1.Analysis of 15 cases of toxic encephalopathy caused by acute benzene poisoning.
Qiong Na ZHENG ; Wen Shuang SHENG ; A Shan PAN
Chinese Journal of Industrial Hygiene and Occupational Diseases 2022;40(9):694-697
In this paper, the MRI manifestations of 15 patients with benzene toxic encephalopathy were analyzed, and the lesion location, shape, scope and signal were observed. The clinical manifestations of 15 patients were mainly central nervous system damage, and the MRI manifestations were characteristic, with a wide range of lesions, and the shapes were "sunflower-like", "flame-like", "bracket-like" and "butterfly-like", and the MRI signal was sheet-like long T(1), long T(2), fluid attenuated inversion recovery (FLAIR) sequence and diffusion weighted imaging (DWI) high signal, apparent diffusion coeffecient (ADC) map low, equal or high signals. When the patient's diagnosis is unclear, MRI examination may provide clinical basis for diagnosis.
Benzene
;
Diffusion Magnetic Resonance Imaging/methods*
;
Humans
;
Magnetic Resonance Imaging
;
Neurotoxicity Syndromes/etiology*
2.Imaging features of 10 patients with toxic encephalopathy caused by diquat.
Chinese Journal of Industrial Hygiene and Occupational Diseases 2022;40(5):362-365
Objective: To explore the CT and MRI imaging findings of diquat toxic encephalopathy. Methods: CT and MRI imaging features of 10 patients with diquat poisoning encephalopathy who had been clinically diagnosed were retrospectively reviewed. Results: CT was performed in all 10 patients, and MRI was performed in 8 patients. In 10 patients, 7 had positive signs on CT, and 8 patients with MRI examination had abnormal changes in the images. The main CT findings were symmetrical hypodensity in bilateral cerebellar hemisphere, brainstem, thalamus and basal ganglia, and swelling of brain tissue. The main MRI findings were symmetrical lesions and brain edema in the deep nuclei of cerebellar hemisphere, brainstem, thalamus and basal ganglia, low signal on T1WI, high signal on T2WI and T2-FLAIR, and cytotoxic edema on diffusion weighted imaging (DWI) . On review after treatment, both CT and MRI showed resorption of the lesion, which narrowed in size. Conclusion: The imaging findings of diquat poisoning encephalopathy are characteristic and the location of the lesion is characteristic, and CT and MRI have a certain diagnostic value in diquat poisoning encephalopathy, which is important for clinical treatment.
Brain Diseases
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Diffusion Magnetic Resonance Imaging/methods*
;
Diquat
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Humans
;
Magnetic Resonance Imaging/methods*
;
Neurotoxicity Syndromes/etiology*
;
Retrospective Studies
3.Neurological responses of embryo-larval zebrafish to short-term sediment exposure to decabromodiphenylethane.
Mei-Qing JIN ; Dong ZHANG ; Ying ZHANG ; Shan-Shan ZHOU ; Xian-Ting LU ; Hong-Ting ZHAO
Journal of Zhejiang University. Science. B 2018;19(5):400-408
Decabromodiphenylethane (DBDPE) has been widely used as an alternative flame retardant due to the restriction or phase-out of traditional polybrominated diphenyl ethers (PBDEs), and is of increasing concern regarding its ubiquity, persistence, and potential adverse effects. In the present study, the toxicological effects of DBDPE were evaluated using zebrafish as an in vivo model. Upon being exposed to DBDPE-polluted sediments for a short term, it was found that the mortality and malformation of zebrafish (including edema, bent notochord, and bent tail) were not affected even at the highest concentration tested (1000.0 µg/kg dry sediment). Regarding behavioral responses, it was found that zebrafish larvae of 48 hours post fertilization (hpf) in all groups escaped successfully with a touch to the dorsal fin. However, when exposed to the highest DBDPE concentration, the larvae of 120 hpf exhibited significantly smaller distances as compared to the control. Moreover, the results of the acetylcholinesterase (AChE) activity, the expression levels of two important nerve-related genes, and the cell apoptosis all indicated that DBDPE posed low neurotoxicity in embryo-larval zebrafish. The results in this study shed some light on the potential risks of DBDPE in the real environment and highlight the application of the sediment exposure route in the future.
Abnormalities, Drug-Induced
;
etiology
;
Animals
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Apoptosis
;
drug effects
;
Behavior, Animal
;
drug effects
;
Bromobenzenes
;
toxicity
;
Geologic Sediments
;
analysis
;
Larva
;
drug effects
;
Neurotoxicity Syndromes
;
etiology
;
Water Pollutants, Chemical
;
toxicity
;
Zebrafish
;
embryology
4.Initial Serum Ammonia as a Predictor of Neurologic Complications in Patients with Acute Glufosinate Poisoning.
