Abstract
The neurotoxicologist is commonly consulted when it is suspected that exposure to a chemical substance has led to an outbreak of human neurological disease. Questions emerge for which answers must be sought by experimental investigation: Is the suspect chemical the culpable agent? What type of disorder is produced? Is it reversible, can it be treated, and what is the prognosis? This paper addresses the orderly analysis of neurotoxic disease, based on experience with a number of human neurotoxins, notably the industrial monomer acrylamide.
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Arezzo, J.C., Schaumburg, H.H., Vaughan, H.G., Jr., Spencer, P.S., and Barna, J., 1982, Hindlimb somatosensory evoked potentials in the monkey: the effects of distal axonopathy. Ann. Neurol. 12: 24.
Auld, R.B., and Bedwell, S.F., 1967, Peripheral neuropathy with sympathetic overactivity from industrial contact with acrylamide. Can. Med. Assoc. J.96: 652.
Bannister, R., 1983, “Autonomic Failure. A Textbook of Clinical Disorders of the Autonomic Nervous System” Oxford University Press, Oxford.
Bisby, W.G., and Bulgar, V.T., 1977, Reversal of axonal transport at a nerve crush. J. Neurochem. 29: 313–320.
Bradley, W.G., and Williams, M.H., 1973, Axoplasmic flow in axonal neuropathies. Brain 96: 235.
Cavanagh, J.B., and Gysbers, M.F., 1980, “Dying-back” above a nerve ligature produced by acrylamide. Acta Neuropathol. 51: 169.
Cavanagh, J.B., and Gysbers, M.F., 1983, Ultrastructural features of the Purkinje cell damage caused by acrylamide in the rat: a new phenomenon in cellular neuropathology. J. Neurocytol. 12: 413.
Chang, L.W., 1980, Mercury. in: “Experimental and Clinical Neurotoxicology,” P.S. Spencer and H.H. Schaumburg, eds., Williams and Wilkins, Baltimore, MD.
Chretien, M., Patey, G., Souyri, F., and Droz, B., 1981, Acrylamide induced neuropathy and impairment of axonal transport of proteins. II. Abnormal accumulations of smooth endoplasmic reticulum at sites of focal retention of fast transported proteins. Electron microscope radioautographic study. Brain Research, 205: 15–28.
De Jong, R.N., 1967, “The Neurological Examination,” Harper & Row, New York.
Fujita, A., Shibata, M., Kato, H., Amoni, Y., Itomi, K., Sujuki, K., Nakajawa, T., and Takahashi, T., I960, Clinical observations on acrylamide poisoning. Nippon Iji Shimpo 1869: 37.
Fullerton, P.M., 1969, Electrophysiological and histological observations on peripheral nerves in acrylamide poisoning in man. J. Neurol. Neurosurg. Psychiat. 32: 186.
Fullerton, P.M., and Barnes, J.M., 1966, Peripheral neuropathy in rats produced by acrylamide. Brit. J. Ind. Med.23: 210.
Garland, T.O., and Patterson, M.W.H., 1967, Six cases of acrylamide poisoning. Brit. Med. J. 4: 134.
Griffin, J.L., Price, D.L., and Drachman, D.B., 1977, Impaired axonal regeneration in acrylamide intoxication. J. Neurobiol. 8: 355.
Hopkins, A.P., 1970, The effect of acrylamide on the peripheral nervous system of the baboon. J. Neurol. Neurosurg. Psychiat. 33: 805.
Hopk ins, A.P., and Gilliatt, R.W., 1971, Motor and sensory nerve conduction velocity in the baboon: normal values and changes during acrylamide neuropathy. J. Neurol. Neurosurg. Psychiat. 35: 163.
Howland, R.D., Vyas, I.L., and Lowndes, H.E., 1980a, The etiology of acrylamide neuropathy: possible involvement of neuron specific enolase. Brain Res. 190: 529.
