Aallam Mina, Nfaoui Nada, Zakaria Yasmina, Chraa Mohamed, Louhab Nissrine
Neurology, Mohammed VI University Hospital Center, Marrakesh, MAR.
Neurology, Mohammed VI University Hospital Center, Cadi Ayyad University, Marrakesh, MAR.
Cureus. 2025 May 13;17(5):e84024. doi: 10.7759/cureus.84024. eCollection 2025 May.
Carbon monoxide (CO) poisoning is the leading cause of death from accidental poisoning worldwide. It is associated with significant mortality and morbidity. The mere notion of exposure to risk should lead to the diagnosis of CO poisoning in an emergency situation. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms: carboxyhemoglobin formation, cytochrome oxidase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon. Delayed neurological sequelae (DNS) or delayed encephalopathy is characterized by a neurological clinical picture that arises after acute CO intoxication and after a period of apparent recovery. The onset of DNS is unpredictable. The true prevalence of DNS is difficult to determine; the estimates range from 1% to 47% of patients after CO poisoning. The exact incidence rate is also unclear. Studies using rigorous methodologies, including neuropsychological testing, report the frequency to be as high as 67%. CO poisoning causes severe neurocognitive after-effects that are rarely studied in the literature. Here, we describe the case of a patient aged 18 years old with no known comorbidities, a victim of accidental CO poisoning, who initially presented with behavioral disorders. The evolution was marked by the occurrence of memory and attention disorders a few weeks later. Neuropsychological assessment revealed a dysfunction of several processes (executive, attentional, and memory). Brain MRI revealed restrictive bilateral occipital, frontal, and temporal lesions of hypoxic origin. The patient underwent three sessions of hyperbaric oxygen therapy and received symptomatic drug treatment and neurocognitive rehabilitation, with a more or less favorable evolution of her disorders.
一氧化碳（CO）中毒是全球意外中毒致死的主要原因。它与显著的死亡率和发病率相关。在紧急情况下，仅仅接触风险这一概念就应促使对CO中毒进行诊断。神经学（昏迷和迟发性神经心理后遗症）和心脏学（冠状动脉正常但有缺血性改变）的临床情况可通过复杂机制来解释：碳氧血红蛋白的形成、细胞色素氧化酶抑制、氧化应激以及缺血再灌注现象。迟发性神经后遗症（DNS）或迟发性脑病的特征是在急性CO中毒后及一段明显恢复时期后出现的神经学临床表现。DNS的发作不可预测。DNS的真实患病率难以确定；估计在CO中毒患者中的比例为1%至47%。确切的发病率也不清楚。使用包括神经心理测试在内的严格方法进行的研究报告其发生率高达为67%。CO中毒会导致严重的神经认知后遗症，而这在文献中很少被研究。在此，我们描述一名18岁、无已知合并症的意外CO中毒患者的病例，该患者最初表现为行为障碍。几周后出现记忆和注意力障碍，病情发展明显。神经心理评估显示多个过程（执行、注意力和记忆）功能障碍。脑部MRI显示双侧枕叶、额叶和颞叶有缺氧性起源的局限性病变。该患者接受了三次高压氧治疗，并接受了对症药物治疗和神经认知康复，其病情或多或少有所好转。
