A case of transient choreoathetosis with amnesic syndrome after acute monoxide poisoning

We report a case of acute CO poisoning, followed after 9 days by the onset of choreoathetosis in the upper limbs and face, in a 24 year old man. The patient also showed memory disturbances that tended to clear gradually within about six months. CT scan and NMR revealed symmetrical bilateral lesions in the globus pallidus.

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Sommario Viene riportato un caso di intossicazione acuta da CO in un uomo di 24 anni, seguita dopo 9 giorni dall'insorgenza di movimenti di tipo coreoatetosico a carico degli arti superiori e del volto. Il p. presentava inoltre turbe mnestiche, sia a breve che a lungo termine, perduranti anche a distanza di mesi dall'epoca dell'intossicazione. Gli esami TC e RMN hanno mostrato la presenza di una lesione pallidale bilaterale e simmetrica.

     

Delayed choreoathetosis following acute carbon monoxide poisoning

Ten days after accidental exposure to carbon monoxide, a 17-year-old youth developed transitory choreoathetosis of both arms, face, and neck, with moderate dysarthria. CT revealed symmetric bilateral infarction in the head of the caudate nucleus, the putamen, and the small parts of the anterolateral globus pallidus.     

A case of delayed post-anoxic encephalopathy after acute carbon monoxide poisoning

The authors report the case of a young 18 year-old man presenting delayed encephalopathy after severe intoxication with carbon monoxide, and transient cerebral swelling. This condition is characterized by diffuse demyelinating lesions of both cerebral hemispheres, the mechanism of which is unknown.     

急性一氧化碳中毒及迟发性脑病的临床与MRI

目的探讨急性一氧化碳中毒(ACOP)及迟发性脑病(DEACMP)患者的临床表现与头颅MRI特点。方法对ACOP 564例、DEACMP 102例患者均行头颅MRI及DWI检查,急性期患者在入院后48h内进行检查,DEACMP在临床出现异常表现后即行头颅MRI检查。结果 ACOP患者临床表现及MRI表现可分为3型:①苍白球受累型;②弥漫性脑肿胀型;③大脑皮质及白质受累型。DEACMP患者临床表现及MRI表现可分为5型:(1)脑白质受累型;(2)基底节受累型;(3)枕叶皮层受累型;(4)小脑半球受累型;(5)多灶型。结论 ACOP及DEACMP的MRI表现既有相同点又有区分点,临床应加以区分,并依据MRI的表现作出不同诊断与治疗。并报道了CO中毒并发皮质盲12例及持续低热3例。     

Severe chorea after acute carbon monoxide poisoning.

Ten days after an acute exposure to carbon monoxide, a 33-year-old woman exhibited severe chorea. CT scan revealed bilateral lucencies of the pallidum and anterior arm of the internal capsule. Chorea was successfully treated by chlorpromazine and did not relapse after treatment withdrawal. The mechanism of chorea in acute carbon monoxide poisoning is discussed.     

Mechanism of delayed encephalopathy after acute carbon monoxide poisoning

Many hypotheses exist regarding the mechanism underlying delayed encephalopathy after acute carbon monoxide poisoning(DEACMP), including the inflammation and immune-mediated damage hypothesis and the cellular apoptosis and direct neuronal toxicity hypothesis; however, no existing hypothesis provides a satisfactory explanation for the complex clinical processes observed in DEACMP. Leucine-rich repeat and immunoglobulin-like domain-containing protein-1(LINGO-1) activates the Ras homolog gene family member A(Rho A)/Rho-associated coiled-coil containing protein kinase 2(ROCK2) signaling pathway, which negatively regulates oligodendrocyte myelination, axonal growth, and neuronal survival, causing myelin damage and participating in the pathophysiological processes associated with many central nervous system diseases. However, whether LINGO-1 is involved in DEACMP remains unclear. A DEACMP model was established in rats by allowing them to inhale 1000 ppm carbon monoxide gas for 40 minutes, followed by 3000 ppm carbon monoxide gas for an additional 20 minutes. The results showed that compared with control rats, DEACMP rats showed significantly increased water maze latency and increased protein and m RNA expression levels of LINGO-1, Rho A, and ROCK2 in the brain. Compared with normal rats, significant increases in injured neurons in the hippocampus and myelin sheath damage in the lateral geniculate body were observed in DEACMP rats. From days 1 to 21 after DEACMP, the intraperitoneal injection of retinoic acid(10 mg/kg), which can inhibit LINGO-1 expression, was able to improve the above changes observed in the DEACMP model. Therefore, the overexpression of LINGO-1 appeared to increase following carbon monoxide poisoning, activating the Rho A/ROCK2 signaling pathway, which may be an important pathophysiological mechanism underlying DEACMP. This study was reviewed and approved by the Medical Ethics Committee of Xiangya Hospital of Central South Hospital(approval No. 201612684) on December 26, 2016.     

