Delayed onset of distal axonal neuropathy in primates after prolonged low-level administration of a neurotoxin.

Short-latency somatosensory evoked potentials were recorded from surface electrodes overlying peripheral nerve, spinal cord, and cortex in 4 monkeys during prolonged intoxication with low levels of acrylamide. A fifth animal served as a longitudinal control subject. Slowing of the response across the spinal-medullary junction was a reliable sign, manifest only after prolonged exposure. Associated morphological changes were preterminal accumulation of axonal neurofilaments without synaptic disruption in the gracile nucleus. The induced alterations in the latency of short-latency somatosensory evoked potentials and in axon morphology were reversible after 7 months of recovery. The extreme delay in onset of subtle neurological dysfunction (940 days) following administration of a presumed safe level of acrylamide suggests that permissible levels of human exposure to toxins of this type should be reassessed.