Original article

Scand J Work Environ Health 2004;30(5):362-370    pdf

https://doi.org/10.5271/sjweh.824 | Issue date: Oct 2004

Central nervous system effects of acute organophosphate poisoning in a two-year follow-up

by Delgado E, McConnell R, Miranda J, Keifer M, Lundberg I, Partanen T, Wesseling C

Objectives Patients hospitalized for acute organophosphate poisoning in León, Nicaragua, were followed for effects on the central nervous system (CNS) over a 2-year period.

Methods Immediate verbal memory (Rey verbal learning), visuomotor performance (digit symbol), and neuropsychiatric symptoms (Q-16) were assessed for 53 poisoned persons at the time of hospital discharge, 7 weeks postpoisoning, and 2 years postpoisoning, and, at the same time intervals, for 28 persons who had never been poisoned. The poisonings were classified as moderate occupational (31), severe occupational (15), and severe through the oral route (7), representing low, medium, and high exposure, respectively. Longitudinal confounder-adjusted between-category comparisons and longitudinal analyses of variance and covariance were used to assess the effects of the exposure.

Results Immediate verbal learning showed deficits in the high-exposure group, in particular at the time of discharge, but the estimate of the difference when compared with the values of the unexposed was imprecise. Visuomotor performance showed a deficit at 7 weeks in the medium-exposure group, but it had improved after 2 years relative to that of the unexposed, for whom improvement had occurred at 7 weeks and persisted during the 2 years of follow-up, possibly a test-retest effect. Neuropsychiatric symptoms were in excess 2 years after the hospital discharge in the low- and medium-exposure groups and all the groups combined. All the results were imprecise for the small high-exposure group.

Conclusions Visuomotor performance and possibly short-term verbal memory seem to be affected early after severe acute organophosphate poisoning and recover, either truly or by some compensatory mechanism. Neuropsychiatric symptoms seem to increase after a longer latency period.

This article refers to the following text of the Journal: 1998;24(1):18-29