Stroke in cancer patients

Abstract

Various causes of cerebrovascular complications exist in patients with malignant tumor. The pathogenesis of thrombosis in malignancy is complex and it has not been completely clarified as yet. A hypercoagulable state in these patients occurs through several interactive processes between the cancer cells and the patient. Tumor cells can directly and indirectly enhance activation of coagulation cascade. Trousseau's syndrome is a paraneoplastic neurologic syndrome which is caused by remote effects of cancers. Tumor cells produce cytokines which promote coagulation and suppress anticoagulant activities, thereby causing stroke in cancer patients. Brain tends to be a target organ of stroke in the conditions of disseminated intravascular coagulopathy (DIC) in cancer patients. Nonbacterial thrombotic endocarditis (NBTE) is characterized by the presence of relatively acellular aggregates of fibrin and platelets attached to normal heart valves. NBTE can be found in DIC. Paradoxical embolism due to patent foramen ovale in patients with deep vein thrombosis is also one of the cause of cerebral infarction. Stroke can occur under various setting of cancer chemotherapy. Tamoxifen increases the risk of stroke in patients with breast cancer. In paticular, it has been reported that the combination of chemotherapy and tamoxifen for breast cancer patients frequently produces thrombotic episodes. Patients with head and neck cancer treated with local radiotherapy have a high risk of developing significant carotid stenosis, and an increased risk of stroke. Malignancy as a risk factor for stroke is becoming increasingly recognized by physicians caring for these patients. The probability of stroke occurring in an individual patient depends on several factors such as intrinsic medical problems, the type of cancer, the clinical stage, performance status, and the treatment modalities employed. Understanding these factors is important for stroke prevention and provision in this population.