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Epstein–Barr virus and the nervous system
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Alexandros C. Tselis, Kumar Rajamani, Pratik Bhattacharya
Pathological findings are scarce because death from EBV encephalitis is rare. Reports have described variable findings on pathological examination of the brain, which points to several possible pathogenetic processes, including typical viral encephalitis and post-infectious acute disseminated encephalomyelitis. Thus, perivascular infiltrates of lymphocytes, as well as diffuse parenchymal infiltrates consisting of both lymphocytes and microglia, have been found in the cortex, as is typical in viral encephalitis [30]. In one patient, both meningeal and diffuse parenchymal white matter perivascular infiltrates of lymphocytes and lymphoblastoid cells (some of which showed mitotic figures, reminiscent of neoplasm) were found. Most of these cells were EBV-infected B cells, but a few T cells and microglia/macrophages were found [21]. Some patients have had typical histopathological findings of acute disseminated encephalomyelitis, with perivenular infiltrates of lymphocytes in the white matter, with lipid-laden macrophages and demyelination [31,32]. Finally, a peculiar case of a fatal EBV-associated acute encephalopathy in an adult was described, with pathological findings of scattered neuronal pyknosis, diffuse cortical edema, and visual cortical perivascular edema but no perivascular infiltrates or microglial nodules [33]. These findings are reminiscent of what has been called a “toxic encephalopathy,” which is a poorly understood parainfectious process seen most often in children [34].
Environmental Toxins and Chronic Illness
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Solvent exposure has been documented to lead to chronic toxic encephalopathy (CTE). Interestingly, in agreement with the issue of decreased detoxification capacity mentioned above, Crinnion (2013) discusses research where individuals on antidepressants were four times more likely to demonstrate persistent CTE compared with those not on these medications. Crinnion (2013) suggests that one reason for this is the fact that many antidepressants inhibit phase I detoxification pathways in the liver. Other research has shown that workers with a genetic propensity for lower glutathione production demonstrated a significantly increased risk for development of CTE. Concerning specific solvents, toluene, which is often present in glues and paints, is highly linked with development of CTE. In one study on printers exposed to toluene, fatigue, impaired memory, impaired concentration, irritability, headaches, mood lability, and depression were often reported. In another study on shipyard painters, in addition to the some of the symptoms mentioned above, dizziness and insomnia were reported as well as a feeling of pressure in the chest and sweating with any work or movement. Finally, another study on female workers reported symptoms relating to manual dexterity, visual scanning, and verbal memory even though there was no overt evidence of classic toxicity.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Trivalent arsenicals (or, more likely an arsenious acid metabolite) bind efficiently to the functional thiol groups of many tissue components, including enzymes. Its affinity for thiol groups in keratin accounts for the accumulation of arsenic in skin, nails, and hair in cases of chronic poisoning. When absorbed across the gut wall, these arsenicals injure the splanchnic vasculature, causing abdominal pain, colic, and diarrhea. Once absorbed into the blood, they cause toxic damage to the liver, kidneys, brain, bone marrow (BM), and peripheral nerves. Liver injury is manifest as hepatomegaly, jaundice, and an increase in circulating hepatocellular enzymes LDH and GOT. Renal damage is reflected in albuminuria, hematuria, pyuria, cylinduria, and then azotemia. Acute tubular necrosis may occur in severe poisoning. Injury to blood-forming tissues can take the form of agranulocytosis, aplastic anemia, thrombocytopenia, or pancytopenia. Toxic encephalopathy may manifest as speech and behavioral disturbances. Peripheral neuropathy occurs in both acute and chronic forms.
Acute diquat poisoning resulting in toxic encephalopathy: a report of three cases
Published in Clinical Toxicology, 2022
Guangcai Yu, Tianzi Jian, Siqi Cui, Longke Shi, Baotian Kan, Xiangdong Jian
A 20-year-old previously healthy man ingested approximately 100 mL of diquat (20 g/100 mL). Gastric lavage and haemoperfusion were performed afterwards. On day 3, he displayed oliguria, agitation, convulsions, and respiratory failure; haemodialysis was performed, and he was put on mechanical ventilation was given. He was admitted to our department the next day. On admission, his heart rate was 111 beats/min, blood pressure was 145/79 mmHg. Coma, anuria, and abdominal distension were the main abnormal signs. Laboratory test results were as follows: creatinine, 882 μmol/L; urea, 37.4 mmol/L; potassium, 3.37 mmol/L; and sodium, 138 mmol/L. The pesticide ingested was confirmed as diquat by the sodium bicarbonate/dithionite test. His main therapeutic options were similar to case 1. On day 6, his urea was 38.6 mmol/L, creatinine was 989 μmol/L. His daily urine volume was 600 mL and increased gradually afterwards. On day 12, he was weaned from mechanical ventilation, but he was still semi-comatose. His brain CT showed a low density in the brainstem region. The next day, toxic encephalopathy was confirmed (Figure 2). After 18 days, he experienced cardiac arrest and died.
Serotonin toxicity from isolated bupropion overdoses
Published in Clinical Toxicology, 2020
Alexander M. Sidlak, Karl O. Koivisto, Ryan T. Marino, Michael G. Abesamis
Over a three-year period, 96 patients were managed by our Medical Toxicology service with a reported bupropion overdose. Eighteen patients were identified as having an overdose on bupropion with no serotonergic co-ingestions. Baseline characteristics are recorded in Table 1. Five patients had GC/MS testing confirming bupropion ingestion. Patients had bupropion toxicity from either a suicide attempt (n = 7), recreational use (n = 8), or accidental ingestion (n = 3). Tachycardia was present in all patients (peak HR: 122 bpm [95% CI: 115–129]). Toxic encephalopathy was the most common sign identified. Incidence of other signs are recorded in Table 2. Records of physical exam findings from the initial presentation of two patients were not available as they were transferred from outside facilities. They were still included in the data, but findings for clonus and hyperreflexia were recorded as absent. Inducible clonus was present in six patients, one of whom did not meet criteria for serotonin toxicity given a lack of hyperthermia, agitation, diaphoresis, or hypertonia.
Methylenedioxymethamphetamine (MDMA)-induced toxic leukoencephalopathy: a case report
Published in Psychiatry and Clinical Psychopharmacology, 2018
Haitham Salem, Travis Barton, Taha Ali, Ashley Anderson, Antonio L Teixeira
On the neurology service, the diagnosis of toxic encephalopathy was confirmed. An EEG showed normal findings for the patient’s age. A comprehensive serological panel was sent. This included Hepatitis A, Hepatitis C, HIV, and an autoantibody workup (AChR ganglionic neuronal antibody, AGNA-1, Amphiphysin Antibody, ANNA-1,-2,-3, Calcium channel antibody N- and P/Q- types, CRMP-5 antibody, Neuronal K-channel antibody, Paraneoplastic antibody, PCA-1 and -2, ACHr binding antibody, striated muscle antibody). The results all came back negative. In addition, cerebrospinal fluid analysis which included a virology profile (VDRL, CMV, EBV, VZV, HIV, HSV1, HSV2, Enterovirus, Cryptococcus, Streptococcus pneumonia) was also unremarkable. After a few days, the patient’s condition remained unchanged. She continued to demonstrate apathy and cognitive impairment. She was discharged from the hospital and will likely require lifelong assisted-living.