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Neurotoxicology
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Sean D. McCann, Trevonne M. Thompson
“Chasing the dragon” is a method of smoking substances of abuse, typically heroin or other opioids, by heating the substance on a piece of aluminum foil and “chasing” the resulting trail of smoke with a tube used to inhale that smoke. This practice has been associated with demyelination of variable regions of white matter termed toxic leukoencephalopathy, most commonly involving white matter of the cerebellum, cerebellar peduncles, posterior cerebrum, and the posterior limb of the internal capsule. Magnetic resonance imaging (MRI) can identify areas of damage and assist in making the diagnosis along with a history of exposure. The exact pathophysiology is unknown, and it remains unclear whether the etiologic agent is heroin itself, a contaminant such as a cutting agent, or the aluminum foil. Treatment is cessation of exposure. Toxic leukoencephalopathy is most commonly associated with substances of abuse but has also rarely been reported in association with chemotherapeutic agents, the topical antibiotic hexachlorophene, arsenic, and other pharmaceuticals.
Outdoor Emissions
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Toxic leukoencephalopathy is a structural alteration of the white matter following exposure to various toxic agents. Kao et al.323 report a 49-year-old man exposed to an explosion of lacquer thinner with brain MRI features atypical from those of chronic toxic solvent intoxication.323
The neurologic approach
Published in Stanley Berent, James W. Albers, Neurobehavioral Toxicology, 2012
Stanley Berent, James W. Albers
In general, there are no conventional CT or MRI imaging abnormalities specific to any given neurotoxicant. There are some imaging abnormalities, however, that can result in a neuroradiology diagnosis of ‘toxic leukoencephalopathy’ (Filley & Kleinschmidt-DeMasters, 2001). ‘Leukoencephalopathy’ is the term used to reflect abnormalities of myelin and more general changes in cerebral white matter, and the abnormalities are believed to manifest primarily in neurobehavioral alterations (Filley, Heaton, & Rosenberg, 1990; Filley & Kleinschmidt-DeMasters, 2001). While, as mentioned elsewhere (see Chapter 5, for instance), neurobehavioral symptoms of this type are non-specific, in general the pattern of symptoms and signs associated with leukoencephalopathy mirrors the distribution and severity of white matter abnormality. That is, neurobehavioral or neurologic abnormalities are bilateral and diffuse, with mild cases exhibiting confusion and inattention, memory impairment, and emotional disturbance, without abnormal language function (Filley & Kleinschmidt-DeMasters, 2001). Of course, the differential diagnosis associated with imaging evidence of a toxic leukoencephalopathy includes numerous conditions associated with many different causes. One of the conditions initially attributed to ‘toxic’ leukoencephalopathy was chronic and massive exposure to toluene, in the form of ‘huffing’ (recreational toluene abuse) (Filley, et al., 1990). That situation, possibly in association with unrecognized hypoxia, produced MRI imaging abnormalities of cerebral atrophy and white matter changes characteristic of leukoencephalopathy. Further, the degree of white matter abnormality on MRI significantly correlated with neuropsychological impairments. Nonetheless, other conditions exist that may produce indistinguishable MRI white matter abnormalities, including hereditary and autoimmune demyelinating diseases, progressive multifocal leukoencephalopathy, acquired immune deficiency syndrome (AIDS), vasculitis, normal pressure hydrocephalus, and exposure to leukotoxic therapies including cisplatin or irradiation. Attribution to a toxic etiology from imaging evidence of a leukoencephalopathy will necessitate meeting criteria, such as Hill (1965), in order to establish causation. While objective documentation of neurologic or neurobehavioral deficits (i.e., the results from neuropsychological evaluation) is necessary (Schaumburg & Spencer 1987), the diagnosis of a leukoencephalopathy also requires that the neuroradiological abnormalities be present (Filley & KleinschmidtDeMasters, 2001). In the identification of imaging abnormalities characteristic of leukoencephalopathy, the results of MRI are the most sensitive of the imaging techniques because of the ability of MRI to image myelin, distinguish between gray matter and white matter, and identify primary and secondary loss of myelin to an extend which considerably exceeds that of CT (Frey, 2000).
The safety of current pharmacotherapeutic strategies for osteosarcoma
Published in Expert Opinion on Drug Safety, 2021
Mariella Spalato, Antoine Italiano
Acute toxic leukoencephalopathy ranges from a subclinical disease, clinically characterized by behavioral changes and inappropriate laughter, to a progressive, devastating encephalopathy, leading to lethargy, coma, aphasia, and focal sensorimotor abnormalities including cortical blindness, dementia, seizures, pyramidal signs, and paresis [96,97]. Additionally, white matter necrosis, loss of oligodendroglia, axonal swelling, microcystic encephalomalacia, and atrophy of the deep cerebral white matter may occur that morphologically match the different degrees of demyelination[98].
Medical outcomes of bromethalin rodenticide exposures reported to US poison centers after federal restriction of anticoagulants
Published in Clinical Toxicology, 2019
Ryan Feldman, Matthew Stanton, Douglas Borys, Mark Kostic, David Gummin
The second fatality report discusses a 24-year-old male found unresponsive in a chair by his parents who later progressed to anoxic brain injury and death. It is not stated in the fatality report if the patient ingested bromethalin, or if there was a history suggestive of exposure, or why in the fatality report bromethalin was a consideration. However, the fatality report states bromethalin exposure could not be ruled out as a cause in post mortem autopsy. Given the possibility of exposure, further description is provided for completeness. On emergency department arrival the patient was unresponsive, had small pupils, decerebrate posturing and seizure-like activity without evidence of trauma or track marks. Initial vital signs revealed a blood pressure of 134/78 mmHg, heart rate of 92 beats per minute, respiratory rate of 22 breaths per minute, oxygen saturation of 93%, and a temperature of 99.5 °F. Laboratory abnormalities included an arterial pH of 7.16, bicarbonate of 16 mmol/L, serum creatinine 1.4 mg/dL, creatinine phosphokinase 32,000 units/L, AST 419 units/L, and ALT 190 units/L. Serum levels of acetaminophen, salicylate, and ethanol were not detectable. The patient’s computed tomography of the head demonstrated no abnormality. Magnetic resonance imaging (MRI) showed toxic leukoencephalopathy and electroencephalogram (EEG) showed diffuse slowing. Herpes simplex virus nucleic acid amplification test was negative. It is unknown if a lumbar puncture was performed. The patient was intubated and sedated, seizure like activity and posturing invariably recurred when sedation was lightened. He was given antiepileptic drugs, antibiotics, and N-acetylcysteine. Liver enzymes returned to normal and N-acetylcysteine was stopped. On day eight, repeat EEG and MRI were consistent with anoxic brain injury; he was transitioned to comfort care and he died on day nine. Antemortem blood taken 1.5 d after presentation was negative for desmethylbromethalin; however, it was noted that too little sample was present and too much time had passed to rule out bromethlain. It is not detailed in the fatality report why bromethalin was a consideration.
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
In conclusion, toxic leukoencephalopathy is a serious pathological finding that should be considered in the differential diagnosis of patients that present with the recent onset of cognitive deficits and are known to have exposure to toxins or drugs of abuse.