By Misty Long, ARRT, RT(R)(N),1 Nick DeLaura CNMT, PET,2 Mohammad Raza Khan, MPhys, MSc1
Data and images courtesy of Provision Diagnostic Imaging, Knoxville, Tennessee, USA
History
A 71-year-old male underwent an evaluation for memory loss and dementia through his primary care physician. A routine workup with MRI revealed moderate global cortical atrophy (GCA)—GCA scale ranges from 0 to 3—with more severity within the medial temporal lobes (GCA 2) as well as mild to moderate chronic small vessel changes
(Figure 1).
The patient was referred to a dementia specialist for further evaluation and amyloid PET/CT imaging. Fifty minutes following the 6.5 mCi (240.5 MBq) intravenous (IV) administration, the patient underwent imaging on Biograph Vision™ PET/CT.
Figure 1: Axial and coronal MRI images.
Findings
Amyloid PET images in Figure 2 show increased tracer uptake in the entire cerebral gray matter reflecting increased amyloid deposition with loss of normal gray-white matter contrast. The uptake in the cerebellum is low as expected, reflecting a physiological pattern. The ventricles appear mildly dilated, which reflects mild age-related atrophy. The extensive abnormal cerebral cortical tracer uptake is most compatible with the presence of amyloid neuritic plaques.
syngo.MI Neuro Cortical Analysis demonstrates high global and regional cortico-cerebellar ratio (global SUVr: 1.96, precuneus SUVr: 2.17, and posterior cingulate SUVr: 2.06), which is significantly higher than the upper level of normal for amyloid burden based on the method by Fleisher et al (Figure 3). The method is based on a multi-center trial, which demonstrated a threshold of SUVrs greater than or equal to 1.17 SUVr, reflects pathological levels of amyloid accumulation associated with Alzheimer’s disease (AD).3
Figure 3: Axial, coronal, and sagittal PET images fused with MRI with syngo.MI Neuro Cortical Analysis.
syngo.via offers quantitative software for the accurate localization and quantification of brain PET images. syngo.MI Neuro DB Comparison and syngo.MI Neuro Cortical Analysis enable physicians to automatically compare beta-amyloid distribution with a normal database and indicate z-score in a heat map as shown in Figure 4, and calculate cortico-cerebellar SUVr, respectively. MRI fusion, normalization to a standard reference template, and the ability to create a custom normal database further enhances syngo.MI Neurology’s capabilities, offering a robust solution for both visual interpretation and quantification, adding further reader confidence to a clinical read.
Figure 4: Axial, coronal, and sagittal amyloid PET images in syngo.MI Neuro DB Comparison.
Discussion
PET imaging of the brain is indicated to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for AD and other causes of cognitive decline.
Amyloid PET imaging alone does not establish a diagnosis of AD, but the findings from such a test must be considered in the context of the person’s medical history, physical examination, and cognitive testing. To guide clinicians on how best to apply amyloid PET in the clinical evaluation of people with cognitive decline, a working group convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging (SNMMI) developed appropriate use criteria (AUC) for brain amyloid PET scans. The AUC represented the primary inclusion criteria for the IDEAS research study. The Imaging Dementia Evidence for Amyloid Scanning (IDEAS) longitudinal study from the Alzheimer’s Association and the American College of Radiology (ACR) showed, “a change in diagnosis from AD to non-AD dementia in 25.1% of cases and a change from non-AD to AD dementia in 10.5% of cases. Furthermore, the study showed a change in patient management in 63.5% of patients with dementia as a result of amyloid PET examination and improved diagnostic confidence among physicians.”4
Recently, the US Food and Drug Administration (FDA) approved immunotherapy agents proven to slow down cognitive decline in the early stages of AD, such as mild cognitive impairment or mild dementia. These disease modifying therapies (DMTs) are beta-directed beta-amyloid monoclonal antibodies that work by reducing beta-amyloid plaques that form in the brain. To qualify for treatment, the presence of beta-amyloid plaque must be confirmed through diagnostic testing. Currently, cerebrospinal fluid (CSF) lab diagnostics and beta-amyloid PET imaging are the only modalities available to evaluate beta-amyloid plaque burden. As required by the label, MRI is required during the initial workup and should be utilized in monitoring patients for potential neurologic side effects or amyloid-related imaging abnormalities (ARIA) related to such new AD treatments.5
Conclusion
A positive beta-amyloid PET scan is not a definitive diagnosis for AD but rather a diagnostic tool to determine the presence of beta-amyloid plaques in the brain to help increase the clinical certainty of AD diagnosis.6
In this particular case, there is generalized increased radiotracer uptake throughout the gray and white matter. These abnormal PET/CT findings are most compatible with moderate to frequent amyloid neuritic plaques consistent with a neuropathological diagnosis of AD. This case demonstrates the clinical utility of Biograph Vision PET/CT imaging and syngo.PET Amyloid Plaque quantification in the evaluation of beta-amyloid plaque density in adult patients with cognitive impairment who are being evaluated for AD and other causes of cognitive decline.
Examination protocol
Scanners: Biograph Vision 450 PET/CT