A head injury, or Traumatic Brain Injury (TBI), occurs when an external force causes brain dysfunction. Strokes happen when blood flow to the brain is interrupted, leading to brain cell death. This interruption is caused by either a blockage (ischemic stroke) or bleeding from a burst blood vessel (hemorrhagic stroke). Research shows a clear biological connection between TBI and stroke, significantly increasing the risk of both immediate and delayed stroke events. Even a mild concussion can raise a person’s lifetime stroke risk.
Direct Trauma to Blood Vessels
The immediate way a head injury can cause a stroke involves direct physical damage to the vascular system. One primary mechanism is arterial dissection, a tear in the inner lining of an artery in the neck or head. These tears often occur in the carotid or vertebral arteries due to the sudden, forceful movements accompanying a TBI.
Arterial Dissection and Clot Formation
When the artery’s inner wall (intima) tears, blood pools between the layers, narrowing the vessel and restricting blood flow. The damaged lining also becomes a site for blood clot formation. A piece of this clot can break off, travel to the brain, and block a smaller artery, causing an ischemic stroke. This process is a significant cause of stroke, especially in younger adults following trauma.
Intracranial Bleeding
Direct trauma can also lead to a hemorrhagic stroke through acute intracranial bleeding. A severe impact may cause blood vessels within the brain tissue or on its surface to rupture immediately. This bleeding, known as an intracranial hemorrhage, displaces and compresses surrounding brain tissue, resulting in a stroke-like injury. Secondary complications, such as brain swelling, can mechanically compress adjacent arteries, causing a secondary ischemic stroke by cutting off the blood supply.
The Role of Systemic Inflammation
Beyond immediate physical damage, a head injury triggers a widespread biological response that creates a delayed stroke risk. This risk is rooted in a prolonged inflammatory cascade following the TBI. The trauma causes the brain to release specific signaling molecules, such as pro-inflammatory cytokines and chemokines, into the bloodstream.
These molecules circulate, initiating systemic inflammation that affects the integrity of blood vessels far from the injury site. This process is called endothelial dysfunction, where the cells lining the blood vessels are damaged. Healthy endothelial cells produce nitric oxide (NO) which helps keep vessels relaxed and prevents clots; after TBI, this function is impaired.
The resulting dysfunction leads to a hypercoagulable state, making the blood more prone to clotting. This systemic change increases the long-term risk for an ischemic stroke because clots are more likely to form in narrowed, inflamed arteries. The stroke risk remains elevated for months and even years after the injury, with the highest risk concentrated in the first few months.
Identifying High-Risk Scenarios
Not every TBI results in a stroke; the risk is modulated by injury characteristics and the patient’s underlying health. While severe injuries are more likely to involve immediate complications like arterial dissection or intracranial hemorrhage, even mild head injuries are associated with a significantly increased risk of ischemic stroke.
Injury Characteristics
The location of the trauma plays a role, especially if the impact causes forceful neck movement that could lead to cervical artery dissection. The risk is also compounded by the frequency of injury. Having two or more head injuries substantially increases the long-term risk of an ischemic stroke compared to a single event, suggesting a cumulative effect on vascular health.
Pre-existing Conditions
Pre-existing patient conditions further amplify the post-TBI stroke risk. Individuals with conditions that affect blood vessel health, such as hypertension, diabetes, or high cholesterol, are more vulnerable to the vascular damage initiated by the TBI. The systemic inflammation from the TBI interacts with these underlying conditions, accelerating atherosclerosis and increasing the likelihood of a subsequent stroke. Managing these pre-existing risk factors is an important strategy for stroke prevention in people with a history of head injury.