Clinical Recovery Without Recanalization in Iron Deficiency Anemia-Associated Cerebral Venous Thrombosis: A Case Report

Cerebral venous thrombosis (CVT) is an uncommon cerebrovascular condition with highly variable clinical presentations and a wide spectrum of underlying causes. Iron deficiency anemia (IDA) has been increasingly recognized as a significant predisposing factor for CVT. We describe the case of a 45-year-old woman who presented with a gradually intensifying headache, followed by acute onset of left facial palsy and left-sided weakness. Laboratory tests demonstrated microcytic, hypochromic anemia, consistent with IDA. Computed tomography (CT), magnetic resonance imaging (MRI), and magnetic resonance venography (MRV) revealed thrombosis of the right transverse sinus, accompanied by venous infarction and intracranial hemorrhage. An extensive workup showed no evidence of hereditary thrombophilia or autoimmune disease. Subsequent evaluation identified a uterine fibroid causing chronic menorrhagia, which was considered the primary source of her IDA. Anticoagulation therapy was started with low-molecular-weight heparin (LMWH) and later transitioned to apixaban. She also received iron supplementation and blood transfusion. Her neurological deficits gradually improved, with no progression of the intracranial hemorrhage and no new thrombotic events. Follow-up imaging showed substantial resolution of venous edema and mass effect; however, MRV continued to demonstrate persistent occlusion of the right transverse sinus. Anticoagulation was stopped four months after disease onset, and no recurrence occurred during subsequent follow-up. This case underscores several key clinical considerations. First, IDA resulting from chronic gynecologic blood loss should be recognized as a modifiable risk factor for CVT. Second, anticoagulation can be used safely in patients with hemorrhagic CVT, even in the presence of severe anemia. Third, good clinical and radiologic outcomes are possible despite incomplete venous recanalization. Collectively, these observations suggest that restoration of overall cerebral venous hemodynamics, rather than recanalization by itself, may be crucial for recovery from CVT.