Dong Keon LEE ; Hyun YOUK ; Hyun KIM ; Oh Hyun KIM ; Jin GO ; Tae Hoon KIM ; Kyoungchul CHA ; Kang Hyun LEE ; Sung Oh HWANG ; Yong Sung CHA
Yonsei Medical Journal 2016;57(1):254-259
PURPOSE: Glufosinate poisoning can cause neurologic complications that may be difficult to treat due to delayed manifestation. Studies assessing possible predictors of complications are lacking. Although serum ammonia level is a potential predictor of severe neurotoxicity, it has only been assessed via case reports. Therefore, we investigated factors that predict neurologic complications in acute glufosinate-poisoned patients. MATERIALS AND METHODS: We conducted a retrospective review of 45 consecutive glufosinate-poisoning cases that were diagnosed in the emergency department (ED) of Wonju Severance Christian Hospital between May 2007 and July 2014. Patients with a Glasgow Coma Scale (GCS) score of <8, seizure, and/or amnesia were defined to a neurologic complication group. RESULTS: The neurologic complication group (29 patients, 64.4%) comprised patients with GCS<8 (27 patients, 60.0%), seizure (23 patients, 51.1%), and amnesia (5 patients, 11.1%). Non-neurologic complications included respiratory failure (14 patients, 31.1%), intubation and ventilator care (23 patients, 51.1%), shock (2 patients, 4.4%), pneumonia (16 patients, 35.6%), acute kidney injury (10 patients, 22.2%), and death (4 patients, 8.9%). Complications of GCS<8, seizure, respiratory failure, and intubation and ventilator care appeared during latent periods within 11 hrs, 34 hrs, 14 hrs, and 48 hrs, respectively. Initial serum ammonia was a predictor of neurologic complications [odds ratio 1.039, 95% confidence interval (1.001-1.078), p=0.046 and area under the curve 0.742]. CONCLUSION: Neurologic complications developed in 64.4% of patients with acute glufosinate poisoning. The most common complication was GCS<8. Initial serum ammonia level, which can be readily assessed in the ED, was a predictor of neurologic complications.
Adult
;
Aged
;
Aged, 80 and over
;
Aminobutyrates/blood/*poisoning
;
Ammonia/*blood
;
*Emergency Service, Hospital
;
Female
;
Glasgow Coma Scale
;
Humans
;
Male
;
Middle Aged
;
Nausea/etiology
;
Neurotoxicity Syndromes/blood/immunology/*physiopathology
;
Respiratory Insufficiency/etiology
;
Retrospective Studies
;
Seizures/etiology
;
Severity of Illness Index
;
Vomiting/etiology
6.Heptachlor induced nigral dopaminergic neuronal loss and Parkinsonism-like movement deficits in mice.
Seokheon HONG ; Joohyun HWANG ; Joo Yeon KIM ; Ki Soon SHIN ; Shin Jung KANG
Experimental & Molecular Medicine 2014;46(2):e80-
Epidemiological studies have suggested an association between pesticide exposure and Parkinson's disease. In this study, we examined the neurotoxicity of an organochlorine pesticide, heptachlor, in vitro and in vivo. In cultured SH-SY5Y cells, heptachlor induced mitochondria-mediated apoptosis. When injected into mice intraperitoneally on a subchronic schedule, heptachlor induced selective loss of dopaminergic neurons in the substantia nigra pars compacta. In addition, the heptachlor injection induced gliosis of microglia and astrocytes selectively in the ventral midbrain area. When the general locomotor activities were monitored by open field test, the heptachlor injection did not induce any gross motor dysfunction. However, the compound induced Parkinsonism-like movement deficits when assessed by a gait and a pole test. These results suggest that heptachlor can induce Parkinson's disease-related neurotoxicities in vivo.
Animals
;
*Apoptosis
;
Astrocytes/drug effects/pathology
;
Cell Line, Tumor
;
Cells, Cultured
;
Dopaminergic Neurons/*drug effects/pathology
;
Gait
;
Heptachlor/*toxicity
;
Humans
;
*Locomotion
;
Mice
;
Neurotoxicity Syndromes/etiology/physiopathology
;
Parkinsonian Disorders/chemically induced
;
Pesticides/*toxicity
;
Substantia Nigra/*drug effects/pathology/physiopathology
8.Relationship between Quality of Life and Nurse-led Bedside Symptom Evaluations in Patients with Chemotherapy-induced Peripheral Neuropathy.
Asian Nursing Research 2014;8(1):36-41
PURPOSE: This cross-sectional study aimed at determining the relationship between patient-reported quality of life (QOL) and nurse-led bedside evaluations of chemotherapy-induced peripheral neuropathy symptoms. METHODS: One hundred ninety-five patients treated at the oncology clinic at our institution were assessed using Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity and nurse-led bedside examinations. The relationship between self-reported QOL and bedside examinations was evaluated using Spearman rank correlations. RESULTS: Scores of upper and lower extremity muscle strength based on the bedside examinations showed a weak negative correlation with the emotional well-being subscale of Functional Assessment of Cancer Therapy-General. Further, weak negative relationships were present between QOL and the following nurse-reported parameters: vibration perception in the hand, upper extremity muscle strength, touch and vibration perception in the feet, and tendon reflexes. CONCLUSION: Collectively, our results indicate that nurse-led bedside evaluation is a noninvasive and useful method for detecting neurotoxicity and evaluating the patient's QOL both during and after treatment.
Aged
;
Antineoplastic Agents/adverse effects
;
*Attitude of Health Personnel
;
Cross-Sectional Studies
;
Female
;
Humans
;
Male
;
Middle Aged
;
Neoplasms/drug therapy
;
Neurotoxicity Syndromes/*diagnosis/etiology
;
Nurses/*psychology
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Peripheral Nervous System Diseases/chemically induced/*diagnosis
;
Platinum Compounds/adverse effects
;
*Quality of Life
;
Questionnaires
;
Symptom Assessment/methods/*standards
;
Taxoids/adverse effects

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