Seven cases of toxic encephalopathy associated with diquat poisoning / 中华急诊医学杂志

Objective:To improve the understanding of the clinical features of toxic encephalopathy associated with diquat poisoning.Methods:This study collected and analyzed the diagnosis and treatment process of 7 patients with acute diquat poisoning combined with central nervous system complications admitted to the First Affiliated Hospital of Zhengzhou University from April 2021 to April 2022. "Diquat" and "Poisoning" were used as keywords to search in CNKI, Wanfang database and PubMed database, and the literature of previous cases was reviewed for summary analysis.Results:Among the 7 patients in our hospital, there were 2 males and 5 females, with an average age of 31 years (range14-57) and an average dose of 23.14 g [(10-40)g]. During the treatment, 3 patients developed irritability and convulsions, 3 patients occurred coma, and one had generalized tonic-clonic seizures. Four patients died and 3 survived, of which 2 patients returned to normal life and study, and one remained abnormal mental behavior (currently in long-term follow-up). All three survivors developed neurological symptoms later than those who died, and were awake about 30 days after taking the drug.Conclusions:Toxic encephalopathy associated with diquat poisoning has rapid progression, poor prognosis and high mortality. This study found that the survival rate of patients with > 48 h of first onset of neurological symptoms is much higher than that of patients with ≤ 48 h of first onset of neurological symptoms, while sex, age, estimated oral dose, and type of presentation of neurological symptoms for the first time have little effect on the survival rate of hospital discharge. The earlier neurological symptoms appear, the greater the likelihood of a poor prognosis.

Imaging features of 10 patients with toxic encephalopathy caused by diquat / 中华劳动卫生职业病杂志

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.

Correlation between endothelial microparticles and subacute 1,2-dichloroethane toxic encephalopathy / 中国职业医学

OBJECTIVE: To explore the correlation between endothelial microparticles(EMPs) and subacute 1,2-dichloroethane(1,2-DCE) toxic encephalopathy. METHODS: A total of 24 patients with subacute 1,2-DCE toxic encephalopathy were selected as the case group, and 24 healthy individuals were selected as the control group using a convenient sampling method. Blood plasma was collected from the fasting venous blood of patients in these two groups, and the level of EMPs in the plasma was detected by flow cytometry. RESULTS: The levels of plasma EMPs of patients in the control group and the case group were(692.0±174.4) ×10~3/L and(839.8±155.8) ×10~3/L respectively. The levels of plasma EMPs in patients with mild, moderate and severe case subgroups were(691.6±101.9) ×10~3/L,(900.6±46.6) ×10~3/L and(1 026.8±69.8)×10~3/L respectively. The EMPs level of patients in the case group was higher than that of the control group(P<0.01). The level of EMPs in the moderate and severe case subgroups was higher than that of the control group and mild case subgroup(P<0.01). CONCLUSION: Endothelial injury was found in patients with subacute 1,2-DCE toxic encephalopathy and endothelial injury is related to the severity of poisoning.

Clinical analysis on 325 cases of trimethyl tin chloride-induced acute toxic encephalopathy / 中国职业医学

OBJECTIVE: To investigate the clinical characteristics of acute toxic encephalopathy caused by trimethyltin chloride(TMT). METHODS: Literatures related to TMT acute poisoning accidents occurred in China from 1998 to 2018 were collected and analyzed using the CNKI, WEIPU Database and WANFANG Database. The clinical manifestations, neuroimaging images, electroencephalography(EEG), treatment and other data were collected and analyzed. RESULTS: A total of 15 literatures were included in the study. These studies involved 15 incidents with 1 339 patients with TMT acute poisoning. Among them, 325 patients(24.3%) presented toxic encephalopathy. They were moderate to severe poisoning.The clinical manifestations were headache, dizziness, limb weakness, abnormal mental behavior and memory loss. Magnetic resonance imaging(MRI) and computed tomography(CT) were performed in 105 and 86 patients, respectively, with 29.5% and 26.7% of abnormal rate. There was no significant difference in the abnormal rate between the above two methods(P>0.05). 294 cases were examined by electroencephalogram. The abnormal rate was 93.9%, which was higher than that of the MRI and CT examination(P<0.05). Patients with toxic encephalopathy were treated with glucocorticoid. Some patients were treated with hyperbaric oxygen, nerve cell nutritional drugs and rehabilitation exercise after the conditions were stable. CONCLUSION: The patients with TMT toxic encephalopathy were moderately and severely poisoned by TMT. EEG examination is helpful for the diagnosis and treatment of TMT toxic encephalopathy.