Delayed hyperbaric oxygen treatment after acute carbon monoxide poisoning

Journal of Neurology -     

依达拉奉联合地塞米松治疗急性一氧化碳中毒后迟发性脑病疗效观察

目的 观察依达拉奉联合地塞米松对急性一氧化碳中毒后迟发性脑病( DEACMP) 的治疗作用.方法 将80 例有昏迷史的DEACMP患者分为治疗组(40例)和对照组(40例).对照组予高压氧、脑细胞活化剂、烟酸治疗.治疗组在对照组治疗的基础上加用依达拉奉30mg+生理盐水100ml静滴,2次/d,连续治疗7～14d;地塞米松10mg静滴,1次/d,连续5d.观察并比较2组治疗效果.结果 治疗组有效率(92.5%)明显高于对照组(70.0%),2组之间差异有统计学意义(χ2=6.65,P<0.01).结论 应用依达拉奉、地塞米松、高压氧等综合治疗DEACMP,多数患者可以获得满意的疗效.     

Parkinsonism after carbon monoxide poisoning

Of 242 patients with carbon monoxide (CO) poisoning examined between 1986 and 1996, parkinsonism was diagnosed in 23 (9.5%). There were 11 men and 12 women. The age at onset ranged from 16 to 69 (mean 45.8) years, with the peak incidence during the 6th decade. The latency before the appearance of parkinsonism varied from 2 to 26 (median 4) weeks, but parkinsonism developed within 1 month after an acute insult in the majority of the patients. All showed encephalopathy with mildly to severely impaired cognitive functions during or immediately after delayed CO sequelae. The common symptoms were gait disturbance, impaired mentality, urinary incontinence, and mutism. The most frequent signs were short-step gait, hypokinesia, masked face, increased muscle tone (rigidity), glabella sign, grasp reflex, and retropulsion. Intentional tremor was occasionally found, but resting tremor could not be seen. There was no correlation between the neuroimaging findings and the development of parkinsonism. Levodopa and anticholinergic drugs were not effective. Of 16 patients followed up for 1 year, 13 (81.3%) recovered spontaneously within 6 months. In conclusion, parkinsonism after CO poisoning is not rare and usually appears as a part of delayed CO encephalopathy. Any drug is not effective, but the prognosis is good.     

急性一氧化碳中毒后迟发性脑病神经元特异性烯醇化酶的测定和意义

目的　探讨急性一氧化碳中毒后迟发性脑病 (DEACMP)患者脑神经元的损伤。方法　应用酶联免疫分析法测定 4 0例DEACMP患者和 30例对照组血清及脑脊液 (CSF)神经元特异性烯醇化酶 (NSE)浓度。应用直线相关分析方法分析NSE浓度与病情严重程度以及预后的关系。结果　对照组血清和CSFNSE浓度分别为 (8.0 1± 6 .78)ug/L和 (6 .74± 5 .31)ug/L。观察组血清和CSFNSE浓度分别为 (15 .2 1± 6 .78)ug/L和 (13.6 1± 5 .2 7)ug/L。观察组与对照组之间存在明显的统计学差异 (P <0 .0 1)。NSE浓度与病情严重程度及预后之间存在相关性。结论　DEACMP患者血清及CSFNSE浓度明显增高 ,NSE浓度的高低可作为脑神经元损伤的量化指标 ,也可能是判断病情、估计预后的重要参数。     