Howland, R.D., Vyas, I.L., Lowndes, H.E., and Argentieri, T.M., 1980b, The etiology of toxic peripheral neuropathies: In vitro effects of acrylamide and 2,5-hexanedione on brain enolase and other glycolytic enzymes. Brain Res.202: I3l.
Igisu, H., Goto, I., Kawamura, Y., Kato, M., Izumi, K., and Kuroiwa, Y., 1975, Acrylamide encephalopathy due to well water pollution. J. Neurol. Neurosurg. Psychiat. 38: 581.
Jakobsen, J., and Sidenius, P., 1983, Early and dose-dependent decrease of retrograde axonal transport in acrylamide-intoxicated rats. J. Neurochem. 40: 447.
Kuperman, A.S., 1958, Effects of acrylamide on the central nervous system of the cat. J. Pharmacol. Exp. Therapeut. 123: 180.
Le Quesne, P., 1980, Acrylamide. in: “Experimental and Clinical Neurotoxicology”, P.S. Spencer and H.H. Schaumburg, eds., Williams and Wilkins, Baltimore, MD.
Leswing, R.J., and Ribelin, W.E., 1969, Physiologic and pathologic changes in acrylamide neuropathy. Arch. Environ. Hlth. 18: 22.
Loeb, A.L., and Anderson, R.J., 1981, Anatagonism of acrylamide neurotoxicity by supplementation with vitamin B6. Neurotoxicology 2: 625.
Lowndes, H.E., Baker, T., Cho, E., and Jortner, B.S., 1978, Position sensitivity of de-afferented muscle spindles in experimental acrylamide neuropathy. J. Pharmacol. 205: 40.
McLeod, J.G., 1983, Distal autonomic neuropathy, in: “Autonomic Failure. A Textbook of Clinical Disorders of the Autonomic Nervous System”, R. Bannister, ed., Oxford University Press, Oxford.
Miller, M.S., Miller, M.J., Burks, T.F., and Sipes, I.G., 1983, Altered retrograde axonal transport of nerve growth factor after single and repeated doses of acrylamide in the rat. Toxicol. Appl. Pharmacol. 69: 96.
Miller, M.S., and Spencer, P.S., in press (a), Single doses of acrylamide reduce retrograde transport velocity. J. Neurochem.
Miller, M.S., and Spencer, P.S., in press (b), Mechanisms of acrylamide axonopathy. Ann. Rev. Pharmacol. Therapeut.
Miller, M.S., and Spencer, P.S., in press, Inhibition by acrylamide of increased ornithine decarboxylase activity and RNA synthesis in dorsal root ganglion following sciatic nerve transection. J. Neurochem.
Morgan-Hughes, J.A., Sinclair, S., and Durston, J.H.J., 1974, The pattern of peripheral nerve regeneration induced by crush in rats with severe acrylamide neuropathy. Brain 97: 235.
Ochs, S., 1982, “Axoplasmic Transport and its Relation to Other Nerve Functions”, John Wiley & Sons, New York.
Pleasure, D.E., Mischner, K.C., and Engel, W.K., 1969, Axonal transport of proteins in experimental neuropathies. Science 166: 524.
Post, E.J., and McLeod, J.G., 1977a, Acrylamide autonomic neuropathy in the cat. I. Neurophysiological and histological studies. J. Neurol. Sci. 33: 353.
Post, E.J., and McLeod, J.G., 1977b, Acrylamide autonomic neuropathy in the cat. II. Effects on mesenteric vascular control. J. Neurol. Sci. 33: 375.
Prineas, J., 1974, The pathogenesis of dying-back polyneuropathies. II. An ultrastructural study of experimental acrylamide intoxication in the cat. J. Neuropathol. Exp. Neurol. 33: 260.
Russell, D.H., and Snyder, S.H., 1968, Amine synthesis in rapidly growing tissues: Ornithine decarboxylase in rat liver. Endocrinology 86: 1414.
