[Detection of neuron-specific enolase in patients with subacute 1, 2-dichloroethane poisoning].

Objective: To investigate the changes of neuron-specific enolase (NSE) in serum and cerebrospinal fluid of patients with subacute 1, 2-dichloroethane (DCE) poisoning. Methods: Ten patients with subacute 1, 2-DCE poisoning hospitalized in Guangzhou 12th Municipal People's Hospital from December 2014 to March 2019 were taken as the subacute 1, 2-DCE poisoning group, 34 typical acute toxic encephalopathy patients hospitalized at the same time as typical acute toxic encephalopathy group, 40 healthy physical examinees as normal control group. The levels of serum NSE in patients of subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy group during onset and improvement were detected by chemiluminescence method, and the results were analyzed statistically. The level of NSE in cerebrospinal fluid of subacute 1, 2-DCE poisoning group was detected and analyzed its correlation with the level of NSE in serum. Using receiver operator characteristic (ROC) curve to analyze the diagnostic efficacy of NSE in subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy (area under curve, AUC) . Results: There was no significant difference between the serum NSE level of the patients with subacute 1, 2-DCE poisoning in the onset group and the normal control group and the improvement group (P>0.05) . The serum NSE level of subacute 1, 2-DCE poisoning in the improvement group was lower than those in the normal control group (P<0.01) . The serum NSE level of the subacute 1, 2-DCE poisoning in the onset group was lower than those in the typical acute toxic encephalopathy in the onset group (P<0.01) . There was no linear correlation between cerebrospinal fluid NSE and serum NSE in patients with subacute 1, 2-DCE poisoning (r=-0.183, P=0.52) . ROC curve showed that the AUC of serum NSE in diagnosing subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy were 0.661 and 0.726, respectively. Conclusion: There is no significant change in serum NSE in patients with subacute 1, 2-DCE poisoning.

[Analysis of 18 cases of toxic encephalopathy caused by occupational acute 1, 2-dichloroethane poisoning].

Retrospective analysis of 18 cases of occupational acute 1, 2-dichloroethane (1, 2-DCE) poisoning. The results showed that all patients have the main manifestations such as dizziness, headache, unresponsiveness and other symptoms of nervous system damage; Brain CT showed varying degrees of diffuse white matter lesions. Brain MRI showed extensive involvement of white matter in both cerebral hemispheres. Affected white matter area presented low intensity on T1WI, hyperintensity on T2WI and T2-Flair; Lumbar puncture examination of cerebrospinal fluid (CSF) pressure (262.5±48.39) mm H(2)O; After treatment, the required time for CSF pressure to restore was (161.56±75.27) days (50-280) days. Summary, Occupational acute 1, 2-DCE poisoning caused by toxic encephalopathy can be manifested as persistent abnormalities in CSF pressure, and the CSF pressure drops slowly during treatment; Early head CT and lumbar puncture examination will be helpful for early detection of intracranial pressure in toxic encephalopathy caused by acute 1, 2-DCE poisoning. Dynamic monitoring of CSF provides guidance for acute 1, 2-DCE poisoning with a long time of treatment and various types of dehydrating agents.

[Dynamic observation of clinical course in patients with subacute 1, 2-dichloroethane poisoning].

OBJECTIVE: To observe the clinical characteristics and regular patterns of subacute 1, 2-dichloroethane poisoning patients for providing evidences to it's diagnosis, treatment and prognosis. METHODS: 51 cases of subacute 1, 2-dichloroethane poisoning analyzed. They were divided into 3 groups according to their main clinical manifestation: group A mainly with intracranial hypertension (n = 25), group B with limbs tremor (n = 18), group C with mental and behavior disorder (n = 8). All cases' clinical symptoms, cranial computer tomography, cerebrospinal pressure (Group A) were observed, the durations of the onset, deterioration, improvement, recovery and whole course of the disease were compared between groups and in each group. RESULTS: In all of 51 cases, only the differences between the deterioration duration of cranial CT and symptom was significantly (t = 2.555, P<0.05), which indicate the deterioration of symptom was earlier than radiological change. The symptom deterioration of group C was the fastest than group A and group B (P<0.00). As to the change of symptom duration, group B's improvement, recovery and whole course was the longest comparing with group A and group C (P<0.05). As to the change of cranial CT duration, group B's recovery duration was the shortest and group A's recovery duration was the longest (P<0.01); group B's whole course was also the shortest and group A's whole course was the longest (P<0.05). The clinical course of symptoms, cranial computer tomography, cerebrospinal pressure (Group A) was compared in each group, in group A, the duration of improvement and whole course of the cranial CT and cerebrospinal pressure change was longer than that of the symptom change (P<0.01), this indicated that group A has longer asymptomatic intracranial hypertension and their cranial radiography recover slowly. In group B, their symptoms (3.94 ± 4.31 days) deteriorated is earlier than cranial CT changes (P<0.05), the recovery (92.39 ± 55.04 days) and whole course of symptom was longer than cranial CT change (all P<0.01). In group C, symptom deterioration was earlier than CT deterioration (P< 0.05). CONCLUSION: The clinical characteristic of subacute 1, 2- dichloroethane poisoning is central nervous system damage, it differs according to the different stage of course, the regions and severity of pathology lesions.

