Toxic Encephalopathy

Abstract

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.

F-18 FDG PET brain imaging in symptomatic arthroprosthetic cobaltism

“…[15] The findings at lower summed scores and their accompanying abnormal clusters begin to demonstrate a pattern comparable with toxic encephalopathy rather than a classical dementia. [24] Also, 85% of the patients showed significant hypometabolism of the right inferior posterior lateral temporal lobe area.…”

“…Since the whole brain is exposed to cobalt, "whole brain" as a reference region was thought to potentially create spuriously underestimated hypometabolism. Likewise, the cerebellum has been reported as hypometabolic by SPECT in mercury, bromine, and manganese poisoning [24]. Data output was recorded for hypometabolism and included number of regions affected, summed score of those regions, along with number of abnormal clusters, their location, and standard deviation.…”

“…As such, the evaluation of data rested, in part, on published articles dealing with other forms of neurotoxicity from organic chemicals and metals such as mercury and manganese. [24,[26][27][28]…”

Sex-specific Profiles of Blood Metal Levels Associated with Metal–Iron Interactions

“…These processes also play an important role in manganese toxicokinetics, which differ from those of nonessential toxic metals such as lead and cadmium. Heavy occupational exposure to manganese can cause a neurologic impairment clinically called “manganism,” a motor syndrome that is similar to but differentiated from idiopathic Parkinson's disease [33–37] . The mechanisms involved in iron absorption are similar to those of divalent metals, particularly manganese [4,27] , and a dietary deficiency of iron can lead to excess absorption of manganese [6–13] .…”

Malaria Prevention, Mefloquine Neurotoxicity, Neuropsychiatric Illness, and Risk-Benefit Analysis in the Australian Defence Force

“…Given that neuropsychiatric effects were evident in mefloquine's safety profile early in its history [ 14 , 16 ] and that concerns over veterans' exposure to neurotoxicants including medicines became prominent in the 1990s [ 42 – 44 ], the literature search then included the discipline of neurotoxicology. This literature describes the manifestation, symptomology, and evidentiary basis of toxic encephalopathies [ 45 – 48 ], neurotoxicity syndromes [ 49 , 50 ], methods for neurotoxicity testing [ 51 – 53 ], and risk assessment [ 54 – 57 ]. This section of the review provided a general frame of reference within which the search and analysis of literature relating specifically to mefloquine toxicity is refined.…”