Chorea following acute carbon monoxide poisoning

The clinical cases of 6 patients suffering with chorea after acute carbon monoxide (CO) poisoning were reviewed. There were 2 men and 4 women, and the age at onset ranged from 11 to 60 (mean 33.0) years. All the patients except one were associated with mild delayed CO encephalopathy. The latency period between CO poisoning and the onset of chorea was 10 to 30 (mean 21.7) days. The duration of chorea after CO poisoning was 14 to 90 (mean 39.8) days. The brain CT findings were bilateral low- density lesions in the basal ganglia and/or in the white matter of the cerebral cortex, and there was no correlation between the lesion sites on the imagings and the development of chorea. Neuroleptic agents alleviated the chorea and the patients did not relapse after neuroleptic agents were halted.     

Evaluation of outcome after acute carbon monoxide poisoning by brain CT.

Of 129 patients with carbon monoxide (CO) poisoning, 62(48.0%) had characteristic computed tomographic (CT) findings. The most common finding, seen in 42 patients, was low-density in the cerebral white matter, and the second characteristic feature, seen in 33 patients, was low-density in both globus pallidi. Abnormal CT findings tended to increase in accordance with the duration of unconsciousness during acute CO poisoning, but such findings occurred even when the mental state was clear during acute illness. The prognosis of acute CO poisoning depended on low-density lesions of the cerebral white matter rather than those of the globus pallidus. There also seemed to be a significant correlation between the cerebral white matter changes in the initial CT scan and the development of delayed neurologic sequelae after acute CO poisoning, particularly in middle age or older patients, but no correlation between the CT findings and the clinical outcome of delayed neurologic sequelae.     

Pathophysiology of brain injuries in acute carbon monoxide poisoning: A novel hypothesis

Acute carbon monoxide (CO) poisoning causes the neurologic symptoms and brain lesions during both acute and delayed phase. We propose that catecholamine crises in globus pallidus and deep white matter are the key pathophysiological factors causing acute and delayed brain injuries respectively. Increased sympathetic activities due to acute CO poisoning is followed by increases of catecholamine levels in synapses or nerve terminals in organs including the brain, especially, limbic system. A dopamine excess in the synaptic cleft of the mesolimbic system, including globus pallidus, may cause the destruction of synapses and nuclei in the globus pallidus. Consequently, the striatal lesion is affected in the acute phase of CO intoxication. Moreover, an increase of catecholamine levels in synapses of deep white matter can persist after the acute stage of CO intoxication. A dopamine excess could lead to oxidative metabolism of dopamine, serotonergic axonal injury, or secondary myelin damage.     

Accidental carbon monoxide poisoning in our homes

Carbon monoxide (CO) is a colorless, odorless, tasteless, nonirritating, but significantly toxic gas. It is a product of combustion of organic matter in presence of insufficient oxygen supply. Symptoms of mild poisoning include headaches, vertigo and flu like effects, whereas larger exposures can lead to significant toxicity of the central nervous system (CNS), heart, and even death. We are reporting two cases that presented to us in the winter months of December to January with history, sign, symptoms, and radiological evidence of suspected CO poisoning.     

Acute carbon monoxide poisoning as the cause of rhabdomyolysis and acute renal failure

Acute renal failure (ARF) is a severe complication of acute CO poisoning which, combined with other organ lesions, may result in lethal outcome. In all vague cases of ARF with nontraumatic rhabdomyolysis, CO poisoning should be considered as a possible etiologic factor. The diagnosis is made on the basis of several simple laboratory tests: determination of carboxyhemoglobin concentration, demonstration of myoglobin in urine or pigment granulated cylindres in urinary sediment, positive orthotoluidine test, and high CPK values originating from skeletal musculature. Many authors report on excellent prognosis in ARF due to nontraumatic rhabdomyolysis of various causes. Our case report shows that the prognosis of CO poisoned patient greatly depends on timely and appropriate treatment, severity of damage to other organs, and success of the treatment of complications such as hospital infections.     

亮蓝G减轻急性CO中毒大鼠海马的损伤

 目的：观察亮蓝G（BBG）对急性一氧化碳中毒（ACMP）引起的大鼠海马组织损伤的影响,探讨配体门控离子通道嘌呤能P2X₇受体（P2X₇R）在一氧化碳中毒脑损伤中的作用。方法：80只8~10周龄SD大鼠分为对照（control）组、ACMP组、ACMP+BBG组和BBG组。采用腹腔注射CO（100 mL/kg）的方法制备大鼠ACMP模型。检测静脉血中的碳氧血红蛋白（HbCO）浓度来判断CO中毒程度。RT-qPCR检测大鼠海马组织P2X₇R的mRNA表达。干湿称重法检测海马组织水肿程度。ELISA法检测海马组织促炎因子白细胞介素1β（IL-1β）、肿瘤坏死因子α（TNF-α）和IL-6的含量。Morris水迷宫实验评价学习记忆能力。HE染色观察海马CA1区细胞形态学改变。结果：与control组（100%）相比,染毒6 h后ACMP组大鼠的存活率降低至55%;海马组织P2X₇R的mRNA表达及促炎因子IL-1β、TNF-α和IL-6的含量均明显增加（P<0.05）;含水量升高到80.72%±0.93%;大鼠逃避潜伏期明显延长,在目标象限探索时间明显缩短。值得注意的是,BBG预处理可以明显改善ACMP诱导的这些海马损伤。另外,大鼠染毒后3 d,海马CA1区的神经元排列紊乱稀疏,细胞形态不完整,细胞核深染、固缩。而BBG预处理能够显著改善CA1区的细胞形态。结论：P2X₇R与ACMP诱导的海马损伤相关。BBG能够增加ACMP大鼠的存活率,减少促炎因子的释放,减轻海马水肿,改善学习记忆能力,减轻ACMP引起的CA1区神经元损伤。