[MRI image analysis of 1,2-dichloroethane chronic toxic encephalopath].

OBJECTIVE: To study the MRI features of 1,2-dichloroethane Chronic Toxic Encephalopathy of 10 cases. METHOD: 10 cases were examined by MRI, slice thickness 8 mm, layer from 2 mm, axial and coronal line scan, T1WI, T2WI, FLAIR imaging. RESULTS: 10 cases show varying degrees of abnormal signal of white matters, low signal intensity on T1WI, high signal intensity on T2WI and FLAIR. MRI could also show extensive abnormal signal in cerebral white matter although the toxic manifestation is mild to moderate. Therefore the symptoms and the shows of MRI could be inconsistent. CONCLUSION: Combined with a history of exposure, the show of varying degrees of abnormal signal of white matter in 1,2-dichloroethane Chronic Toxic Encephalopathy cases are characteristic.

Establishment of a poisoned animal model of toxic encephalopathy induced by 1,2-dichloroethane.

1,2-dichloroethane(1,2-DCE) is toxic, especially by inhalation due to its high vapour pressure. Inhalation of concentrated 1,2-DCE vapor can induce effects on the human nervous system, even encephalopathy. However, 1,2-DCE toxic encephalopathy has seldom been reported, and no adequate data were available to evaluate the encephalopathy of 1,2-DCE in experimental animals. The aim of the present study was to establish a toxic experimental animal model induced by 1,2-DCE. Dose effect and time effect of 1,2-DCE on the nervous system were detected. The rats were treated by 1,2-DCE at various concentrations of 0, 2.5, 5.0, 10.0 g/m3 for 6 h and treatment of rats at 10.0 g/m3 for 0, 3, 6, and 12 h. Morphology of brain tissue was observed by HE staining and TEM under light and electron microscope, besides water contents in the cortex and medulla of rats were analyzed. The results indicated that 1,2-DCE induced abnormal histopathology, and significantly higher water content were confirmed in the cerebral cortex of toxic animal model in a dose- and time-dependent manner. To declare that 1,2-DCE could induce toxic encephalopathy with a pathological feature of cerebral edema is very important for the medical rescue in urgent toxic accidents.

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.

[Clinical and cranial MRI analysis on five cases of toxic encephalopathy induced by dichloroethane].

OBJECTIVE: To investigate the clinical features, cranial MRI and treatment of toxic encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE). METHODS: The clinical, MRI features and treatment of 5 patients with toxic encephalopathy induced by 1,2-DCE were observed and analyzed. RESULTS: Five patients all presented with subacute onset with a history of direct exposure to 1,2-DCE. Lumbar cerebrospinal fluid pressures were all increased in 5 patients. All 5 patients had obvious intracranial hypertension. Liver and kidney function had no obvious abnormalities; Cranial MRI showed T1WI low signal and T2WI high signal in bilateral hemispheric white matter, cerebellar dentate nucleus and globus pallidus. After the treatment of dehydrating agent, glucocorticoid and supportive treatment, four patients were clearly improved, and one patient had cerebral hernia formation. CONCLUSION: The main neurological clinical features in patients with 1,2-DEC poisoning is obvious intracranial hypertension. The prognosis is usually good with early and long term use of glucocorticoids and dehydrating agent in poisoning patients.

[Effect of nicotinamide on the reactions of peroxide oxidation of biomolecules in the rat brain and erythrocytes in 1,2-dichloroethane toxic injury].

It was established that acute poisoning of rats by 1,2-dichloroethane induced considerable changes in lipid peroxidation indices, glutathione content and activity of antioxidant enzymes--superoxidase, catalase, glutathione peroxidase in the brain tissue, erythrocytes and blood plasma. It was shown that nicotinamide in the dose of 200 mg/kg prevented considerable degree of the intoxication caused by 1,2-dichloroethane as well as activation of lipid peroxidation and inhibition of antioxidant defens enzyme activities in tissue of experimental animals.