A brain infarct describes an area of localized tissue death within the brain. This tissue death occurs when the blood supply to a specific region is severely reduced or completely blocked. The brain is uniquely sensitive to any interruption in blood flow because it does not store oxygen or glucose. A continuous supply of oxygenated blood is therefore necessary to maintain the high metabolic demands of brain cells. When this supply fails, the resulting tissue death is what physicians commonly refer to as an ischemic stroke, which accounts for the vast majority of all stroke cases.
The Mechanism of Ischemia
The condition that immediately precedes an infarct is ischemia, which is the restriction of blood flow to the tissue. This restriction is almost always caused by a physical blockage within one of the arteries supplying the brain. The two main types of physical blockage are a thrombosis and an embolism, each originating in a different location.
A thrombotic event occurs when a blood clot forms directly inside a brain artery, typically at a site of pre-existing damage. This local formation is often linked to atherosclerosis, where fatty plaques build up and narrow the vessel walls. The clot grows slowly at the site of the plaque, eventually becoming large enough to stop blood flow entirely, leading to an infarct.
An embolism involves a clot that forms elsewhere in the body and then travels through the bloodstream until it lodges in a smaller brain vessel. These clots frequently originate in the heart, particularly in individuals with conditions like atrial fibrillation, or they can break off from atherosclerotic plaques in the large carotid arteries of the neck. The resulting blockage is often sudden and highly destructive.
How Oxygen Deprivation Causes Cell Death
Once the blood supply is cut off, the death of brain cells begins. The immediate consequence of oxygen and glucose deprivation is the failure of the cells to produce adenosine triphosphate (ATP), the primary energy molecule. Without ATP, the energy-dependent ion pumps that maintain the electrical balance across the cell membrane cease to function.
This failure of the ion pumps causes a massive disruption in the concentration of ions, particularly sodium and calcium, inside the cell. Water rushes into the neurons and glial cells to balance the osmotic pressure, causing the cells to swell, a process known as cytotoxic edema. This swelling can further compress capillaries, worsening the lack of blood flow in the surrounding area.
The high concentration of intracellular calcium triggers the excessive release of glutamate, a neurotransmitter that overstimulates neighboring neurons. This phenomenon, called excitotoxicity, defines the core area of the infarct, or ischemic core, where damage is irreversible within minutes.
Surrounding this core is an area of tissue called the ischemic penumbra, which is severely compromised but still receiving marginal blood flow. The penumbra is metabolically active but functionally impaired. Timely medical intervention aims to restore blood flow to this penumbra before the cascade of cell death spreads.
Categorizing Brain Infarcts
Brain infarcts are classified in several ways to describe the extent of the damage and its likely origin. One common method uses the size and location of the affected area. Lacunar infarcts, for instance, are very small lesions, typically less than 15 millimeters, that occur deep within the brain structures.
These small infarcts are caused by the blockage of tiny perforating arteries, often seen in individuals with a history of chronic high blood pressure or diabetes. In contrast, territorial infarcts are much larger, involving a wide region of the brain supplied by one of the major cerebral arteries, such as the middle cerebral artery.
Infarcts can also be categorized by their presumed cause. Etiological classifications include large artery atherosclerosis, cardioembolic stroke, where the blockage originates in the heart, and small vessel occlusion.
Recognizing and Confirming an Infarct
A brain infarct involves the sudden onset of neurological deficits that correspond to the affected area of the brain. Common signs include sudden facial drooping, weakness or numbness in one arm or leg, or difficulty speaking or understanding language. Recognizing these symptoms quickly is crucial.
To confirm the diagnosis and determine the appropriate immediate treatment, diagnostic imaging is necessary. The initial step is typically a non-contrast Computed Tomography (CT) scan of the head, which is performed rapidly to rule out a hemorrhagic stroke. The presence of hemorrhage would immediately change the treatment course, as the medications used for an ischemic infarct could worsen bleeding.
Magnetic Resonance Imaging (MRI), particularly a sequence called Diffusion-Weighted Imaging (DWI), is the most sensitive and specific method for confirming an acute infarct. DWI can detect the cellular changes associated with tissue death within minutes of the event. This imaging helps physicians to precisely map the extent of the core damage and the surrounding at-risk penumbra.