Jed A Barash, Jeremy D Schmahmann, Zhongcong Xie, Michael H Lev, Georges El Fakhri
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引用次数: 0
Abstract
Since 2012, individuals with a history of opioid misuse have infrequently been observed to develop a sudden-onset amnestic syndrome associated with bilateral hippocampal-restricted diffusion on MRI. Follow-up imaging of this opioid-associated amnestic syndrome (OAS) has revealed persistent hippocampal abnormalities. Given these observations, as well as neuropathological studies demonstrating excessive tau deposition in the hippocampi and other brain regions of individuals with opioid misuse, we describe longitudinal imaging of a patient with a history of OAS from presentation through 53 months later, when tau positron emission tomography (PET) was performed. Our patient was a 21-year-old woman with a history of attention-deficit hyperactivity disorder and substance use disorder, including opioids (intravenous heroin), who was hospitalized for acute-onset, dense anterograde amnesia. Her urine toxicology screen was positive for opiates. On presentation, her brain MRI showed restricted diffusion as well as T2 and fluid-attenuated inversion recovery (FLAIR) hyperintensity of the hippocampi and globi pallidi. On day 3, magnetic resonance spectroscopy of a right hippocampal region of interest showed a mild reduction of N-acetyl aspartate/creatine, slight elevation of choline/creatine, and the appearance of lactate/lipid and glutamate/glutamine peaks. At 4.5 months, there was resolution of restricted diffusion on MRI, although a minimal anterior T2 and FLAIR hyperintense signal in the right hippocampus persisted. However, by 53 months, when mild memory loss was reported, the hippocampi appeared normal on MRI, and [ 18 F]T807 (tau) PET showed no uptake suggestive of tau deposition. This case report supports the investigation into the hypothesis that OAS may follow a trajectory of reversible metabolic injury.
期刊介绍:
Cognitive and Behavioral Neurology (CBN) is a forum for advances in the neurologic understanding and possible treatment of human disorders that affect thinking, learning, memory, communication, and behavior. As an incubator for innovations in these fields, CBN helps transform theory into practice. The journal serves clinical research, patient care, education, and professional advancement.
The journal welcomes contributions from neurology, cognitive neuroscience, neuropsychology, neuropsychiatry, and other relevant fields. The editors particularly encourage review articles (including reviews of clinical practice), experimental and observational case reports, instructional articles for interested students and professionals in other fields, and innovative articles that do not fit neatly into any category. Also welcome are therapeutic trials and other experimental and observational studies, brief reports, first-person accounts of neurologic experiences, position papers, hypotheses, opinion papers, commentaries, historical perspectives, and book reviews.