Tsai Carolyn, O'Reggio Abigail, Mehrabyan Anahit, Williams Dena, Dujmovic Basuroski Irena
Neurology, University of North Carolina at Chapel Hill, Chapel Hill, USA.
Cureus. 2022 Jun 29;14(6):e26435. doi: 10.7759/cureus.26435. eCollection 2022 Jun.
Hippocampal ischemia is a rare complication of cocaine abuse that has been thought to arise from vasospasm, anoxic injury, and/or catecholaminergic excitotoxicity. We present two cases of patients abusing cocaine, who presented with an acute onset anterograde amnesia due to bilateral hippocampal ischemia, and had different outcomes. Case 1 is a 49-year-old male with a history of IV heroin abuse who presented after being found down for an unknown period of time. He awoke with no memory of events leading up to hospitalization and was unable to retain new information. Urine toxicology was positive for cocaine and opiates. Traditional vascular risk factors included obesity, hypertension, and hyperlipidemia. His recovery was complicated by continued drug use and one episode of cardiac arrest. Despite cognitive rehabilitation, only minimal improvements in his anterograde memory were observed during his annual follow-up. Case 2 is a 23-year-old male with a history of attention deficit disorder treated with dexmethylphenidate and a history of consistent marijuana and cocaine abuse, who presented with nausea, vomiting, chest pain, shortness of breath, and acute-onset short-term memory loss. Urine toxicology was negative for cocaine and opiates and positive for marijuana. He had no known vascular risk factors. With cognitive rehabilitation and discontinuation of illicit drug use, he demonstrated a significant improvement in his memory function over the course of six months. Brain MRI in both patients showed symmetric bilateral hippocampal diffusion restriction without post-contrast enhancement with corresponding hyperintensities on fluid-attenuated inversion recovery sequences. In both patients, cerebrospinal fluid (CSF) studies were unremarkable for inflammation or infection, and electroencephalograms were normal in awake and drowsy states. Bilateral hippocampal ischemia should be considered as a potential cause of acute onset anterograde amnesia in patients with a history of cocaine abuse. Other substances such as heroin and dexmethylphenidate may potentially increase susceptibility for hippocampal ischemia in patients using cocaine. Discontinuation of illicit drug abuse can influence the degree of recovery from acute bilateral hippocampal ischemia.
海马体缺血是可卡因滥用的一种罕见并发症，一直被认为是由血管痉挛、缺氧损伤和/或儿茶酚胺能兴奋性毒性引起的。我们报告了两例滥用可卡因的患者，他们因双侧海马体缺血而出现急性顺行性失忆，且结局不同。病例1是一名49岁男性，有静脉注射海洛因滥用史，在被发现昏迷了一段时间后前来就诊。他醒来后对入院前的事情毫无记忆，并且无法记住新信息。尿液毒理学检查显示可卡因和阿片类药物呈阳性。传统血管危险因素包括肥胖、高血压和高脂血症。他的康复因持续吸毒和一次心脏骤停而复杂化。尽管进行了认知康复治疗，但在年度随访期间，他的顺行性记忆仅出现了极小的改善。病例2是一名23岁男性，有注意力缺陷障碍病史，曾使用右哌甲酯治疗，并有持续滥用大麻和可卡因的病史，他出现了恶心、呕吐、胸痛、呼吸急促和急性短期记忆丧失。尿液毒理学检查显示可卡因和阿片类药物呈阴性，大麻呈阳性。他没有已知的血管危险因素。通过认知康复治疗和停止非法药物使用，他在六个月的时间里记忆功能有了显著改善。两名患者的脑部磁共振成像均显示双侧海马体对称弥散受限，增强扫描无强化，在液体衰减反转恢复序列上有相应的高信号。两名患者的脑脊液研究均未发现炎症或感染迹象，脑电图在清醒和嗜睡状态下均正常。对于有可卡因滥用史的患者，双侧海马体缺血应被视为急性顺行性失忆的潜在原因。其他物质，如海洛因和右哌甲酯，可能会增加使用可卡因患者海马体缺血的易感性。停止非法药物滥用可影响急性双侧海马体缺血的恢复程度。
