443 those of types 10 and 19 inhibited its infectivity. Unlike the prototype strains of types 10 and 19 which are completely neutralised by the homologous antiserum, the Bristol isolates break through antisera to these two types but inhibition is more marked with antiserum to type-10 adenovirus. Similar results have been obtained elsewhere with one adenovirus isolated from a case of conjunctivitis in the past year.’ More detailed reports of the clinical and epidemiological features of the infections and of the infecting agent are being prepared. However, we thought it worthwhile to draw attention to this outbreak of keratoconjunctivitis associated with an adenovirus related to types 10 and 19 and to the difficulties likely to be encountered in typing the virus. Bristol

Eye Hospital

Bristol Royal Infirmary, Bristol BS2 8HW

A. B. TULLO P. G. HIGGINS

SOMATOSENSORY EVOKED POTENTIALS IN RETROBULBAR NEURITIS

SIR,-It is generally accepted that the only common cause of retrobulbar neuritis is multiple sclerosis (M.S.), of which it is often the first symptom. In every series, however, there are some patients who do not have other evidence of neurological disease, no matter how long the period of follow-up. It would be useful to be able to distinguish between these two groups at the time of the attack of retrobulbar neuritis. In the diagnosis of M.s. averaging techniques have been successfully used to demonstrate abnormalities of visual,6 auditory,’ and somatosensory8 evoked potentials in the absence of relevant clinical signs and presumed to be due to "silent" plaques of demyelination. It therefore seemed logical to seek such evidence of more widespread disease in patients with retrobulbar neuritis. Since 1974 cortical and cervical somatosensory evoked potentials (S.E.P.) were examined by the method described by Matthews et al.9in 39 patients presenting with unilateral acute retrobulbar neuritis as an isolated event. Abnormalities were present in only 4 patients (10%). This is not far from Kur)and’s"’estimate of a 13 c chance of m.s. developing after an attack of retrobulbar neuritis but is much lower than the more convincing figure of a 78‘%, chance of acquiring mt.s. within fifteen years."In my series the period of follow-up has been brief and information is incomplete. Of the 4 patients with abnormal s.E.P. only 1 has developed signs of M.S. Of those with normal S.E.P. 2 now have mt.s. The technique is not, therefore, likely to be of value in the prediction of M.S. after retrobulbar neuritis, either because it is insensitive or, probably, because in most such patients plaques are not present in the sensory pathways of the cervical spinal cord or brainstem. I thank the staff of the Oxford Eye Hospital who referred most of these patients and Marian Small and Erika Pountney for technical assistance.

Department of Clinical Neurology, University of Oxford, Churchill Hospital, Headington, Oxford OX3 7LJ

W. B. MATTHEWS

CREATINE KINASE IN MYOCARDIAL INFARCTION

Sm,—Ienjoyed your editorial (Feb. 11, p. 313) and the many previous articles on the latest methods of measuring one or other isoenzyme of creatine kinase to help in the diagnosis and management of myocardial infarction. Alas, the chemical

pathologists

of my district are so underfunded that they will the ordinary creatine kinase of my coronary

not measure even

patients. St. Charles Hospital, London W10

PRETRANSPLANT LYMPHOCYTOTOXINS AND BONE-MARROW GRAFT REJECTION

SIR,-Dr Gale and colleagues (Jan. 28, p. 170) found that

aplastic anaemia patients with pretransplant serum-lymphocytotoxins were more likely to reject bone-marrow grafts than those without. My study of 30 HLA-identical bone-marrow grafts from siblings in 29 aplastic patients reached a different conclusion. The grafting procedure followed the Seattle group’s protocol. Before grafting 17 patients were conditioned by donor buffycoat cells followed by cyclophosphamide (50 mg/kg, 4 times), 9

given cyclophosphamide, procarbazine, and antilymphocyte globulin,and 3 patients were given cyclophosphamide (60 mg/kg twice) and total body irradiation. Serum samples were obtained before grafting, twice weekly during the first two months, and occasionally thereafter. HLA antibodies were determined by microlymphocytotoxicity tests2 against a panel of lymphocytes from 25 normal donors. Non-HLA antibodies-i.e., cold lymphocytotoxins, autolymphocytotoxins, and anti-B-lymphocyte antibodies-were excluded from the study. 13 grafts were made in patients who did not have HLA antibodies either before or after grafting; 6 were rejected (46%). In the other 16 patients, including 1 patient grafted twice, patients

were

who had HLA antibodies before grafting, 10 grafts were rejected (58%). These results were not statistically different, suggesting that the absence of HLA antibodies, even when donor leucocytes have been transfused, does not make marrow graft rejection less likely. In patients with pretransplant HLA antibodies, the antibodies persisted after in 9 grafts and disappeared within a few weeks in after 8. All the patients with persisting antibodies but only whose antibodies disappeared rejected their grafts. This difference was statistically significant (Fisher’s exact test,

P=0.0008). What happens to HLA antibodies after grafting may reflect the immunosuppressive treatment; antibodies disappeared in the 3 patients given cyclophosphamide and total body irradiation, which is more immunosuppressive than cyclophosphamide alone. My results show a relationship between pretransplant lymphocytotoxins and graft outcome different to that found by the U.C.L.A. group. The discrepancy might be explained by the difference in pretransplant treatment; 14 of the U.C.L.A. patients were given total body irradiation after which rejection seldom happens. It is hard to compare these patients with a group on cyclophosphamide alone. In addition, Gale et al. gave no details about the type of lymphocytotoxins observed; multitransfused patients frequently develop nonHLA lymphocytotoxins of unknown significance. There is no correlation between these pre-graft lymphocytotoxins and the outcome of the graft. 3.4 In my opinion pre-graft HLA antibodies are of little or no value in predicting the outcome of the graft but when followed up after grafting may indicate the degree of immunosuppression of the graft recipient. Institut de Recherche sur les Maladies du U.E.R. d’Hématologie, Centre Hayem,

Hôpital Saint-Louis, 5. Pereira, M. S. Personal communication. 6. Halliday, A. M., McDonald, W. I., Mushin, J. Br. med. J. 1973, iv, 661. 7. Robinson, K., Rudge, P. Brain, 1977, 100, 19. 8. Small, D. G., Matthews, W. B., Small, M. J. neurol. Sci. 1978, 35, 211. 9. Matthews, W. B., Beauchamp, M., Small, D. G. Nature, 1974, 252, 230. 10. Kurland, L. T., Beebe, G. W., Kurtzke, J. F., Nagler, B., Auth, T. L., Lessel, S., Nefzger, M.D. Acta neurol. scand. 1966, suppl. 19, p. 157. 11.Hutchinson, W. M. J. Neurol. Neurosurg. Psychiat. 1976, 39, 283.

J. H. BARON

75010 Paris

Sang,

E. GLUCKMAN

Storb, R., and others. Blood, 1976,48, 817. Mittal, K. K., Mickey, M. R., Singal, O. P., Terasaki, P. I. Transplantation, 1968, 6, 913. 3. Gluckman, E., Andersen, E., Dausset, J. Lancet, 1977, ii, 146. 4. Gluckman, E., Gluckman, J. C., Andersen, E. Lancet, 1976, i, 1244. 1. 2.