An MRI report mentioning “plaque” in the brain is a common finding, though it is often a cause for concern. Neurologists and radiologists refer to these findings as “lesions” or “white matter hyperintensities” (WMH). These bright spots on the scan represent areas where the brain’s communication network has been altered or damaged. The presence of WMHs does not automatically indicate a serious disease, but they can signal various underlying conditions, ranging from normal age-related changes to significant neurological issues. Determining the cause of these lesions requires careful correlation with a patient’s symptoms, medical history, and physical examination.
Understanding “Plaque” on a Brain MRI
The brain is composed of gray matter, where processing occurs, and white matter, which consists of insulated nerve fibers called axons. White matter acts as the communication highway, facilitating rapid signaling between different brain regions. This white color comes from myelin, a fatty protective sheath wrapped around the axons.
Damage to the white matter, whether from inflammation, poor blood flow, or demyelination, changes the tissue’s water content. These changes are what the Magnetic Resonance Imaging (MRI) machine detects. On specific MRI sequences, particularly T2-weighted and FLAIR (Fluid-Attenuated Inversion Recovery), these areas of altered tissue appear visibly bright, earning them the name “hyperintensities.”
White matter hyperintensities are not a specific diagnosis but a descriptive finding that points to a variety of pathological processes. These bright spots signify areas where the myelin sheath has been lost, where local inflammation has occurred, or where small blood vessels have failed to supply adequate oxygen. The location, size, shape, and number of these hyperintensities provide the necessary clues to differentiate between potential causes. An increased lesion load is associated with a greater likelihood of clinical symptoms or future neurological risk.
Plaque Associated with Vascular Health Issues
The most frequent cause of white matter hyperintensities, particularly in older adults, is chronic damage related to the health of the brain’s smallest blood vessels. This condition is known as Cerebral Small Vessel Disease (SVD). Long-standing health issues like uncontrolled hypertension, diabetes, and high cholesterol compromise the integrity of these tiny arteries and arterioles.
The vessel walls can thicken and narrow, which reduces necessary blood flow. This chronic lack of blood flow results in low-grade, long-term ischemia, or oxygen deprivation, in the deep white matter. On an MRI, these lesions typically appear symmetrically, often clustering around the ventricles (periventricular) and deep within the cerebral hemispheres (subcortical).
These vascular lesions are directly linked to an increased risk of stroke, specifically lacunar infarcts, which are small strokes deep in the brain. They are also a major contributor to cognitive decline, frequently leading to vascular dementia characterized by executive dysfunction and slowed processing speed. Extensive deep white matter hyperintensities can impair pathways controlling movement and balance, manifesting as subtle but progressive gait disturbances.
Plaque Associated with Demyelinating Conditions
A second major category of white matter lesions is rooted in immune-mediated inflammation, most notably seen in Multiple Sclerosis (MS). In MS, the body’s immune system mistakenly attacks the myelin sheath, causing inflammation and subsequent demyelination. The core difference from vascular lesions is that MS lesions are primarily inflammatory, rather than ischemic.
These lesions are often ovoid, or egg-shaped, and tend to be distributed asymmetrically across the brain and spinal cord. A characteristic pattern is the presence of “Dawson’s fingers,” which are elongated lesions that align perpendicularly to the fluid-filled spaces of the lateral ventricles.
MS lesions also frequently appear in locations that are typically spared by vascular disease. These include the juxtacortical regions, where the lesions are in direct contact with the gray matter cortex, and the infratentorial region, which includes the brainstem and cerebellum. To determine if a lesion is actively inflamed, a contrast agent containing gadolinium is injected during the MRI scan. If the lesion is “active,” the gadolinium leaks out of the temporarily compromised blood-brain barrier and causes the lesion to “enhance” on the image.
Monitoring and Clinical Follow-Up
The discovery of white matter hyperintensities, whether incidentally found or linked to symptoms, initiates a focused clinical workup. The first step involves a comprehensive physical and neurological examination combined with a detailed review of the patient’s medical history. This correlation helps determine if the lesions are “silent” findings or if they explain a patient’s current symptoms.
Further investigation often includes a panel of blood tests to screen for modifiable vascular risk factors and other potential causes. These tests routinely check cholesterol levels, blood sugar control via Hemoglobin A1c (HbA1c), and sometimes markers for autoimmune diseases. Management for vascular lesions centers on intensive control of underlying risk factors, such as optimizing blood pressure and managing diabetes, to prevent the progression of SVD.
If the lesion pattern or clinical presentation suggests an inflammatory cause like MS, a lumbar puncture, or spinal tap, may be performed. This procedure analyzes the cerebrospinal fluid (CSF) for signs of immune system activity, such as the presence of oligoclonal bands. Follow-up MRI scans are often necessary to monitor for changes in the number and size of lesions over time, providing evidence of disease progression or activity.