An aggravated return-to-work case of organic solvent induced chronic toxic encephalopathy

BACKGROUND: Organic solvent-induced chronic toxic encephalopathy (CTE) is known as a non-progressive disorder that does not progress after diagnosis. The authors present a case those symptoms worsened after continued exposure to organic solvent after returning to work. Because such a case has not been reported in South Korea to the best of our knowledge, we intend to report this case along with literature review. CASE PRESENTATION: A 59-year-old man, who performed painting job at a large shipyard for 20 years, was receiving hospital treatment mainly for depression. During the inpatient treatment, severe cognitive impairment was identified, and he visited the occupational and environmental medicine outpatient clinic for assessing work relatedness. In 1984, at the age of 27, he began performing touch-up and spray painting as a shipyard painter. Before that he had not been exposure to any neurotoxic substances. In 2001, at the age of 44, after 15 years of exposure to mixed solvents including toluene, xylene and others, he was diagnosed with CTE International Solvent Workshop (ISW) type 2A. After 7 years of sick leave, he returned to work in 2006. And he repeated return-to-work and sick leave in the same job due to worsening of depressive symptoms. He had worked four times (2006–2010, 2011–2011, 2011–2011, 2016–2017) for a total of 5 years as a shipyard painter after first compensation. During the return-to-work period, the mean values of the mixed solvent index ranged from 0.57 to 2.15, and except for a one semiannual period, all mean values were above the standard value of 1. We excluded other diseases that can cause cognitive impairment like central nervous system diseases, brain injury, psychological diseases and metabolic diseases with physical examinations, laboratory tests, and brain image analysis. And finally, throughout neuropsychological tests, an overall deterioration in cognitive function was identified compared to 2002, and the deterioration types was similar to that often shown in the case of CTE; thus a diagnosis of CTE (ISW) type 3 was made. CONCLUSION: This case is showing that CTE can go on with continued exposure to mixed solvents. Appropriate “fitness to work” should be taken to prevent disease deterioration especially for the sick leave workers.

Clinical effect of electroencephalographic biofeedback therapy in treatment of memory disorders in patients with acute severe toxic encephalopathy / 中华劳动卫生职业病杂志

Objective@#To investigate the clinical effect and safety of electroencephalographic biofeedback therapy in improving memory disorders in patientsin the recovery stage of acute severe toxic encephalopathy.@*Methods@#A total of 52 patients in the recovery stage of acute severe toxic encephalopathy who were hospitalized in our hospital from March 2013 to December 2016 were enrolled and randomly divided into observation group with 27 patients and control group with 25 patients. Both groups were given the drugs to promote the metabolism of brain cells,and the patients in the observation group were given electroencephalographic biofeedback therapy in addition. The Chinese revised version of Wechsler Memory Scale Type A was used to measure memory ability before and after each course of treatment. The treatment outcome was evaluated for both groups.@*Results@#There were no significant differences in the scores of long-term memory,short-term memory, immediate memory, and memory quotient between the two groups before treatment(P>0.05).After the first course of treatment ended, the observation group had significant increases in the scores of forward task,backward task,association,and memory quotient(P<0.05); compared with the control group, the observation group had a significant reduction in the score of backward task(P<0.05).After the second course of treatmentended, the observation group had significant increases in the scores offorward task,backward task,memorization of pictures,reproduction,association,comprehension,and memory quotient,and the control group had significant increases in the scores of reproduction,association,comprehension,and memory quotient(P<0.05); compared with the control group, the observation group had significant increases in the scores of forward task,backward task,memorization of pictures, reproduction, association, comprehension, and memory quotient(P<0.05).Two patients experiencedchest distress, palpitation, and dysphoria during treatment, which did not affect the treatment.@*Conclusion@#Electroencephalographic biofeedback therapy has a certain effect in the treatment of memory disorders in patients with acute severe toxic encephalopathy.

Research progress in heavy metal toxic damage of nervous system / 中国药理学与毒理学杂志

With the development of modern industry,heavy metal pollution in China is becoming increasingly serious.Large-scale water sources and farmland have been severely contaminated.Frequent contact with heavy metal in life or at work has caused a marked increase in heavy metal poisoning in recent years.Nervous system damage caused by heavy metal poisoning is extremely common in clinic,and poses a threat to a patient's life,bringing heavy burden to society and families.Therefore,early prevention and treatment are crucial.This article takes commonpoisoning several common heavy metals as an example and combine the domestic and foreign research to review the damage to the nervous system caused by heavy metal poisoning.We aim to make patients and medical staff more alert to such poisoning and provide the basis for clinical prevention,diagnosis,treatment and research.

A Case of Optic Neuropathy Associated with Methyl Bromide Intoxication

PURPOSE: In this study, a case of toxic encephalopathy and optic neuropathy due to methyl bromide poisoning is reported. CASE SUMMARY: A 31-year-old male presented with dysarthria, gait disturbance and bilateral visual impairment. He was treated with intravenous methylprednisolone for bilateral optic neuritis 1 year prior. He previously worked in a fumigation warehouse and was exposed to methyl bromide in the past 3 years. His corrected visual acuity was 20/30 in both eyes. The patient had reduced color vision and enlarged central scotoma in both eyes. His mentality was alert but exhibited slow response, ataxia and dysarthria. Brain magnetic resonance imaging (MRI) revealed high signals in the brainstem, cerebellum and midbrain. His serum and urine methyl bromide concentrations were significantly elevated. The patient was treated with intravenous methylprednisolone 1.0 g/day for 5 days. MRI showed resolution of the multiple brain lesions observed previously. Ten days after steroid therapy, his visual acuity was 20/20 in both eyes and his neurologic manifestations were completely recovered at 2 months after treatment. CONCLUSIONS: Taking a detailed occupational history is necessary in patients with optic neuropathy. The probability of toxic optic neuropathy should be considered when patients are exposed to toxic materials.

