11 December 1965 Motor Neurone Disease Serum

degree, in amyotrophic lateral sclerosis. The possibility that myelotoxic antibodies may be formed secondarily to myelin destruction, arising perhaps from some non-immune cause, is a very real one in view of the finding of antibody to encephalitogenic factor in a variety of neurological conditions reported by Field, Caspary, and Ball (1963). Nevertheless, their undoubted occurrence in multiple sclerosis and experimental allergic encephalomyelitis might well be of some pathogenetic importance because of the lowered blood-brain barrier at lesions in this disease (Broman, 1947, 1964) and in experimental allergic encephalomyelitis (Barlow, 1956; Vulp6, Hawkins, and Rozdilsky, 1960; Field, 1961). Finally, the occurrence of two examples of myelotoxicity among our 20 normal sera should be compared with the 2 out of 26 reported by Bornstein and Appel (1965). Lumsden (1965) does not report upon normals, but in view of the findings of Hashem and Barr (1963) it is possible that normal subjects may -become sensitized to brain or its degeneration products if these are ingested. The possibility exists also that laboratory workers or others habitually exposed to brain might show some antibody responses. In this connexion Field et al. (1963) were able to demonstrate antibody to an encephalitogenic factor in 20.4% of 44 normal subjects. There is, however, no evidence that human antibodies demonstrated by the tanned-cell method parallel serum myelotoxicity.