title: Three-dimensional brain metabolic imaging in patients with toxic encephalopathy.
abstract: Thirty-three workers, ages 24 to 63, developed clinical toxic encephalopathy after exposure to neurotoxins and were studied by SPECT brain scans. Five were exposed to pesticides, 13 were acutely exposed to mixtures of solvents, 8 were chronically exposed to mixtures of hazardous wastes that contained organic solvents, 2 were acutely exposed to phosgene and other toxins, and 5 had exposures to hydrogen sulfide. Twenty-nine had neuropsychological testing and all had a medical history and physical. Of the workers who had a clinical diagnosis of toxic encephalopathy, 31 (93.9%) had abnormal SPECT brain scans with the most frequent areas of abnormality being temporal lobes (67.7%), frontal lobes (61.3%), basal ganglia (45.2%), thalamus (29.0%), parietal lobes (12.9%), motorstrip (9.68%), cerebral hemisphere (6.45%), occipital lobes (3.23%), and caudate nucleus (3.23%). Twenty-three out of 29 (79.3%) neuropsychological evaluations were abnormal. Other modalities when performed included the following percentages of abnormals: NCV, 33.3%; CPT sensory nerve testing, 91.3%; vestibular function testing, 71.4%; olfactory testing, 89.2%; sleep EEG analysis, 85.7%; EEG, 8.33%; CT, 7.14%; and MRI brain scans, 28.6%. The complex of symptoms seen in toxic encephalopathy implies dysfunction involving several CNS regions. This series of patients adds to the previous experience of brain metabolic imaging and demonstrates that certain areas of the brain are typically affected despite differences in toxin structure, that these lesions can be globally defined by SPECT/PET brain scans, that these lesion correlate well with clinical and neuropsychological testing, and that such testing is a useful adjunct to previous methods. EEG and structural brain imaging such as CT and MRI are observed to have poor sensitivity in this type of patient. Additional metabolic imaging studies need to be done to explore dose, time, and specific toxin effects as well as mechanisms of toxicity and olfactory migration.
authors: Med-Health, Ltd. Clinic, Environmental and Occupational Medical Research Institute, Lafayette, Louisiana 70503.
authors: T J
authors: TJ
authors: Callender
authors: L
authors: L
authors: Morrow
authors: K
authors: K
authors: Subramanian
authors: D
authors: D
authors: Duhon
authors: M
authors: M
authors: Ristovv
mesh_terms: D000293:Adolescent; D000328:Adult; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001927:Brain Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D004569:Electroencephalography; D005260:Female; D006801:Humans; D006862:Hydrogen Sulfide / Q000009:adverse effects; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D009498:Neurotoxins / Q000009:adverse effects*; D010575:Pesticides / Q000009:adverse effects; D010705:Phosgene / Q000009:adverse effects; D012997:Solvents / Q000009:adverse effects; D014055:Tomography, Emission-Computed; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D009498:Neurotoxins; D010575:Pesticides; D012997:Solvents; D010705:Phosgene; D006862:Hydrogen Sulfide