Toxic encephalopathy, vision loss, and memory disorder caused by acute acrylamide exposure.

Acrylamide (ACR) is an irritant that can cause damage to the eyes, skin, and nervous and reproductive systems. This study aims to illustrate a case of central nervous system and optic nerve damage from exposure to ACR. In this case, a 49-year-old male material handler was accidentally splashed with ACR solution on both of his upper limbs. Consequently, he was admitted to the hospital with toxic encephalopathy, characterized by cerebellar ataxia and slurred speech. Magnetic resonance imaging scan, a brain computed tomography scan blood sample analyses, optic coherence tomography, electroneuromyogram, and visual evoked potentials examination were performed. After 20 days of receiving symptomatic support treatment, the patient continued to experience disturbances in consciousness. Then, he developed vision loss, memory disorders, and symptoms of peripheral neuropathy such as skin peeling, extremity weakness, and absent tendon reflexes. This case report underscores the severe consequences of acute dermal exposure to high concentrations of ACR, resulting in toxic encephalopathy, visual impairment, and memory disorders, which will contribute to a broader understanding of ACR toxicity.

[A case report of death from toxic encephalopathy caused by emamectin·chlorfenapyr].

Emamectin·chlorfenapyr is insecticide compounded by emamectin benzoate and chlorfenapyr. There is no special antidote after poisoning, and the mortality rate of patients is very high. We admitted a case of toxic encephalopathy caused by oral administration of emamectin·chlorfenapyr. The clinical manifestations of patient were gastrointestinal symptoms, profuse sweating, high fever, changes in consciousness. After admitted to the hospital, despite active comprehensive treatment, the patient died of ineffective rescue eventually.

Non convulsive refractory status epilepticus induced by thiocolchicoside (TCC) intrathecal injection: A case report.

TCC is a semisynthetic molecule widely used in clinical settings as a pain killer and myorelaxant. Several neurological side effects have been reported in association with TCC treatment including somnolence, confusion and seizure, the latter in a lower percentage of patients. Some previous reports described seizure onset after TCC intake in adulthood. However, major epileptological complication, namely status epilepticus, has never been previously reported in association with TCC treatment. In our report, we describe a case of acute refractory non-convulsive status epilepticus (NCSE) in the context of a TCC-induced acute toxic encephalopathy (ATE) in a woman without any previous neurological or physical comorbidities.

[Analysis of 15 cases of toxic encephalopathy caused by acute benzene poisoning].

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.

[Imaging features of 10 patients with toxic encephalopathy caused by diquat].

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.

Acute toxic encephalopathy following bromadiolone intoxication: a case report.

BACKGROUND: Clinically, bromadiolone poisoning is characterized by severe bleeding complications in various organs and tissues. Bromadiolone-induced toxic encephalopathy is extremely rare. Here, we report a special case of bromadiolone-induced reversible toxic encephalopathy in a patient who had symmetrical lesions in the deep white matter. CASE PRESENTATION: A 23-year-old woman mainly presented with dizziness, fatigue, alalia and unsteady gait after the ingestion of bromadiolone. The laboratory examinations showed normal coagulation levels. Brain magnetic resonance imaging (MRI) showed apparent diffusion restriction in the bilateral deep white matter. The clinical manifestations and MRI alterations were reversible within one month of treatment with vitamin K. The neuropsychological assessment showed no neurodegenerative changes at the 2-year follow-up. CONCLUSION: With the increased use of bromadiolone as a rodenticide, more cases of ingestion have been reported annually over the past several years. Bromadiolone-induced toxic encephalopathy has no special clinical manifestations and is potentially reversible with timely treatment. Because of the reversible restricted diffusion on diffusion-weighted images (DWI) and low apparent diffusion coefficient (ADC) values, transient intramyelinic cytotoxic oedema is thought to be the cause rather than persistent ischaemia. The underlying pathophysiological mechanism is still unknown and may be coagulant-independent. This clinical case extends the current knowledge about neurotoxicity in cases of bromadiolone poisoning and indicates that MRI is useful for the early detection of bromadiolone-induced toxic encephalopathy.