急性一氧化碳中毒后迟发性脑病发病的危险因素分析

目的探讨急性一氧化碳中毒后迟发性脑病(DEACMP)发病的相关危险因素。方法以2001—2014年在豫北地区10家医院符合入组标准和排除标准的急性一氧化碳中毒(ACMP)752例住院患者为研究对象,收集临床资料,并随访90d以上,根据以后是否发生DEACMP分为ACMP组和DEACMP组,对所有患者的年龄、昏迷时间、昏迷程度、吸烟饮酒史等26个指标进行统计归纳,分析ACMP后患者发生DEACMP的可能危险因素。结果 752例ACMP患者中127例发生DEACMP,发生率16.9%。单因素分析结果显示,ACMP患者男性较女性更易患DEACMP,差异有统计学意义(P0.05);昏迷时间12h者DEACMP发生率明显升高,48h者58.3%发生DEACMP;中度以上昏迷、病理征阳性、丧偶、吸烟史、饮酒史、重大精神刺激等患者发生DEACMP风险大于无此类病史者,差异均有统计学意义(P0.05);ACMP急性期颅脑CT异常、并存其他疾病其DEACMP发生率较高,差异有统计学意义(P0.05)。多因素回归分析显示,性别、丧偶、头颅CT异常、昏迷程度、昏迷时间是发生DEACMP的独立危险因素。结论发生DEACMP的危险因素较多,尤其对40岁以上、男性、有丧偶史、头颅CT异常、中度昏迷以上、昏迷时间12h的ACMP患者应特别注意加强临床监测,提前采取干预措施给予病前预防性治疗。     

急性一氧化碳中毒后迟发性脑病的预后因素分析

目的探讨影响急性一氧化碳中毒后迟发性脑病（DEACMP）预后的因素。方法回顾性分析2008年7月至2011年3月在川北医学院附属医院神经内科住院的42例DEACMP患者临床资料,根据其恢复情况将患者分为无效组（n=21）和好转组（n：21）,分别比较两组患者年龄、性别、基础疾病、中毒时间、意识丧失时间、假愈期、入院时日常生活活动量表（ADL）评分、并发症、是否在急性期接受高压氧（HBO）治疗、头颅CT是否异常、头颅MRI是否异常以及是否使用神经节苷脂（GM1）、依达拉奉、多奈哌齐治疗等可能影响DEACMP预后的因素。结果年龄、假愈期、人院时ADL评分以及并发症与DEACMP患者预后相关（P〈0．05）,其中年龄和最低ADL评分更具意义（P〈0．01）,而其余因素对DEACMP患者预后无明显影响（P〉0．05）。结论年龄较大、假愈期较短、入院时ADL评分较低以及出现并发症均提示DEACMP患者预后不良,应高度警惕。     

A case of cortical blindness due to carbon monoxide poisoning

We report a case of cortical blindness occurring 7 days after acute CO poisoning with no other neurological or psychic deficits apart from denial of the blindness with visual confabulation and slight loss of retentive memory. There was scant correlation between the course of the clinical pattern, which cleared completely within 6 days, and the electroencephalographic pattern with marked and diffuse slowing, which did not recede completely during 3 months observation. CT scanning of the skull, initially within normal limits, displayed 2 weeks later a faint but diffuse hypodensity of the white substance, more marked in the occipital region, which was no longer present 80 days after the first scan.

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Sommario Viene descritto un caso di cecità corticale comparsa sette giorni dopo un 'intossicazione acuta da CO, senza altri deficit neurologici e psichici, tranne anosognosia con confabulazioni limitate alla sfera visiva e lieve deficit della memoria di fissazione. Si rileva una scarsa corrispondenza tra l'evoluzione del quadro clinico, risoltosi completamente entro il sesto giorno dall'esordio, e la persistenza di marcati rallentamenti elettroencefalografici diffusi, non completamente regrediti nei tre mesi successivi di osservazione. L'esame TC del cranio, inizialmente nella norma, evidenzia, dopo due settimane, una sfumata ipodensità diffusa della sostanza bianca, più marcata a livello occipitale, che scompare al successivo controllo effettuato dopo 80 giorni.

     

一氧化碳中毒迟发性脑病临床和MRI特点分析

目的 探讨急性一氧化碳(CO)中毒迟发性脑病(DEACMP)的临床及MRI特点. 方法 中国医科大学附属盛京医院神经内科自2007年1月至2011年7月共收治23例DEACMP患者,回顾性分析患者的临床表现、影像学资料. 结果 DEACMP临床症状主要为智能障碍(91.3％)、锥体外系损害(65.2％)及精神行为异常(52.2％).MRI改变包括双侧皮质下白质和(或)侧脑室周围白质损害11例,双侧基底节(主要为双侧苍白球)损害4例,皮质下白质和(或)侧脑室周围白质与基底节同时受损害8例,其中单纯苍白球损害预后较好.均予高压氧、改善脑血循环药物、脑细胞营养药及对症治疗后,治疗总有效率为86.9％. 结论 头颅MRI检查对急性CO中毒后DEACMP的早期诊断、疗效观察和判定预后有重要的临床意义,及时足疗程的高压氧是重要和有效的治疗手段.