Certain neuropathic pain states, including postherpetic neuralgia and trigeminal neuralgia, show a dramatically increased incidence in the aged. Two recent experimental observations, unrelated a priori, might provide insight into why this is so. The first observation appeared unexpectedly during the course of a quantitative morphometric study aimed at determining the kinetics of retrograde cell death in dorsal root ganglia (DRGs) of adult male rats after nerve injury. Although the expected falloff in the ratio of neurons on the operated side versus the contralateral intact side was confirmed, much of the change resulted from an increase in the number of cells on the intact side. DRG cell counts were then carried out in intact, unoperated rats of various ages, and an increase in neuronal populations with age and size was confirmed. However, as the rats entered "old age" (greater than 400 days of age), proliferation ceased and there was an indication of secondary cell loss (involution). This is consistent with other data on DRG involution in the aged. The second observation is that regressive changes in DRGs following nerve injury are associated with enhanced generation of ectopic impulse discharge in the DRG, and potentiated cross-excitation among neighboring DRG neurons. It is likely that these post-injury changes in DRG electrogenesis contribute to the neuropathic sensory abnormalities, including chronic pain, that are associated with traumatic nerve injury. Considering both observations together, it is possible that DRG involution in the aged triggers electrical changes in the DRG resembling those associated with DRG involution following nerve injury. If so, this process could account for the special susceptibility of elderly patients to certain neuropathic pain states.