[Clinical analysis of 15 cases of acute glufosinate poisoning].

The glufosinate poisoning can cause damage to the respiratory system and nervous system. In severe cases, respiratory failure and toxic encephalopathy are life-threatening. It should be paid attention to and supportive treatment.In this paper, 15 cases of acute oral glyphosate poisoning diagnosed by toxicant test in the Poisoning Treatment Center of the Army from March to August 2018 were analyzed, and the clinical characteristics and treatment effect of acute glyphosate poisoning were summarized, so as to improve the understanding, diagnosis and treatment level of the disease.

[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.

Acute reversible toxic encephalopathy during capecitabine and oxaliplatin treatment.

INTRODUCTION: Capecitabine is a fluoropyrimidine commonly used in the treatment of colorectal cancer which may cause central nervous system toxicity, namely cerebellar dysfunction. CASE REPORT: We describe a 77-year-old man undergoing adjuvant treatment of colon cancer with capecitabine and oxaliplatin who presented with acute cerebellar ataxia and encephalopathy that progressed to coma. Diagnosis of toxic encephalopathy was made after the exclusion of alternative causes of neurological dysfunction and complete resolution of clinical findings with permanent discontinuation of chemotherapy. DISCUSSION: When patients with cancer develop symptoms and signs of central nervous dysfunction, metabolic and infectious causes plus tumor involvement of central nervous system must be sought. However, chemotherapy may also cause toxicity to the central nervous system. Capecitabine is no exception, although cerebellar dysfunction is rarely reported. CONCLUSION: Although rare, capecitabine-induced encephalopathy may be severe and physicians should be aware of this possible side effect.

General Pathophysiology of Astroglia.

Astroglial cells are involved in most if not in all pathologies of the brain. These cells can change the morpho-functional properties in response to pathology or innate changes of these cells can lead to pathologies. Overall pathological changes in astroglia are complex and diverse and often vary with different disease stages. We classify astrogliopathologies into reactive astrogliosis, astrodegeneration with astroglial atrophy and loss of function, and pathological remodelling of astrocytes. Such changes can occur in neurological, neurodevelopmental, metabolic and psychiatric disorders as well as in infection and toxic insults. Mutation in astrocyte-specific genes leads to specific pathologies, such as Alexander disease, which is a leukodystrophy. We discuss changes in astroglia in the pathological context and identify some molecular entities underlying pathology. These entities within astroglia may repent targets for novel therapeutic intervention in the management of brain pathologies.

Diagnosing solvent-induced chronic toxic encephalopathy: the effect of underperformance in neuropsychological testing.

Objective: The diagnoses of solvent-induced chronic toxic encephalopathy (CSE) can be supported by neuropsychological tests. However, since results not only reflect cognitive functioning but also the patient's effort to perform well, this study examines to what extent underperformance impacts neuropsychological outcomes in individuals referred for suspected CSE. Methods: A retrospective study of 48 suspected CSE patients having completed ten neuropsychological tests assessing different domains of cognition. Underperformance was identified using the Amsterdam Short-Term Memory Test and the Rey 15-item Memory Test (FIT). Multiple linear regression was applied to examine the effect of insufficient effort on test performance. Results: A total of 54.1% of the patients were identified as having underperformed on one or both performance validity tests. Analyses showed a significant effect of underperformance on most tests barring letter-number sequencing. Conclusions: Most of the neuropsychological tests evaluated showed significant effects of underperformance. Performance on letter-number sequencing was not affected. In case of underperformance, the results of the neuropsychological assessment should be disregarded when weighing the final multi-disciplinary diagnosis, with the exception of letter-number sequencing. Key points A total of 54.1% of patients with suspected CSE referred for neuropsychological assessment was identified as having underperformed on one or both PVTs. Underperformance has a significant effect on most neuropsychological tests with the exception of letter-number sequencing assessing attention and working memory. In case of underperformance, the results of the neuropsychological assessment should be disregarded when weighing the final multi-disciplinary diagnosis, with the exception of letter-number sequencing.

