CONCENTRATION-RELATED EFFECTS OF HEXANE ON EVOKED RESPONESES FROM BRAIN AND PERIPHERAL NERVE
|Publication Date:||1 January 1982|
n-Hexane produces, by way of its metabolite 2,S-hexanedione, peripheral and central axonopathies with secondary myelinopathies [ 1 ]. Extensive ncuromorphologic investigations have described the anatomic changes associated with hexane exposures [2. 3], but there have been few studies of the functional, electrophysiologic, consequences of hexacarbon neuropathy. Of these studies, most have focused on the peripheral nervous system, even though the central nervous system (CNS) is known to undergo morphologic changes |4]. Ciancetti el al. |5J, for example, observed electromyographic and nerve conduction velocity changes in a large number of exposed shoe-industry workers, and several investigators have described similar changes in animals with experimentally induced hexacarbon polyneuropathy [6, 7]. In an earlier study (^ we showed, by measuring the brainstem auditory-evoked response (BAER) and action potential (AP) of the ventral caudal nerve of the rat's tail, that hexane causes a nerve conduction delay in auditory brainstem tracts as well as in peripheral nerve. This finding, and a report that n-hexane causes pathology in the hypothalamus and optic tracts of cats , suggest that manifestations of hexane poisoning would be evident in evoked responses obtained from several sensory systems. Indeed, Seppatainen et al.  found, that n-hexane Induced changes in the visual-evoked response (VER) of exposed workers.
In order to characterize further the electrophysiologic concomitants of hexacarbon neuropathy, biopotentials«voked in peripheral nerve and brain by somatosensory, auditory, and visual stimulation were studied in rats exposed by inhalation to three concentrations of hexane.