Schneider J S, Tobe E H, Mozley P D, Barniskis L, Lidsky T I
Thomas Jefferson University Medical School, Department of Pathology, Philadelphia, PA 19107, USA.
Occup Med (Lond). 1998 May;48(4):255-60. doi: 10.1093/occmed/48.4.255.
This case study describes the long-term after-effects of hydrogen sulphide exposure in a previously health 27-year-old male. Upon hospital admission the patient had a Glasgow Coma Score (CGS) of 3; with emergency treatment including hyperbaric oxygen treatments, he progressed to a GCS of 15 on day 7. Although both CT and MRI scans were unremarkable, PET using F-18 deoxyglucose administered 3 years after the accident showed abnormally decreased metabolism bilaterally in the temporal and inferior parietal lobes as well as the left thalamus. Uptake in the striatum was heterogeneous and abnormal. A cerebral perfusion study using SPECT performed 3.5 years after the accident revealed bilaterally decreased flow in the putamen but no cortical abnormalities. Neuropsychological and neurofunctional testing revealed the following impairments: microsmia, psychomotor slowing, extrapyramidal signs and deficits in memory and executive/planning functioning. These findings are discussed in the context of hydrogen sulphide's known mechanisms of toxicity and the functions of the basal ganglia.
本案例研究描述了一名既往健康的27岁男性硫化氢中毒的长期后遗症。入院时患者格拉斯哥昏迷评分（GCS）为3分；经过包括高压氧治疗在内的紧急治疗，他在第7天GCS进展至15分。尽管CT和MRI扫描均无异常，但在事故发生3年后进行的使用F-18脱氧葡萄糖的PET检查显示，双侧颞叶、顶叶下部以及左侧丘脑代谢异常降低。纹状体摄取不均匀且异常。事故发生3.5年后进行的使用SPECT的脑灌注研究显示双侧壳核血流减少，但无皮质异常。神经心理学和神经功能测试显示存在以下损伤：嗅觉减退、精神运动迟缓、锥体外系体征以及记忆和执行/计划功能缺陷。将结合硫化氢已知的毒性机制和基底神经节的功能对这些发现进行讨论。
