What Does Plaque on Brain MRI Indicate for Neurological Health?

Brain MRI scans reveal structural abnormalities that provide critical clues about neurological health. One such finding is plaque, which appears as distinct areas of altered tissue. While not always indicative of a specific disease, plaque is associated with neurological conditions affecting cognitive and motor function.

Understanding its significance requires examining its characteristics, causes, and relationship to brain pathology.

Imaging Characteristics Of Plaque

Magnetic resonance imaging (MRI) offers a detailed view of brain tissue, enabling radiologists to identify plaques based on size, shape, distribution, and signal intensity. These lesions often appear as hyperintense or hypointense regions depending on the imaging sequence. On T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences, plaques typically appear bright, indicating increased water content due to demyelination or gliosis. In contrast, T1-weighted imaging may show hypointense plaques, particularly in chronic cases where axonal loss and atrophy have occurred. Gadolinium contrast helps distinguish active from inactive plaques by highlighting blood-brain barrier disruption, a feature of newly forming lesions.

The location of plaques provides insight into their significance. Periventricular plaques, found around the lateral ventricles, are common in demyelinating disorders, while cortical and subcortical plaques may indicate neurodegenerative processes. Deep gray matter involvement, particularly in the thalamus and basal ganglia, suggests more widespread pathology. The pattern—whether focal, confluent, or diffuse—also aids in diagnosis. For instance, Dawson’s fingers, where plaques extend perpendicularly from the ventricles, are a hallmark of certain demyelinating diseases.

Advanced imaging techniques further refine plaque assessment. Diffusion-weighted imaging (DWI) differentiates acute from chronic lesions by detecting cytotoxic edema, which appears as restricted diffusion in active plaques. Magnetic resonance spectroscopy (MRS) provides metabolic insights, revealing changes in markers such as N-acetylaspartate (NAA), a neuronal integrity indicator, and choline, which reflects membrane turnover. A reduction in NAA suggests neuronal loss, while increased choline may indicate ongoing inflammation or demyelination. Susceptibility-weighted imaging (SWI) detects iron deposition, linked to chronic neurodegenerative changes in certain plaque-associated disorders.

Key Conditions Involving Plaque

Plaque on a brain MRI is associated with several neurological conditions, each with distinct pathological mechanisms and clinical implications. These plaques may result from neurodegeneration, demyelination, or other structural changes affecting brain function. Recognizing the conditions that contribute to plaque formation helps interpret MRI findings and guide further evaluation.

Alzheimer-Type Changes

In Alzheimer’s disease (AD), plaques consist of extracellular amyloid-beta deposits that accumulate in the cerebral cortex and hippocampus. MRI does not directly visualize amyloid plaques but infers their presence through structural changes such as cortical thinning and hippocampal atrophy. Amyloid PET scans are more effective in detecting these deposits. However, MRI can reveal secondary effects, such as white matter hyperintensities, which may indicate small vessel disease or neuroinflammation.

Studies, including a 2021 review in The Lancet Neurology, show that individuals with significant amyloid burden often experience progressive brain volume loss, particularly in the medial temporal lobe. This distribution correlates with cognitive decline, reinforcing MRI’s role in tracking disease progression. Functional MRI (fMRI) studies suggest amyloid deposition disrupts network connectivity, especially in the default mode network, which is involved in memory processing.

Multiple Sclerosis

Multiple sclerosis (MS) is a demyelinating disorder characterized by plaques resulting from myelin loss in the central nervous system. These lesions are typically found in the periventricular white matter, corpus callosum, brainstem, and spinal cord. MRI is central to MS diagnosis, with hallmark features including ovoid or confluent hyperintensities on T2-weighted and FLAIR sequences. A defining characteristic is Dawson’s fingers—plaques oriented perpendicular to the ventricles, following perivascular spaces. Gadolinium-enhanced imaging differentiates active from chronic lesions, as active plaques show contrast enhancement due to blood-brain barrier disruption.

The 2017 McDonald Criteria emphasize the importance of lesion dissemination in space and time, which MRI can confirm by detecting new plaques on follow-up scans. Longitudinal studies in Brain indicate that lesion load correlates with disability progression, making MRI essential for monitoring disease activity and treatment response.

Other Plaque-Forming Disorders

Beyond Alzheimer’s and MS, other conditions contribute to plaque formation. Cerebral small vessel disease (CSVD) results in white matter hyperintensities resembling plaques on MRI, linked to chronic ischemia, cognitive impairment, and stroke risk. Neurosarcoidosis, a granulomatous inflammation, produces plaque-like lesions, often affecting the basal meninges and deep brain structures. MRI findings may include leptomeningeal enhancement and periventricular nodules.

Progressive multifocal leukoencephalopathy (PML), a demyelinating disease caused by JC virus reactivation in immunocompromised individuals, presents as asymmetric, subcortical white matter lesions without mass effect, distinguishing it from MS. Leukodystrophies, a group of genetic disorders affecting myelin metabolism, can present with diffuse white matter plaques, often symmetrically distributed. Recognizing these patterns on MRI aids in differentiating conditions and guiding clinical management.

Neuroinflammation And Plaque Formation

Plaque development in the brain is closely linked to neuroinflammation, which influences both formation and progression. Chronic inflammation within the central nervous system alters neural tissue, leading to structural changes visible on MRI. This inflammatory activity disrupts the blood-brain barrier, allowing proteins and immune mediators to accumulate, contributing to myelin degradation, neuronal damage, and abnormal protein deposition.

Neuroinflammation also affects astrocytes and microglia, which maintain neural homeostasis. When activated, these cells release pro-inflammatory cytokines and reactive oxygen species, exacerbating tissue injury and promoting lesion formation. Research in Nature Neuroscience (2022) highlights how prolonged microglial activation leads to oxidative stress and lipid peroxidation, both implicated in plaque-related neurodegeneration. This cycle of inflammation and tissue breakdown fosters further plaque accumulation, reinforcing disease progression.

The metabolic consequences of neuroinflammation shape plaque development, particularly in conditions with impaired energy metabolism. PET imaging studies show regions with high inflammatory activity often exhibit altered glucose uptake, reflecting neuronal dysfunction. This is especially evident in disorders where plaques form in metabolically vulnerable areas, such as deep gray matter and periventricular white matter. The interplay between inflammation and metabolic dysfunction suggests plaques are not merely structural byproducts but active sites of disease pathology, where ongoing biochemical changes drive their evolution.