Elevated Plasma Factor VIII in Non-Pyogenic Cerebral Venous Thrombosis after Head Trauma without Skull Fracture

Cerebral Venous Thrombosis (CVT) is a relatively uncommon but important cause of stroke that tends to affect young adults, especially women. Head trauma with or without skull fracture was reported to be triggering factors for CVT, but the underlying pathophysiology was not well elucidated. Endothelial injury and coexistent hypercoagulability were supposed to contribute to CVT after head trauma without skull fracture. We report a 49-year-old female patient who presented with headache with vomiting after head trauma and was initially diagnosed as post-traumatic Intracerebral Hemorrhage (ICH), but subsequently, progressed to CVT that resulted in cerebral venous infarction with hemorrhagic transformation. Magnetic Resonance brain Venography (MRV) confirmed CVT in superior sagittal sinus as well as right transverse and sigmoid sinuses. She was treated with endovascular mechanical thrombectomy followed by anticoagulation. The coagulopathy panel was checked both in hospital and in outpatient clinic for evaluating the etiology underlying post-traumatic nonpyogenic CVT. Persistently elevated level of plasma Factor VIII was identified. We should consider that patients with recent head trauma history without skull fracture and coexistent hypercoagulability could develop CVT resulting in cerebral venous infarction with hemorrhagic transformation even when the patient showed no definite focal neurologic deficit or the patient’s initial CT scan revealed no intracranial hemorrhage.

Elevated Lipocalin-2 Can Indicate the Vascular Inflammation in Patients with Ischemic Stroke

Purpose: Elevated level of Lipocalin-2 (LCN2), a new acute phase adipokine, was described after ischemic stroke. A number of researchers feel as though that LCN2 originated from the infiltrating neutrophils and other cells in brain after stroke. Others measured elevated LCN2 expression in arteriosclerotic plaque. Therefore we have investigated LCN2 relative gene expression level of blood neutrophil granulocytes in patients with ischemic stroke to assess if elevated LCN2 is the cause or consequence of ischemic stroke. Methods: Laboratory and anamnestic data were collected, which could have a role in development of thrombo-embolic events in patients with ischemic stroke. RNA based method was used to evaluate the relative gene expression level of LCN2. We calculated Odds Ratio (OR) and Confidence Interval (CI) for the association between LCN2 and ischemic stroke. Results: 34 samples were available for evaluation. The LCN 2 relative gene expression level was decreased in 12 cases. In this group, 91% of patients have Atrial Fibrillation (AF) at the time of hospitalisation. The mean LCN2 relative gene expression value was 64.25% (ranges: 34%-115%) in patients with AF. It was significantly lower than in patients with normal sinus rhythm (409.2%; ranges: 127%-1127%; p=0.0003). The elevated LCN2 relative gene expression level significantly (p=0.012) increases the risk of stroke (OR: 12.6) independently from other factors. Conclusions: High LCN2 expression level seems to have strong positive predictive value on ischemic stroke, and may be useful in thrombotic risk stratification of plaque vulnerability in these patients.