ischemic Stroke

Abstract

Hypertension is a major risk factor for stroke. Neurovascular compression (NC) of the left ventrolateral medulla oblongata may cause arterial hypertension. We evaluated the relationship between the two ischemic stroke patients. We classified 69 patients under 50 years old (49 men and 20 women, aged 43.6 ± 7.3 years) based on magnetic resonance imaging findings as follows: NC patients (n = 38; 10 with NC on the right side, 18 with NC on the left side, and 10 with NC on both sides) and non-NC patients (n = 31). We compared the following clinical characteristics between the two groups: (1) risk factors for stroke, including hypertension, diabetes mellitus, hypercholesterolemia, and smoking and (2) stroke subtype. Hypertension was more frequent in the NC group than in the non-NC group (58 vs. 19%, p = 0.001). Hypertension was more frequent in patients with left-side NC than in those with right-side NC (78 vs. 20%, p = 0.005). No other differences were observed between the two groups. Twelve patients presented with atherothrombotic stroke, 16 with cardioembolic stroke, 24 with lacunar stroke and 17 with stroke of miscellaneous etiology. NC was significantly more common in patients with lacunar stroke as compared with those affected by other stroke subtypes (p = 0.015). We found a significant relationship between hypertension and NC of the ventrolateral medulla oblongata on the left side in ischemic stroke patients younger than 50 years of age. Some patients with lacunar stroke may have hyptertension related to NC.

Blood Pressure and Acute Ischemic Stroke

“…In some specific cases, infarction involving the lateral medulla (Wallenburg syndrome), leads to hypertension and it can be shown that this region of brain is important in blood pressure control. 1,2 Similarly infarction of the insula may result in varying degrees of autonomic dysfunction, including acute hypertension. Acute hypertension may also been seen as a terminal event among patients with massive edema and rostral-caudal herniation, either due to malignant middle cerebral artery or cerebellar infarction; however, this occurs usually in the 24-96hour timeframe after stroke onset.…”