Cerebral atherosclerosis is a form of vascular disease defined by the narrowing and hardening of arteries that supply blood to the brain. This condition develops when fatty deposits, known as plaque, accumulate within the artery walls. The buildup causes the vessels to thicken and lose elasticity, restricting the flow of oxygenated blood to brain tissue. This process affects large arteries in the neck, such as the carotid arteries, and smaller arteries deep inside the brain.
The Mechanism of Plaque Buildup in Cerebral Arteries
The pathology begins with chronic injury to the endothelium, the thin layer of cells lining the artery wall. This damage often stems from high blood pressure, elevated cholesterol levels, or toxins from cigarette smoke. Once the endothelial lining is compromised, it becomes permeable, allowing low-density lipoprotein (LDL) cholesterol particles to seep into the artery wall.
These cholesterol particles trigger an inflammatory response, attracting white blood cells (monocytes and T-lymphocytes) to the site of injury. Monocytes transform into macrophages, which consume the trapped LDL cholesterol, forming foam cells. The accumulation of these foam cells, along with connective tissue and extracellular matrix, creates the atherosclerotic plaque.
As the plaque grows, it pushes the vessel wall inward, a process called stenosis, which reduces the artery’s internal diameter. This narrowing limits the volume of blood passing through to the brain, leading to chronic hypoperfusion or reduced blood flow. The plaque consists of a soft, lipid-rich core covered by a fibrous cap composed of smooth muscle cells and collagen. The stability of this cap determines the immediate risk of a severe event.
Cerebral atherosclerosis targets extracranial arteries (like the carotid) and intracranial arteries deep within the brain, such as the middle cerebral and basilar arteries. Although the process is the same as in other parts of the body, the smaller size and location of intracranial arteries make them vulnerable to severe consequences from minor blockages. Plaque buildup obstructs blood flow and creates a rough surface where blood clots can easily form, increasing the likelihood of an acute blockage.
Contributing Factors and High-Risk Groups
The development of cerebral atherosclerosis is linked to several modifiable and non-modifiable factors that accelerate plaque formation. Chronic hypertension (persistently high blood pressure) is a significant modifiable risk factor for intracranial lesions. High pressure physically stresses and damages the delicate endothelial lining of the cerebral arteries, initiating plaque development.
Dyslipidemia, characterized by abnormal levels of circulating lipids, is a major contributor, specifically high levels of LDL cholesterol and low levels of high-density lipoprotein (HDL). High LDL provides the primary material for the plaque core, while low HDL impairs the body’s ability to remove excess cholesterol. Diabetes mellitus also increases risk, as high blood sugar levels contribute to vascular inflammation and damage the vessel walls.
Lifestyle choices, such as cigarette smoking, introduce toxic chemicals that harm the endothelium and speed up plaque buildup. Smoking also contributes to the inflammatory state within the vessels, further destabilizing the plaque. Non-modifiable factors include increasing age (risk rises noticeably in men over 45 and women over 55) and a genetic predisposition. Individuals of Asian, Hispanic, and African American ancestry have a higher prevalence of intracranial atherosclerotic disease compared to white populations.
Recognizing the Signs and Symptoms
In its early stages, cerebral atherosclerosis often produces no noticeable symptoms, as the brain compensates for minor reductions in blood flow. As arterial narrowing progresses, some individuals may experience subtle, chronic signs due to sustained reduction in oxygen delivery. These can include unexplained headaches, facial pain, or persistent mild cognitive changes, indicating insufficient blood flow.
The most concerning symptoms are those associated with acute, temporary disruptions of blood flow, known as a Transient Ischemic Attack (TIA). A TIA, often called a “mini-stroke,” occurs when the blockage is temporary, causing stroke-like symptoms that resolve within minutes to a few hours. Since brain tissue does not die during a TIA, the symptoms disappear, but the event serves as a warning of impending, permanent damage.
Symptoms of a TIA are identical to those of a full stroke and require immediate medical attention. These include:
- Sudden weakness or numbness on one side of the body (face, arm, or leg).
- Sudden difficulty speaking or slurred speech.
- Temporary loss of vision in one eye or double vision.
- A sudden, severe headache with no clear cause.
The sudden onset of these neurological deficits indicates the brain’s blood supply is at high risk of failure due to atherosclerotic plaque.
Diagnosis and Immediate Medical Consequences
Confirming cerebral atherosclerosis involves non-invasive imaging techniques to visualize the cerebral arteries and the extent of the plaque. Doctors frequently use Magnetic Resonance Angiography (MRA) and Computed Tomography Angiography (CTA). These tests use magnetic fields or X-rays, along with contrast dye, to create detailed images of the blood vessels and measure the degree of stenosis (narrowing).
Another common method is Transcranial Doppler (TCD) ultrasound, which uses high-frequency sound waves to measure the speed and direction of blood flow through major arteries inside the skull. By detecting changes in flow velocity, doctors can infer significant narrowing caused by plaque. These tools help determine the patient’s risk profile based on the location and severity of the disease.
The most immediate consequence of advanced cerebral atherosclerosis is an ischemic stroke, resulting from the complete loss of blood supply to a part of the brain. This occurs through two primary mechanisms:
Thrombotic Stroke
The plaque grows large enough to completely block the artery at the site of its formation.
Embolic Stroke
The fibrous cap of the plaque ruptures, exposing the lipid core to the bloodstream. This triggers the formation of a blood clot that either fully occludes the vessel or breaks off (thromboembolism). The traveling clot then moves downstream to block a smaller artery.