Sabri, M.I., 1983, Mechanism of action of acrylamide on the nervous system. Biol. Mem. 8: 16.
Sabri, M.I., and Ochs, S., 1971, Inhibition of gIyceraldehyde-3-phosphate dehydrogenase in mammalian nerve by iodoacetate. J. Neurochem. 13:1509.
Sabri, M.I., Dairman, W., Juhasz, L., Bischoff, M.C., Spencer, P.S., 1981, Is acrylamide neurotoxicity pyruvate sensitive? Trans. Amer. Soc. Neurochem. 12: 147.
Sabri, M.I., and Spencer, P.S., 1980, Inhibition of glyceraldehyde-3-phosphate and other glycolytic enzymes by acrylamide. Neurosci. Lett. Suppl. 5: 455.
Sahenk, Z., and Mendell, J.R., 1981, Acrylamide and hexanedione neuropathies: abnormal bidirectional transport rate in distal axons. Brain Res. 219:397.
Satchel, P.M., and McLeod, J.G., 1981, Megaoesophagus due to acrylamide neuropathy. J. Neurol. Neurosurg. Psychiat. 44: 906.
Satchell, P.M., Harper, B., and Goodman, A.H., 1982, Abnormalities in the vagus nerve in acrylamide neuropathy. J. Neurol. Neurosurg. Psychiat. 45: 609.
Schaumburg, H.H., Wisniewski, H.M., and Spencer, P.S., 1974, Ultrastructural studies of the dying-back process. I. Peripheral nerve terminal and axon degeneration in systemic acrylamide intoxication. J. Neuropathol. Exp. Neurol. 33: 260.
Sidenius, P., and Jakobsen, J., 1983, Anterograde axonal transport in rats during intoxication with acrylamide. J. Neurochem. 40: 687.
Spencer, P.S., Hanna, R.B., and Pappas, G.D., 1977a, Acrylamide inactivation of Pacinian corpuscle function: a freeze-fracture study. J. Neuropathol. Exp. Neurol. 36: 631.
Spencer, P.S., Hanna, R.B., Sussman, M., and Pappas, G., 1977b, Inactivation of Pacinian corpuscle mechanosensitivity by acrylamide. J. Gen. Physiol. 70: 17a.
Spencer, P.S., and Schaumburg, H.H., 1974, A review of acrylamide neurotoxicity. II. Experimental animal neurotoxicity and pathologic mechanisms. Canad. J. Neurol. Sci. 1: 152.
Spencer, P.S., and Schaumburg, H.H., 1977, Ultrastructural studies of the dying-back process. IV. Differential vulnerability of PNS and CNS fibers in experimental centra I-peripheral distal axonopathies. J. Neuropathol. Exp. Neurol. 36: 300.
Spencer, P.S., and Schaumburg, H.H., 1980, “Experimental and Clinical Neurotoxicology”. Williams and Wilkins, Baltimore, MD.
Sumner, A.J., and Asbury, A.K., 1975, Physiological studies of the dying-back phenomenon. Muscle stretch afferents in acrylamide neuropathy. Brain 98: 91.
Takahashi, M., Ohara, T., and Hashimoto, K., 1971, Electrophysiological study of nerve injuries in workers handling acrylamide. Int. Arch. Arbeitsmed. 28: 1–11
Weir, R.L., Glaubiger, G., and Chase, N., 1978, Inhibition of fast axoplasmic transport by acrylamide. Environ. Res. 17: 251.
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© 1988 Plenum Press, New York
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Spencer, P.S., Schaumburg, H.H. (1988). Analysis Of Neurotoxic Disease: The Acrylamide Experience. In: Galli, C.L., Manzo, L., Spencer, P.S. (eds) Recent Advances in Nervous System Toxicology. NATO ASI Series, vol 100. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0887-4_9
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DOI: https://doi.org/10.1007/978-1-4613-0887-4_9
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