Lewy body dementia (LBD) is a progressive neurodegenerative disorder resulting from the accumulation of abnormal protein deposits called Lewy bodies in the brain. Diagnosing LBD can be challenging because its symptoms, which include cognitive decline, fluctuating attention, and movement issues, often overlap with other conditions. While magnetic resonance imaging (MRI) is a standard procedure in the evaluation of dementia, it does not provide a definitive diagnosis for LBD itself. The structural MRI scan serves instead as a powerful tool to eliminate other possibilities, offering indirect evidence that supports a clinician’s suspicion of LBD based on clinical presentation.
The Primary Role of MRI in Diagnosis
The first and most important function of an MRI scan in the context of a potential LBD diagnosis is to exclude other causes of cognitive impairment. Many conditions that mimic dementia symptoms are structurally visible on an MRI and are sometimes treatable. The scan effectively rules out major space-occupying lesions such as brain tumors, chronic subdural hematomas, or large, acute strokes.
The MRI also helps identify conditions like normal pressure hydrocephalus (NPH), which causes symptoms similar to dementia but involves the buildup of cerebrospinal fluid. By confirming the absence of these confounding pathologies, the MRI establishes that the patient’s symptoms are likely the result of a primary neurodegenerative process. This exclusionary process verifies that the clinical picture is consistent with a form of dementia rather than a reversible or surgically treatable condition.
Typical Structural Appearance of the Brain
Structural MRI provides high-resolution images of the brain’s anatomy, allowing clinicians to assess for patterns of tissue loss, known as atrophy. In many cases of LBD, the brain’s overall atrophy is subtle or minimal, especially in the early stages of the disease. This relative preservation of brain volume, particularly in specific regions, becomes an important diagnostic clue.
A frequently observed finding in LBD is the relative preservation of the medial temporal lobe structures, including the hippocampus and amygdala, which are responsible for memory. These areas are often spared significant shrinkage until later in the disease course. In contrast to the specific, severe atrophy seen in Alzheimer’s disease, LBD often shows more generalized cortical thinning or atrophy that affects areas outside of the medial temporal lobe.
Using Imaging for Differential Diagnosis
The pattern of atrophy, or lack thereof, on the MRI is used to differentiate LBD from other common forms of dementia. Comparing the structural MRI findings of a patient with LBD to those with Alzheimer’s disease (AD) is a primary use of the scan. Patients with AD typically exhibit pronounced and measurable atrophy of the medial temporal lobe, especially the hippocampus, early in the disease process.
The relative preservation of medial temporal lobe volume in LBD serves as a significant feature to distinguish it from AD. Differentiating LBD from Vascular Dementia (VaD) involves looking for signs of cerebrovascular disease. VaD is characterized on MRI by the presence of small vessel disease, lacunar infarcts (small strokes), or extensive white matter hyperintensities, which indicate damage from reduced blood flow. An MRI showing widespread vascular damage without the specific LBD clinical profile often points toward VaD as the primary diagnosis.
Beyond Structural Scans: Functional Imaging
The limitation of a standard structural MRI is that it only visualizes the anatomy and the physical size and shape of brain structures, not how they are functioning. Because LBD is a functional disease related to chemical imbalances and protein buildup, functional imaging scans are often required to confirm the diagnosis. These specialized scans measure activity or the presence of specific neurotransmitters.
A common functional study used for LBD is the dopamine transporter scan, or DaTscan, a type of single-photon emission computed tomography (SPECT). This scan uses a radioactive tracer that binds to dopamine transporters in the striatum, a brain region involved in movement. In LBD, the characteristic loss of these dopamine transporters shows up as a distinctly abnormal pattern of reduced tracer uptake on the scan. Other functional techniques, like \(\text{^{18}F}\)-FDG PET, may reveal reduced metabolism in the occipital lobe, which correlates with visual hallucinations.