León-Ruiz M, Jiménez-Jiménez F J, Benito-León J
Hospital Quirónsalud San José, Madrid, España.
Hospital Universitario del Sureste, Arganda del Rey, España.
Rev Neurol. 2022 Jun 16;74(12):403-407. doi: 10.33588/rn.7412.2021288.
Cadmium is an important heavy metal in neurobiology, with potential neurotoxic effects, often in the form of polyneuropathy (PNP).
We present an exceptional case of PNP due to cadmium of toxic-occupational origin, specifically a 47-year-old man, aeronautical mechanic, with a 5-year clinical picture, consisting of a tingling sensation having a 'glove and stocking' distribution of symptoms and bimanual manipulative clumsiness. The neurological examination revealed bilateral achilles hyporeflexia and protopathic-thermal-algesic exteroceptive hypoesthesia in hands and feet. The following complementary rests were requested: toxic-metabolic-infectious-vitamin profile, full craniospinal MRI, electroneurographic-electromyographic study (ENG-EMG) of the upper and lower limbs, PET-CT body and 24-hour video-electroencephalogram. The results were consistent with an axonal, distal, symmetric sensory-motor PNP, of moderate intensity, chronic evolution, with active denervation, of toxic-occupational origin due to cadmium. The patient continued on sick leave to cease exposure to cadmium, initiating intensive multimodal neurorehabilitation program, with serial analytical determinations of toxins and new ENG-EMG studies every 6 months. With normalization of the altered values ??and complete clinical restitution at one-year follow-up.
This case highlights the importance of including the toxicological determination of cadmium in case of suspicion of a PNP of toxic-occupational origin, once ruled out other etiologies, in order to early interrupt occupational exposure, as it is a potentially reversible cause of peripheral neuropathy. Currently there is no specific pharmacological treatment against cadmium tested in humans. Randomized clinical trials carried out in these patients are warranted to develop an anti-cadmium drug in refractory cases despite the end of exposure.
镉是神经生物学中的一种重要重金属,具有潜在的神经毒性作用,常表现为多发性神经病(PNP)。
我们呈现了一例因职业性镉中毒导致的PNP特殊病例,具体为一名47岁的男性航空机械师,有5年的临床表现,包括呈“手套和袜套”样分布的刺痛感以及双手操作笨拙。神经系统检查显示双侧跟腱反射减弱,手足原发性热痛觉减退。要求进行以下辅助检查:毒理学 - 代谢 - 感染 - 维生素谱、全颅脊髓MRI、上下肢神经电图 - 肌电图研究(ENG - EMG)、全身PET - CT以及24小时视频脑电图。结果符合轴索性、远端、对称性感觉运动型PNP,强度中等,慢性进展,伴有失神经活动,由职业性镉中毒引起。患者继续休病假以停止接触镉,启动强化多模式神经康复计划,每6个月进行毒素系列分析测定和新的ENG - EMG研究。在一年随访时,异常值恢复正常且临床完全恢复。
该病例强调了在怀疑职业性中毒导致的PNP且排除其他病因后,进行镉的毒理学测定的重要性,以便早期中断职业接触,因为这是周围神经病变的一个潜在可逆原因。目前尚无针对镉的经过人体试验的特异性药物治疗。尽管接触已停止,但对这些患者进行随机临床试验以开发难治性病例的抗镉药物是有必要的。