RSNA 2017

Abstract Archives of the RSNA, 2017


Assessment of the Neurologic Effects of Intracranial Gadolinium Deposition Using a Large Population Based Cohort

Wednesday, Nov. 29 3:00PM - 3:10PM Room: N226

Robert J. McDonald, MD, PhD, Rochester, MN (Presenter) Consultant, General Electric Company; Investigator, General Electric Company
Jennifer S. McDonald, PhD, Rochester, MN (Abstract Co-Author) Research Grant, General Electric Company
Terry Therneau, PhD, Rochester, MN (Abstract Co-Author) Nothing to Disclose
Laurence J. Eckel, MD, Rochester, MN (Abstract Co-Author) Nothing to Disclose
David F. Kallmes, MD, Rochester, MN (Abstract Co-Author) Research support, Terumo Corporation Research support, Medtronic plc Research support, Sequent Medical, Inc Research support, Benvenue Medical, Inc Research support, General Electric Company Consultant, General Electric Company Consultant, Medtronic plcConsultant, Johnson & Johnson
Rickey Carter, PhD, Rochester, MN (Abstract Co-Author) Nothing to Disclose
Clifford R. Jack JR, MD, Rochester, MN (Abstract Co-Author) Stockholder, Johnson & Johnson Research Consultant, Eli Lilly and Company
Ronald C. Petersen, MD, PhD, Rochester, MN (Abstract Co-Author) Nothing to Disclose

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The neurotoxic potential of intracranial gadolinium (Gd) deposition following intravenous administration of gadolinium based contrast agents (GBCAs) is undefined. In the current study, we used the world's largest prospective population-based cohort on aging to study the effects of Gd exposure on neurologic and neurocognitive function.


The Mayo Clinic Study of Aging (MCSA) cohort was enumerated from the Rochester Epidemiology Project in 2004 to study the incidence and natural history of cognitive impairment and dementia. All participants underwent extensive longitudinal clinical (neurologic evaluation, neuropsychological testing) assessment at baseline and 15-month follow-up intervals. Neurologic and neurocognitive scores were compared using standard multivariate methods between MCSA patients with no history of prior Gd exposure and those who underwent prior Gd-enhanced MRI. Progression from normal cognitive status to mild-cognitive impairment and dementia was assessed using multistate Markov model analysis.


Among 4261 cognitively normal study participants aged 50-90 (mean age (SD): 71.9 yrs (10.7), mean study participation (SD): 3.7 yrs (3.0)), 1092 (25.6%) received one or more GBCA doses (median: 2 doses, range: 1-28 doses) unrelated to their participation in the MCSA. Median time since first Gd exposure was 5.6 years (IQR=2.2-9.3 years). After adjusting for age, sex, education level, baseline neurocognitive performance, Charlson comorbidity index, and ApoE4 status, GBCA exposure was not a significant predictor of cognitive decline (changes in clinical dementia rating (p=.48), Blessed dementia scale (p=.68), or mental status exam score (p=.55)), diminished neuropsychological performance (p=.13), or diminished motor performance (Unified Parkinson's Disease Rating Scale (p=.43)). No dose-related effects were observed among these metrics (p=.89-.20). Finally, Gd exposure was not an independent risk factor in the rate of cognitive decline from normal cognitive status to dementia in this cohort (p=.91).


GBCA administration was not associated with worse overall neurologic or neurocognitive performance nor does it significantly affect the natural progression of cognitive decline in a large population-based cohort.


Despite evidence of Gd accumulation following intravenous GBCA administration, Gd exposure is not associated with adverse neurologic outcomes.