443

those of types 10 and 19 inhibited its infectivity. Unlike theprototype strains of types 10 and 19 which are completely neu-tralised by the homologous antiserum, the Bristol isolates

break through antisera to these two types but inhibition ismore marked with antiserum to type-10 adenovirus. Similarresults have been obtained elsewhere with one adenovirus iso-lated from a case of conjunctivitis in the past year.’More detailed reports of the clinical and epidemiological fea-

tures of the infections and of the infecting agent are being pre-pared. However, we thought it worthwhile to draw attentionto this outbreak of keratoconjunctivitis associated with anadenovirus related to types 10 and 19 and to the difficultieslikely 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 INRETROBULBAR NEURITIS

SIR,-It is generally accepted that the only common causeof retrobulbar neuritis is multiple sclerosis (M.S.), of which itis often the first symptom. In every series, however, there aresome patients who do not have other evidence of neurologicaldisease, no matter how long the period of follow-up. It wouldbe useful to be able to distinguish between these two groups atthe time of the attack of retrobulbar neuritis. In the diagnosisof M.s. averaging techniques have been successfully used todemonstrate abnormalities of visual,6 auditory,’ and somato-sensory8 evoked potentials in the absence of relevant clinicalsigns and presumed to be due to "silent" plaques of demyelina-tion. It therefore seemed logical to seek such evidence of morewidespread disease in patients with retrobulbar neuritis.Since 1974 cortical and cervical somatosensory evoked

potentials (S.E.P.) were examined by the method described byMatthews et al.9 in 39 patients presenting with unilateral acuteretrobulbar 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 anattack of retrobulbar neuritis but is much lower than the more

convincing figure of a 78‘%, chance of acquiring mt.s. withinfifteen years."In my series the period of follow-up has beenbrief and information is incomplete. Of the 4 patients withabnormal s.E.P. only 1 has developed signs of M.S. Of thosewith 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. afterretrobulbar neuritis, either because it is insensitive or, prob-ably, because in most such patients plaques are not present inthe sensory pathways of the cervical spinal cord or brainstem.

I thank the staff of the Oxford Eye Hospital who referred most ofthese patients and Marian Small and Erika Pountney for technical as-sistance.

Department of Clinical Neurology,University of Oxford,Churchill Hospital,Headington, Oxford OX3 7LJ W. B. MATTHEWS

CREATINE KINASE IN MYOCARDIAL INFARCTION

Sm,—I enjoyed your editorial (Feb. 11, p. 313) and themany previous articles on the latest methods of measuring oneor other isoenzyme of creatine kinase to help in the diagnosisand management of myocardial infarction. Alas, the chemical

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.

pathologists of my district are so underfunded that they willnot measure even the ordinary creatine kinase of my coronarypatients.St. Charles Hospital,London W10 J. H. BARON

PRETRANSPLANT LYMPHOCYTOTOXINS ANDBONE-MARROW GRAFT REJECTION

SIR,-Dr Gale and colleagues (Jan. 28, p. 170) found thataplastic anaemia patients with pretransplant serum-lymphocy-totoxins were more likely to reject bone-marrow grafts thanthose without. My study of 30 HLA-identical bone-marrowgrafts from siblings in 29 aplastic patients reached a differentconclusion.

The grafting procedure followed the Seattle group’s protocol.Before grafting 17 patients were conditioned by donor buffy-coat cells followed by cyclophosphamide (50 mg/kg, 4 times),9 patients were given cyclophosphamide, procarbazine, andantilymphocyte globulin, and 3 patients were given cyclophos-phamide (60 mg/kg twice) and total body irradiation. Serumsamples were obtained before grafting, twice weekly during thefirst two months, and occasionally thereafter. HLA antibodieswere determined by microlymphocytotoxicity tests2 against apanel of lymphocytes from 25 normal donors. Non-HLA anti-bodies-i.e., cold lymphocytotoxins, autolymphocytotoxins,and anti-B-lymphocyte antibodies-were excluded from thestudy.

13 grafts were made in patients who did not have HLA anti-bodies either before or after grafting; 6 were rejected (46%).

In the other 16 patients, including 1 patient grafted twice,who had HLA antibodies before grafting, 10 grafts wererejected (58%). These results were not statistically different,suggesting that the absence of HLA antibodies, even whendonor leucocytes have been transfused, does not make marrowgraft rejection less likely.

In patients with pretransplant HLA antibodies, the anti-bodies persisted after in 9 grafts and disappeared within a fewweeks in after 8. All the patients with persisting antibodies butonly whose antibodies disappeared rejected their grafts. Thisdifference was statistically significant (Fisher’s exact test,

P=0.0008).What happens to HLA antibodies after grafting may reflect

the immunosuppressive treatment; antibodies disappeared inthe 3 patients given cyclophosphamide and total body irradia-tion, which is more immunosuppressive than cyclophospha-mide alone. My results show a relationship between pretrans-plant lymphocytotoxins and graft outcome different to thatfound by the U.C.L.A. group. The discrepancy might beexplained by the difference in pretransplant treatment; 14 ofthe U.C.L.A. patients were given total body irradiation afterwhich rejection seldom happens. It is hard to compare thesepatients with a group on cyclophosphamide alone. In addition,Gale et al. gave no details about the type of lymphocytotoxinsobserved; multitransfused patients frequently develop non-HLA lymphocytotoxins of unknown significance. There is nocorrelation between these pre-graft lymphocytotoxins and theoutcome of the graft. 3.4 In my opinion pre-graft HLA anti-bodies are of little or no value in predicting the outcome of thegraft but when followed up after grafting may indicate thedegree of immunosuppression of the graft recipient.Institut de Recherche sur les Maladies du Sang,U.E.R. d’Hématologie,Centre Hayem, Hôpital Saint-Louis,75010 Paris E. GLUCKMAN

1. Storb, R., and others. Blood, 1976,48, 817.2. 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.