Longitudinal Imaging in a Patient With Opioid-associated Amnestic Syndrome.

IF 1.3 4区 医学 Q4 BEHAVIORAL SCIENCES Cognitive and Behavioral Neurology Pub Date : 2023-09-01 DOI:10.1097/WNN.0000000000000347
Jed A Barash, Jeremy D Schmahmann, Zhongcong Xie, Michael H Lev, Georges El Fakhri
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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.

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阿片类药物相关AmnesticSyndrome患者的纵向成像。
自2012年以来,很少观察到有阿片类药物滥用史的人在MRI上出现与双侧海马受限扩散相关的突发遗忘综合征。阿片类药物相关遗忘综合征(OAS)的随访影像学显示持续的海马异常。鉴于这些观察结果,以及神经病理学研究表明,阿片类药物滥用患者的海马和其他大脑区域存在过量的tau沉积,我们描述了一名有OAS病史的患者从出现到53个月后进行tau正电子发射断层扫描(PET)时的纵向成像。我们的患者是一名21岁的女性,有注意力缺陷多动障碍和物质使用障碍病史,包括阿片类药物(静脉注射海洛因),因急性发作、严重顺行性健忘症住院。她的尿液毒理学检查结果显示鸦片类药物呈阳性。在介绍中,她的大脑MRI显示海马和苍白球的T2和液体衰减反转恢复(FLAIR)高信号扩散受限。第3天,右侧海马感兴趣区域的磁共振波谱显示N-乙酰天冬氨酸/肌酸轻度减少,胆碱/肌酸轻度升高,并出现乳酸/脂质和谷氨酸/谷氨酰胺峰。在4.5个月时,MRI上出现了限制性扩散的消退,尽管右侧海马中持续存在最小的前部T2和FLAIR高信号。然而,到53个月时,当报告轻度记忆丧失时,海马在MRI上显示正常,[18F]T807(tau)PET没有显示提示tau沉积的摄取。该病例报告支持对OAS可能遵循可逆代谢损伤轨迹的假设的调查。
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来源期刊
CiteScore
2.40
自引率
7.10%
发文量
68
审稿时长
>12 weeks
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.
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