A stroke occurs when blood flow to the brain is interrupted or reduced, depriving brain cells of oxygen and nutrients. This interruption is usually caused by a blockage (ischemic stroke) or, less commonly, by a burst blood vessel (hemorrhagic stroke). Cancer, characterized by the uncontrolled division of abnormal cells, significantly increases the risk of ischemic stroke. This heightened risk involves biological changes caused by the tumor and the effects of necessary cancer treatments.
Cancer’s Effect on Blood Clotting
Cancer promotes stroke primarily by inducing hypercoagulability, meaning the blood has an increased tendency to clot. Tumor cells disrupt the normal clotting balance by releasing pro-coagulant factors into the bloodstream. A significant factor is Tissue Factor, which initiates the coagulation cascade and leads to an overproduction of thrombin. This process causes blood to form clots more easily and frequently.
This systemic hypercoagulability is sometimes termed Trousseau Syndrome, referring to migratory thrombophlebitis. While historically linked to venous clots, this syndrome also encompasses arterial events like ischemic stroke. The thrombi formed in cancer-associated stroke are distinct, often showing a high proportion of platelets and thrombin.
The risk of clotting-related stroke is high with certain cancer types, including mucin-producing adenocarcinomas such as pancreatic, lung, gastric, and colorectal cancers. This risk is elevated in the first six months after diagnosis and in cases of metastatic or advanced disease. High levels of D-dimer, a byproduct of clot breakdown, can serve as a marker for this hypercoagulable state and indicate an underlying malignancy.
Tumor Emboli and Vascular Damage
Stroke can also result from physical blockages originating from the cancer or its inflammatory effects on blood vessels. Nonbacterial thrombotic endocarditis (NBTE), or Marantic Endocarditis, involves sterile vegetations composed of fibrin and platelets forming on heart valves. These fragile vegetations can break off, travel to the brain, and cause an embolic ischemic stroke. NBTE is strongly associated with advanced malignancy, especially mucin-releasing adenocarcinomas of the lung, pancreas, and stomach.
In rare instances, tumor fragments can break away and travel through the bloodstream, lodging directly in a cerebral artery to cause a stroke. This is known as tumor embolism and is most often seen with cancers that have invaded the heart chambers or pulmonary veins, such as lung cancer. Cancer also triggers a generalized state of inflammation that can damage the lining of blood vessels, a process known as paraneoplastic vasculopathy. This inflammation can lead to the narrowing or complete occlusion of cerebral blood vessels, causing stroke.
Stroke Risk from Cancer Therapies
Cancer treatments, while life-saving, can independently increase the risk of stroke through various mechanisms. Chemotherapy agents are a known cause of vascular toxicity, which damages the endothelial lining of blood vessels and triggers clot formation. For example, platinum-based drugs like cisplatin increase the risk of vascular events, potentially by damaging the endothelium or inducing a pro-thrombotic state.
The chemotherapy agent L-asparaginase, frequently used for acute lymphoblastic leukemia, is strongly associated with both thrombotic and hemorrhagic cerebrovascular events. This drug depletes plasma proteins involved in coagulation and clot-dissolving systems, leading to an imbalance that favors clotting. This often results in clot formation in the cerebral veins or dural sinuses.
Radiation therapy directed at the head and neck poses a significant, often delayed, stroke risk. The radiation causes chronic damage to the carotid arteries, accelerating atherosclerosis (the hardening and narrowing of the arteries). This radiation-induced vasculopathy can increase the relative risk of ischemic stroke by at least double, with the risk continuing to rise years after treatment. Newer targeted therapies and immunotherapies, such as immune checkpoint inhibitors, also carry a risk of vascular side effects. These can include rare complications like Posterior Reversible Encephalopathy Syndrome (PRES) or other thromboembolic events.
Recognizing Stroke Symptoms in Cancer Patients
Given the multiple ways cancer and its treatments can lead to a stroke, rapid recognition of symptoms is important. A stroke is a medical emergency where every minute counts, requiring immediate action to preserve brain function. The most practical tool for identifying a stroke is the FAST mnemonic.
The FAST mnemonic outlines key symptoms:
- F stands for Face drooping; check if one side of the face is numb or if the smile is uneven.
- A stands for Arm weakness; ask the person to raise both arms and note if one drifts downward.
- S is for Speech difficulty, which can manifest as slurred words or an inability to understand a simple sentence.
- T stands for Time to call emergency services if any of these signs are present.
Cancer patients, particularly those undergoing active treatment, should be monitored closely, as stroke can be subtle and difficult to distinguish from other cancer-related neurological issues. Prompt diagnosis involves brain imaging, such as MRI, and specialized lab work to look for markers of hypercoagulability. Awareness and quick response are the best defenses against the devastating effects of a cancer-associated stroke.