Evaluation of chronic neurological sequelae after acute pesticide exposure using spect brain scans

Abstract

A case in which SPECT brain imaging was used in the diagnosis and treatment of chronic effects from acute acetylcholinesterase inhibitor poisoning is presented. The patient was exposed to an insecticide mixture containing phosphorothiate, pyrethrin, piperonyl butoxide, and petroleum distillates, which produced symptoms consistent with acute acetylcholinesterase inhibitor poisoning as well as an upper respiratory tract irritant. Delayed sequelae of gross neurologic symptoms followed, that is, coarse tremor, intermittent hemiballistic movements of the right arm and leg, flaccid muscular tone, fasciculations of muscle groups, muscle cramps, and sensory disturbances. A brain single-photon emission computerized tomography (SPECT) scan was performed 34 mo postexposure, revealing significantly decreased blood flow to the left temporal lobe and to the right and left basal ganglia. The patient's paresthesias were treated with phenytoin, which resulted in worsening of her movement disorder. A trial of amantadine and selegiline (Deprenyl) resulted in a dramatic reduction in dysfunctional movements and ataxia. Post amantadine and selegiline therapy, brain SPECT images revealed significantly improved blood flow with minimally decreased blood flow to the right and left basal ganglia. The use of SPECT scan techniques helped to elucidate objective chronic central nervous system effects subsequent to an acute insecticide exposure and also assisted in the evaluation of the effectiveness of therapeutic intervention.

Neurotoxicity in single photon emission computed tomography brain scans of patients reporting chemical sensitivities†

“…While a complete statistical analysis is not yet complete, it is our collective finding that neurotoxic changes, as reported herein and elsewhere, are seen in over 90% of those chemically sensitive patients, who allege neurocognitive deficits from exposure to low levels of commonly encountered chemicals. We feel that this is an important finding, which corroborates the findings also published by Heuser et al (1994) and Callender et al (1994). We believe that the findings are especially important, as these neurotoxic findings appear to be very different from the metabolic brain changes that have been reported in psychiatric disease (Frazen, 1975;Mathew et al, 1980;Gemmell et al, 1987).…”

“…The authors felt that this suggested a primary cortical effect, possibly due to a vasculitis process. Callender et al (1994) reported on a case study in which SPECT imaging was used in the evaluation and follow-up of a patient who had a complex pesticide exposure. Initial symptoms were consistent with both an irritant effect and acetylcholinesterase inhibitor poisoning.…”

Italian Expert Consensus on Clinical and Therapeutic Management of Multiple Chemical Sensitivity (MCS)

“…Despite MCS patients often displaying a normal neurological exam, environmental exposures may negatively modulate the nervous system (spatial disorientation, short-term memory loss, tinnitus, tremors, convulsions) in susceptible subjects [ 1 ]. Thus, the neurological armamentarium may also include the following clinical and instrumental tests: Pupillography [ 75 ]; Simple and choice reaction time tasks [ 76 ]; Balance tests [ 77 ]; Visual contrast tests [ 78 , 79 , 80 , 81 ]; Visual color tests [ 82 ]; Tests of the perception of vibrations [ 77 ]; Electroencephalography (EEG) [ 82 ]; Single-photon emission computed tomography (SPECT) [ 83 , 84 , 85 , 86 ]. …”

Neuropsychology

“…It has been suggested that neurotoxic damage is not a result of anatomical changes such as demyelination and atrophy that would be picked up on structural imaging scans, but rather may be associated with a "vasculitis mechanism" that is best determined with functional imaging (Heuser, Mena, & Alamos, 1994). Several studies using SPECT have found diminished blood flow to both cortical and subcortical areas, with particular diminution of temporal and frontal cortical areas and the basal ganglia and thalamus subcortically (Callender, Morrow, & Subramanian, 1994;Callender, Morrow, Subramanian, Duhon, & Ristov, 1993;Heuser et at., 1994;Heuser, Mena, Goldstein, Thomas, & Alamos, 1993;Simon et ai., 1994).…”