Toxic encephalopathy caused by occupational exposure to 1, 2-Dichloroethane.

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.