[Peculiarities of barbituric acid derivatives acute poisoning clinical picture in patients of elderly and senile age and their therapy.]

In this article materials obtained during treatment of 61 patients with acute poisoning with phenobarbital, which is part of Corvalol and Valocordin, are presented. It has already been established that phenobarbital acute poisoning in elderly and senile patients is accompanied by more frequent development of central nervous system, respiratory system (pneumonia) and cardiovascular system complications, which cause more severe clinical course and risk of an adverse outcome of acute poisoning. This research has shown that for hypoxia correction during phenobarbital acute poisoning in elderly and senile patients it is advisable to include Reamberin in the treatment regimen, which has no adverse effects on central haemodynamic parameters and effectively reduces severity of metabolic disorders.

Subcortical brain atrophy in Gulf War Illness.

Gulf War Illness (GWI) is a multisystem disorder that has affected a substantial number of veterans who served in the 1990-1991 Gulf War. The brain is prominently affected, as manifested by the presence of neurological, cognitive and mood symptoms. Although brain dysfunction in GWI has been well documented (EBioMedicine 12:127-32, 2016), abnormalities in brain structure have been debated. Here we report a substantial (~10%) subcortical brain atrophy in GWI comprising mainly the brainstem, cerebellum and thalamus, and, to a lesser extent, basal ganglia, amygdala and diencephalon. The highest atrophy was observed in the brainstem, followed by left cerebellum and right thalamus, then by right cerebellum and left thalamus. These findings indicate graded atrophy of regions anatomically connected through the brainstem via the crossed superior cerebellar peduncle (left cerebellum â†’ right thalamus, right cerebellum â†’ left thalamus). This distribution of atrophy, together with the observed systematic reduction in volume of other subcortical areas (basal ganglia, amygdala and diencephalon), resemble the distribution of atrophy seen in toxic encephalopathy (Am J Neuroradiol 13:747-760, 1992) caused by a variety of substances, including organic solvents. Given the potential exposure of Gulf War veterans to "a wide range of biological and chemical agents including sand, smoke from oil-well fires, paints, solvents, insecticides, petroleum fuels and their combustion products, organophosphate nerve agents, pyridostigmine bromide, …" (Institute of Medicine National Research Council. Gulf War and Health: Volume 1. Depleted uranium, pyridostigmine bromide, sarin, and vaccines. National Academies Press, Washington DC, 2000), it is reasonable to suppose that such exposures, alone or in combination, could underlie the subcortical atrophy observed.

[Clinical effect of electroencephalographic biofeedback therapy in treatment of memory disorders in patients with acute severe toxic encephalopathy].

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.

The dangers of "Chasing the dragon": a fatal case of heroin-induced leukoencephalopathy.

Heroin-induced leukoencephalopathy (HLE) is a rare toxic encephalopathy associated primarily with heroin inhalation, commonly referred to as "chasing the dragon." This study presents a clinical case of a 27-year-old polydrug user diagnosed with HLE during hospitalization for rapidly progressive flaccid tetraplegia and aphasia. The clinical manifestations encompassed cerebellar and bulbar dysfunction, coupled with motor impairment and altered consciousness. Based on the clinical data and MRI results, HLE was identified as the most likely cause. This article aims to provide insights into the clinical and radiological aspects of HLE, emphasizing the diagnostic significance of radiological findings. The gold standard examination for diagnosis is MRI, crucial due to the difficulties in obtaining histological confirmation for this rare condition.

Heroin-induced leukoencephalopathy: Chasing the imaging findings.