A Rare Case of Viagra Induced Toxic Encephalopathy

Viagra has been prescribed worldwide to treat men with erectile dysfunction. Clinical trials have shown that Viagra may cause various kinds of adverse effects include some central nervous system (CNS) adverse effects. Although extremely rare, toxic encephalopathy also can be one of those effects. This report presents a case of encephalopathy caused by Viagra in correlation with its radiologic findings. Its pharmacologic mechanism and potential effects on the biochemistry of the CNS are reviewed.

Toxic Encephalopathy

This article schematically reviews the clinical features, diagnostic approaches to, and toxicological implications of toxic encephalopathy. The review will focus on the most significant occupational causes of toxic encephalopathy. Chronic toxic encephalopathy, cerebellar syndrome, parkinsonism, and vascular encephalopathy are commonly encountered clinical syndromes of toxic encephalopathy. Few neurotoxins cause patients to present with pathognomonic neurological syndromes. The symptoms and signs of toxic encephalopathy may be mimicked by many psychiatric, metabolic, inflammatory, neoplastic, and degenerative diseases of the nervous system. Thus, the importance of good history-taking that considers exposure and a comprehensive neurological examination cannot be overemphasized in the diagnosis of toxic encephalopathy. Neuropsychological testing and neuroimaging typically play ancillary roles. The recognition of toxic encephalopathy is important because the correct diagnosis of occupational disease can prevent others (e.g., workers at the same worksite) from further harm by reducing their exposure to the toxin, and also often provides some indication of prognosis. Physicians must therefore be aware of the typical signs and symptoms of toxic encephalopathy, and close collaborations between neurologists and occupational physicians are needed to determine whether neurological disorders are related to occupational neurotoxin exposure.

Toxic Encephalopathy

This article schematically reviews the clinical features, diagnostic approaches to, and toxicological implications of toxic encephalopathy. The review will focus on the most significant occupational causes of toxic encephalopathy. Chronic toxic encephalopathy, cerebellar syndrome, parkinsonism, and vascular encephalopathy are commonly encountered clinical syndromes of toxic encephalopathy. Few neurotoxins cause patients to present with pathognomonic neurological syndromes. The symptoms and signs of toxic encephalopathy may be mimicked by many psychiatric, metabolic, inflammatory, neoplastic, and degenerative diseases of the nervous system. Thus, the importance of good history-taking that considers exposure and a comprehensive neurological examination cannot be overemphasized in the diagnosis of toxic encephalopathy. Neuropsychological testing and neuroimaging typically play ancillary roles. The recognition of toxic encephalopathy is important because the correct diagnosis of occupational disease can prevent others (e.g., workers at the same worksite) from further harm by reducing their exposure to the toxin, and also often provides some indication of prognosis. Physicians must therefore be aware of the typical signs and symptoms of toxic encephalopathy, and close collaborations between neurologists and occupational physicians are needed to determine whether neurological disorders are related to occupational neurotoxin exposure.

Metronidazole Induced Encephalopathy in a Patient with Brain Abscess

Metronidazole is commonly used for brain abscess but is not well known for its neurotoxic complications. Metronidazole-induced encephalopathy (MIEP) is toxic encephalopathy associated with the use of metronidazole. We experienced a case of brain abscess which developed reversible severe MIEP during treatment period. Although MIEP occurs in typical locations, it is not easy to differentiate from other conditions such as cerebral infarction, demyelinating diseases and metabolic diseases. Neurosurgeons should be aware that severe MIEP can occur during the use of metronidazole though it is not common.

A Case of Acute Toxic Encephalopathy due to an Oxycodone Overdose

Acute encephalopathies can be defined as an acute central nervous system (CNS) insult, due to an underlying pathology. The clinical symptoms almost always include an acute state of confusion and cognitive impairment. Toxic encephalopathies can occur acutely or chronically depending on the toxic drugs and other substances as well as the individual metabolism of the drug. The organs acutely affected include the heart, lung and kidneys. However, the brain, spinal cord and sympathetic nerves can be affected chronically. If the toxic substance passes through the bloodbrain barrier into the hypothalamus and the posterior pituitary gland, the result can be diabetes insipidus. If the substance affects the anterior pituitary gland, the result can include hormone dysfunction, impaired immune function and altered cognition or personality. We report a patient that developed acute toxic encephalopathy after the prescribed dose of oxycodone was exceeded.