Semnic Isidora, Rački Valentino, Perković Olivia, Vuletić Vladimira
Department of Neurology, Clinical Hospital Centre Rijeka, Rijeka, Croatia.
Department of Neurology, Faculty of Medicine, University of Rijeka, Rijeka, Croatia.
Front Toxicol. 2025 Sep 9;7:1580275. doi: 10.3389/ftox.2025.1580275. eCollection 2025.
The association between neurological symptomatology and heavy metal exposure has been reported in the literature. A few cases of extrapyramidal symptomatology and subacute combined degeneration have been described as manifestations of mercury intoxication. We highlight a case of a patient presenting with Parkinsonian features (tremor, rigidity, and bradykinesia), pyramidal deficits, dysarthria, paresthesia, mild cognitive decline, and emotional lability, with proven elevated mercury levels in blood and hair and elevated arsenic in urine.
A 60-year-old man, with history of mercury exposure while working at the Centre for Waste Management and Environmental Protection presented to a neurologist after 10 months of persistent tremors, muscle spasms, paresthesia, and irritability, followed by the onset of bradykinesia, slurred speech, rigidity, insomnia, and subtle cognitive decline. Laboratory investigations revealed functional vitamin B12 and vitamin D deficiencies, while toxicological quantitative analysis showed elevated blood mercury levels (15.2 μg/L) and hair root levels (3 μg/g). MRI of the brain was normal, whereas MRI of the posterior cervical spine detected signs of myelopathy. Florodeoxyglucose (FDG) Positron Emission Tomography (PET) of the brain revealed bilateral temporal and parietal glucose hypometabolism, most pronounced in the left inferior parietal and left superior temporal regions. Single-Photon Emission Computed Tomography (SPECT) imaging of dopaminergic neurons in the striatum was negative, and the patient was unresponsive to levodopa. Multivitamin therapy (vitamins B, E, and D) with selenium, in combination with symptomatic therapy (benzodiazepines, muscle relaxants, and antidepressants) provided minimal relief, leading to the introduction of N-acetyl cysteine, which resulted in moderate improvement of symptoms. Physical and speech therapy were of great importance in this case.
This case is unique because it represents the development of therapy-resistant extrapyramidal symptoms over 3 years of mercury exposure, likely leading to subacute combined degeneration due to functional vitamin B12 deficiency. Epidemiological data describe methylmercury poisoning, known as Minamata disease, which presents with -somatosensory deficits, ataxia, parkinsonism, dysarthria, and visual and hearing impairments.
Toxicological screening for heavy metals in blood and urine should be considered in patients presenting with unexplained, levodopa-resistant extrapyramidal symptoms, behavioral and sleep disturbances, cognitive decline, and other non-specific neurological signs.
文献中已报道神经症状与重金属暴露之间的关联。少数锥体外系症状和亚急性联合变性病例被描述为汞中毒的表现。我们重点介绍一例患者,其表现出帕金森氏症特征(震颤、僵硬和运动迟缓)、锥体束征、构音障碍、感觉异常、轻度认知衰退和情绪不稳定,经证实血液和头发中的汞含量升高,尿液中的砷含量升高。
一名60岁男性,有在废物管理与环境保护中心工作时接触汞的病史。在持续震颤、肌肉痉挛、感觉异常和易怒10个月后,出现运动迟缓、言语含糊、僵硬、失眠和轻微认知衰退,随后就诊于神经科医生。实验室检查显示功能性维生素B12和维生素D缺乏,而毒理学定量分析显示血液汞水平升高(15.2μg/L)和发根汞水平升高(3μg/g)。脑部MRI正常,而后颈部脊柱MRI检测到脊髓病迹象。脑部氟脱氧葡萄糖(FDG)正电子发射断层扫描(PET)显示双侧颞叶和顶叶葡萄糖代谢减低,在左下顶叶和左上颞叶区域最为明显。纹状体多巴胺能神经元的单光子发射计算机断层扫描(SPECT)成像为阴性,且患者对左旋多巴无反应。多种维生素疗法(维生素B、E和D)联合硒,再加上对症治疗(苯二氮䓬类、肌肉松弛剂和抗抑郁药)仅提供了轻微缓解,随后引入N - 乙酰半胱氨酸,症状有中度改善。在该病例中,物理治疗和言语治疗非常重要。
该病例独特之处在于,在3年的汞暴露过程中出现了对治疗耐药的锥体外系症状,可能由于功能性维生素B12缺乏导致亚急性联合变性。流行病学数据描述了甲基汞中毒,即水俣病,其表现为躯体感觉缺陷、共济失调、帕金森综合征、构音障碍以及视觉和听力损害。
对于出现无法解释的、对左旋多巴耐药的锥体外系症状、行为和睡眠障碍、认知衰退以及其他非特异性神经体征的患者,应考虑进行血液和尿液重金属毒理学筛查。