We present a case of a 29-year-old male who was brought into the hospital due to unresponsiveness and found to have heroin inhalational leukoencephalopathy (HLE). HLE is one component of a broad spectrum of opioid encephalopathies that is associated with heroin inhalation and other opioids. There is considerable overlap of HLE with other toxic and hypoxic-ischemic encephalopathies; however, the specific territories of brain involvement help distinguish it from other cerebral insults. The goal of this study is to help elucidate the findings of HLE and compare these findings to other toxic and hypoxic-ischemic encephalopathies.

Tralopyril poisoning due to respiratory exposure.

INTRODUCTION: Tralopyril is a metabolite of the pesticide chlorfenapyr. Direct toxicity by tralopyril has not been described. We report two cases of tralopyril poisoning via inhalation. CASE PRESENTATIONS: Two workers developed heat intolerance, diaphoresis, and weight loss after occupational inhalational exposure to tralopyril. Patient 1: The exposure was due to the absence of respiratory protection. Magnetic resonance imaging showed abnormal signals in the bilateral periventricular white matter, corpus callosum, basal ganglia, brainstem, and spinal cord. The patient's blood tralopyril concentrations on days 1, 3, 5, 8, and 11 post-admission were 1.09 mg/L, 1.04 mg/L, 1.01 mg/L, 0.71 mg/L, and 0.313 mg/L, respectively. Haemoperfusion (HA330), haemoperfusion (HA380), and haemodiafiltration were performed on days 1-3, 5-8, and 9-10, respectively. Patient 2: The patient's symptoms followed inappropriate use of respiratory protection. His blood tralopyril concentrations on days 1, 4, 5, and 6 were 0.592 mg/L, 0.482 mg/L, 0.370 mg/L, and 0.228 mg/L, respectively. DISCUSSION: The patients presented with features typical of chlorfenapyr poisoning, which suggests that tralopyril is the main toxic metabolite of chlorfenapyr. CONCLUSION: Tralopyril can be absorbed by inhalation, leading to delayed clinical symptoms and organ damage, including toxic encephalopathy and spinal cord damage.

Neem oil poisoning: Case report of an adult with toxic encephalopathy.

Neem oil has widespread use in Indian subcontinent due to its many bioactive properties. Azadirachtin, an active ingredient, is implicated in causing the effects seen in neem oil poisoning. Neem oil poisoning is rare in adults. This report highlights the toxicity associated with neem oil poisoning in an elderly male. The patient presented with vomiting, seizures, metabolic acidosis, and toxic encephalopathy. The patient recovered completely with symptomatic treatment.

Acute Toxic Encephalopathy in Occupational Exposure with Polyvinyl Chloride (PVC) Fumes: A Case Series.

Background: Toxic encephalopathy is a spectrum of central nervous system disorders caused by exposure to toxins, especially from occupational workplace. Polyvinylchloride (PVC) is a synthetic chemical polymer that is used widely in daily activities of living. PVC is produced by polymerization of monomer units of vinyl chloride. Its manufacturing requires multiple procedures and additives for heat and light stabilization involving heavy metals. Objective: In this novel case series, we present the diverse clinical presentation of 10 patients, working in plastic recycling factory having inhalational exposure to PVC fumes, manifesting as acute toxic encephalopathy. Materials and Methods: All the patients were screened for the causes of acute encephalopathy including heavy metals, methanol poisoning, and organotins along with arterial blood gas analysis, brain imaging, and electroencephalogram. Memory loss, confusion, vertigo, headache, and nausea were complained in all the patients while seizure occurred in three patients. Neurocognitive status was grossly impaired in all the patients. Metabolic acidosis in presence of hyponatremia and/or hypokalemia was observed in nine cases. Five of the patients were having evidence of white matter involvement in brain imaging. The screening for heavy metal, methanol, and organotin were negative. Hemodialysis was done in six patients. Recovery was good in everyone and the average discharge was by 10.8 days (range: 2-25 days). All the patients were symptom-free at 3-months follow-up. Conclusion: Early suspicion and aggressive management can have favorable outcome in PVC toxic encephalopathy. Occupational hazards due to PVC toxicity are increasing in the present industrial era but it is very less identified.