TY - JOUR
T1 - Toxic encephalopathy caused by occupational exposure to 1, 2-Dichloroethane
AU - Liu, Jian Ren
AU - Fang, Shan
AU - Ding, Mei Ping
AU - Chen, Zhi Cai
AU - Zhou, Jia Jun
AU - Sun, Fen
AU - Jiang, Biao
AU - Huang, Jian
N1 - Funding Information:
This work was supported by grant (No. 30600193 ) from the National Natural Science Foundation of China (J.R. Liu), the grant (No. 2009R10022 ) of Qianjiang talent project from Bureau of Science and technology of Zhejiang province, China (J.R. Liu), the Youth Talent Special Fund of the Health Bureau of Zhejiang Province, China (No. 2004QN012 , J.R. Liu), and the Health Bureau of Zhejiang Province, China ( 2007A100 , J.R. Liu).
PY - 2010/5/15
Y1 - 2010/5/15
N2 - This study describes the clinical and neuroimaging features of five patients with 1, 2-Dichloroethane (DCE) toxic encephalopathy. From January 1st 1998 to June 30th 2009, five patients who were subsequently diagnosed with DCE toxic encephalopathy were admitted to our hospital. All were female workers who had been in contact with DCE and subsequently had had seizures or symptoms of intracranial hypertension, including headache, nausea, and vomiting. The cranial MRI showed extensive brain edema in either the subcortical white matter, bilateral globus pallidus, and cerebellar nucleus dendatus, or the cortices. Of the five patients in the study, three had vasogenic edema, one had cytotoxic edema, and one had both types of edema. Following treatment with steroids and mannitol for 3 to 10 weeks, all patients made either a partial or complete recovery. The imaging findings were resolved on a follow-up MRI. It is clear that occupational exposure to DCE can cause severe toxic encephalopathy. Moreover, extensive brain edema, secondary to blood-brain barrier damage or neuronal injury, is the major neuroimaging feature and the cause of clinical manifestations. Early diagnosis and prompt treatment leads to a good outcome.
AB - This study describes the clinical and neuroimaging features of five patients with 1, 2-Dichloroethane (DCE) toxic encephalopathy. From January 1st 1998 to June 30th 2009, five patients who were subsequently diagnosed with DCE toxic encephalopathy were admitted to our hospital. All were female workers who had been in contact with DCE and subsequently had had seizures or symptoms of intracranial hypertension, including headache, nausea, and vomiting. The cranial MRI showed extensive brain edema in either the subcortical white matter, bilateral globus pallidus, and cerebellar nucleus dendatus, or the cortices. Of the five patients in the study, three had vasogenic edema, one had cytotoxic edema, and one had both types of edema. Following treatment with steroids and mannitol for 3 to 10 weeks, all patients made either a partial or complete recovery. The imaging findings were resolved on a follow-up MRI. It is clear that occupational exposure to DCE can cause severe toxic encephalopathy. Moreover, extensive brain edema, secondary to blood-brain barrier damage or neuronal injury, is the major neuroimaging feature and the cause of clinical manifestations. Early diagnosis and prompt treatment leads to a good outcome.
KW - 1,2-Dichloroethane
KW - Brain edema
KW - Diffusion weighted MR imaging
KW - MR imaging
KW - Neuroimaging
KW - Occupational exposure
KW - Toxic encephalophy
UR - http://www.scopus.com/inward/record.url?scp=77949874193&partnerID=8YFLogxK
U2 - 10.1016/j.jns.2010.01.022
DO - 10.1016/j.jns.2010.01.022
M3 - Article
C2 - 20163807
AN - SCOPUS:77949874193
SN - 0022-510X
VL - 292
SP - 111
EP - 113
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
IS - 1-2
ER -