A stroke occurs when blood flow to a part of the brain is interrupted, causing brain cells to die. Magnetic Resonance Imaging (MRI) is the most sensitive method for diagnosing this event and tracking the resulting damage over time. The appearance of a stroke on an MRI is not static; it changes dramatically as the brain tissue evolves through phases of injury, repair, and permanent loss. Understanding this temporal evolution allows physicians to determine the approximate time a stroke occurred and how long the signs of the injury will remain visible.
Immediate Detection: The Acute Phase (0-48 Hours)
The earliest detection relies on identifying the failure of brain cells due to lack of oxygen. This failure causes a shift of water from the extracellular space into the cells, a process called cytotoxic edema, which begins within minutes of the blood flow blockage.
The most sensitive MRI technique for visualizing this immediate damage is Diffusion-Weighted Imaging (DWI). DWI maps the random movement of water molecules; because the water is trapped inside the swollen cells, its movement is restricted. This restriction causes the affected area to appear brightly hyperintense on the DWI sequence, often within 30 minutes to six hours of symptom onset, making it the standard for acute stroke diagnosis.
The corresponding Apparent Diffusion Coefficient (ADC) map confirms this finding by showing a dark, hypointense signal in the same area. The ADC map provides a quantitative measure of water restriction, with values typically dropping by about 40% compared to healthy brain tissue. This dark signal on the ADC map is crucial because it distinguishes a true acute stroke from other lesions that might look bright on DWI. During this initial 48-hour window, other standard MRI sequences, like T2-weighted imaging or Fluid-Attenuated Inversion Recovery (FLAIR), may still appear completely normal.
The Evolving Lesion: Subacute Changes (Days 3 to Weeks 4)
As the acute phase gives way to the subacute phase, the stroke lesion undergoes a dynamic transformation as the body begins clearing the damaged tissue. This phase typically starts around 48 hours and can last for up to four weeks. The initial cytotoxic edema resolves, and a new type of swelling, called vasogenic edema, takes hold as the blood-brain barrier breaks down and fluid leaks into the surrounding tissue.
It is during this period that the lesion becomes clearly visible on other sequences, specifically T2-weighted and FLAIR imaging. The increased water content from the vasogenic edema causes the infarcted tissue to appear bright, or hyperintense, on both T2 and FLAIR scans, peaking in clarity around one to two weeks after the event. While the DWI signal remains bright during the first week, the ADC values start to rise, a phenomenon called “pseudonormalization,” where the ADC signal temporarily returns to near-normal levels around seven to fifteen days.
A notable occurrence in the subacute phase, particularly around two to three weeks, is the “fogging effect.” This is a transient period where the hyperintense signal on T2 and FLAIR images can temporarily fade or normalize, making the stroke lesion appear less obvious. This temporary normalization is caused by the infiltration of inflammatory cells and macrophages into the area. This transient invisibility makes imaging interpretation challenging, often requiring a look at earlier DWI scans to confirm the diagnosis.
Permanent Markers: Chronic Visibility (Months and Years Later)
The final outcome of an ischemic stroke, known as the chronic phase, begins once the dynamic period of tissue breakdown and inflammation subsides, typically after four weeks. The signs of a stroke remain visible indefinitely, for years and decades, because the damaged brain tissue is permanently lost.
The necrotic tissue is gradually removed by macrophages, and the resulting space is replaced by cerebrospinal fluid (CSF), a process known as encephalomalacia. On MRI, this permanent tissue loss is characterized by a fluid-filled cavity that follows the signal characteristics of CSF on all sequences. This includes appearing dark on FLAIR and T1-weighted images, and bright on T2-weighted images.
The edges of the permanent cavity are often lined with gliosis, a form of glial scarring where supporting brain cells proliferate in response to the injury. This scarring appears as a thin rim of hyperintensity on FLAIR imaging surrounding the fluid-filled space. The combination of the fluid-filled cavity (encephalomalacia) and the surrounding scar tissue (gliosis) represents the permanent, irreversible marker of the past stroke. These structural changes are permanent features that will be detected on any subsequent MRI scan, confirming the history of a cerebral infarction.