Clinical and pathological study of ischaemic neuropathy.

For many years a number of workers have studied the relation between arterial occlusion or compression in man, produced by various pathological processes, and peripheral nerve abnormality. The whole subject was authoritatively reviewed by Richards (1951). There is ample evidence, clinical, histological, and electrical, that ischaemia of a nerve has an adverse effect upon it. Persisting nerve damage from ischaemia may be produced by arterial injury (Tinel, 1917; Holmes, Highet and Seddon, 1944), by embolism (Blackwood, 1944; Haimovici, 1950), by chronic occlusive arterial disease (Joffroy and Achard, 1889; Priestley, 1931; Hutchinson and Liversedge, 1956; Gairns, Garven, and Smith, 1960), by polyarteritis nodosa (Kemohan and Woltman, 1938), and by other, rarer, causes. Experimentally ischaeiia has been produced in animal nerves by variou means (Adams 1943; Roberts, 1948) and electrical studies have been carried out on ischaemic nerves (Bentley and Schlapp, 1943; Porter and Wharton, 1949). Lewis, Pickering, and Rothschild (1931) showed in their classical experiments that changes may be produced in nerve function by ischaemia. The histological changes described in the nerves have been fairly consistent and non-specific, and involve patchy degeneration in nerve fibres together with endoneurial fibrosis. However, many reports have not distinguished between changes occurring in nerves after an acute ischaemic episode and those resulting from chronic longstanding ischaemia, and no attempt has been made to determine the type of degeneration in ischaemic nerve fibres by individual examination. In addition, many of the earlier reports on nerves in arteriosclerotic limbs were from cases complicated by diabetes mellitus. Some of the studies also were carried out on digital nerves, but it has been shown (Gairns et al., 1960) that the digital nerves even of healthy young subjects may reveal damage due to repeated minor injuries. The state of the vasa nervorum in peripheral arteriosclerosis has been commented upon incidentally by a few authors while studying the nerves (Joffroy and Achard, 1889; Woltman and Wilder, 1929). Cottrell (1940) found occlusive changes present in the vasa nervorum of the aged. Detailed examination of the smaller vessels has, however, been neglected both by workers on nerve ischaemia and by those studying arteriosclerosis. It has been shown that there are two types of degenerative change that occur in nerve fibres: Wallerian degeneration and segmental demyelination (Gombault, 1880; Vizoso and Young, 1948; Thomas and Young, 1949; Vizoso, 1950; Lubin'ska, 1958 and 1959). It is a common clinical experience to find abolition of vibration sensitivity and diminution or loss of ankle jerks in the feet of the aged (Pearson, 1928; Critchley, 1931). Lascelles and Thomas (1966) studied isolated nerve fibres from the sural nerves of subjects of various ages, and found degenerative changes present in those over the age of 65 years, segmental demyelination being the predominant abnormality. They suggested a possible relationship between these clinical findings and nerve changes and atheromatous occlusion of the vasa nervorum. The present investigation was designed to determine the degree of neurological abnormality, as assessed clinically, in the affected limbs of patients with chronic occlusive arterial disease of the legs. This was combined with a study of the pathological changes in sensory nerves from the affected limbs, by both light and electron microscopy, with particular reference to the alterations in the vasa nervorum and the detailed study of the nerve fibres themselves.