Evaluation of blink reflex results obtained from workers previously diagnosed with solvent-induced toxic encephalopathy.
We reviewed blink reflexes recorded from 51 railroad workers with long-term occupational exposure to solvents who were diagnosed by others with solvent-induced toxic encephalopathy. No worker fulfilled conventional clinical criteria for dementia or trigeminal mononeuropathy. All workers had normal R1 and R2 blink reflex latencies. R1 latencies correlated significantly with several nerve conduction measures, including F wave latencies, suggesting that some intersubject variability reflected intrinsic conduction properties, not isolated brain-stem function. Although normal, the workers' R1 latencies were significantly prolonged compared with historical control groups, including gender-matched control subjects of similar mean age (11.2 ms vs 9.9 ms; P < 0.0001). Stepwise multiple regression models demonstrated significant associations of R1 latency with age and use of CNS-active prescription medications (P = 0.003), but duration of occupational solvent exposure did not enter into the models. Paradoxically, workers using CNS-active medications had significantly shorter R1 latencies compared with workers not using such medications (10.9 vs 11.7 ms; P = 0.01). Job title, another potential surrogate measure of exposure, was not significantly related to reflex latencies. The geographical site of predominant solvent exposure did influence R1 latency, and workers from one site had longer exposure duration and longer R1 latencies than remaining workers. However, an interaction between age and exposure duration (r = 0.39; P = 0.003) confounded interpretation of this observation. Disability or work status, mental status findings, or classification of encephalopathy did not influence blink reflex latencies. The overall results do not support, but do not entirely exclude, a possible relationship between subclinical blink reflex abnormalities and occupational exposure to solvents. Nevertheless, it is clear from these results that the small group differences in R1 latency between exposed workers and control subjects are of no diagnostic importance and of uncertain physiologic importance, and they may reflect unrecognized confounders and technical factors.
Albers
J W
JW
Departments of Neurology and Psychiatry, Neurobehavioral Toxicology Program, University of Michigan Health System, USA.
Wald
J J
JJ
Trask
C L
CL
Garabrant
D H
DH
Berent
S
S
D000328:Adult; D000367:Age Factors; D000437:Alcoholism / Q000150:complications; D000704:Analysis of Variance; D001767:Blinking; D001927:Brain Diseases / Q000139:chemically induced* / Q000175:diagnosis; D003704:Dementia / Q000139:chemically induced; D003863:Depression / Q000150:complications; D006801:Humans; D016014:Linear Models; D008875:Middle Aged; D008962:Models, Theoretical; D009431:Neural Conduction; D009460:Neurologic Examination; D009784:Occupational Diseases / Q000139:chemically induced* / Q000175:diagnosis; D016273:Occupational Exposure / Q000009:adverse effects*; D011890:Railroads; D011930:Reaction Time; D012307:Risk Factors; D012997:Solvents / Q000009:adverse effects*; D013997:Time Factors; D014944:World Health Organization
D012997:Solvents