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antibody hypothesis, such as that of Burnet’s clonalselection.4 4

We have been able to reproduce these findings in othersubjects, but in Mantoux-negative persons the same

degree of inhibition by o.T. was not obtained. Hydro-cortisone succinate inhibited the action of o.T., thoughother bacterial antigens were less affected, and at the samedilutions of hydrocortisone succinate the action of P.H.A.was not inhibited.

Fuller details and discussion of this will be published later.





SiR,-In an interesting leading article 5 you suggesteda hippocampal-mammillary anatomical substrate for theability to memorise recent events, a conclusion sincereached elsewhere 6 Loss of this ability, however, notonly follows bilateral lesions of the mammillary bodies orof the hippocampus,8-10 but also bilateral damage to theanterior cingulate cortex.lll2 It seems reasonable thereforeto suggest that such


memorising "

may be a function ofthe whole limbic lobe, a concept which certain electricalphenomena might be interpreted as supporting.

Thus, not only have slow waves been shown to occur in thehippocampus during a particular phase of learning or condi-tioning in cats,13 but also in 15 of the 17 abnormal records from21 patients with Korsakow’s syndrome of probable mammillaryorigin, the pathological slow and fast E.E.G. activity foundpredominated anteriorly,14 a finding which might be relatedto loss of cingulate function since this presumably depends tosome extent at least upon the mammillothalamic tract relayed bythe anterior thalamic nucleus, and the cingulate cortex hasprojections to the cerebral frontal convexity.15

It is true that Barbizet refers to two neurosurgical reports ofbilateral section of the fornix in which no such disorder of

memory was recorded, but this might have been because thepathological lesions for which the operative sections were made,were so gross and of such longstanding that the plastic brainhad adapted itself to manage without fornix function in thesepatients (much as it adapts to congenital absence of the corpuscallosum apparently), especially since in a third report ofbilateral fornix section 16 the memory defect in question wasobserved and carefully investigated psychologically. Ervin,incidentally, also refers briefly to three instances of lesions ofthe mammillothalamic tract and one of the anterior thalamus,which led to similar memory defects, although lesions of theanterior thalamic nuclei 17 or of the cingulate areas 18 in

experimental animals led to no specific behavioural disturbancebeing observed. Mrs. Beck has recently informed me, however,that in her experiments, in collaboration with Dr. Brierley,attempts were not made to train the animals with a view to

demonstrating the presence or absence of such defects, and thesame may apply therefore to the findings of Gomez andMettler. As Barbizet and Sweet et al. make so clear, thedefects are not of perception, of immediate nor of long-4. Burnet, F. M. The Clonal Selection Theory of Acquired Immunity.

Cambridge, 1959.5. Lancet, 1957, i, 918.6. Barbizet, J. J. Neurol. Psychiat. 1963, 26, 127.7. Russell, W. R. Proc. R. Soc. Med. 1958, 51, 9.8. Victor, M., Angevine, J. B., Jr., Mancall, E. L., Fisher, C. M. Arch.

Neurol. 1961, 5, 244.9. Hall, P. Lancet, 1963, i, 752.

10. Crawford, J. P. Proc. R. Soc. Med. 1957, 50, 704.11. Whitty, C. W. M., Lewin, W. Brain, 1960, 83, 648.12. Eysenck, H. J. Dynamics of Anxiety and Hysteria. London, 1957.13. Adey, W. R., Dunlop, C. W., Hendrix, C. E. Arch. Neurol. 1960, 3, 74.14. Gorman, W. F., Stearns, E., Wortis, S. B. Amer. J. Psychiat. 1950,

107, 20.15. Ward, A. A., Jr. Ass. Res. nerv. Dis., Proc. 1948, 27, 438.16. Sweet, W. H., Talland, G. A., Ervin, F. R. Trans. Amer. Neurol. Ass.

1959, 84, 7.17. Brierley, J. B., Beck, E. Ciba Foundation Symposium on the Neuro-

logical Basis of Behaviour; p. 90. London, 195818. Gomez, J. A., Mettler, F. A. J. Neurol. Psychiatl 1962, 25, 387.

standing memory, but of failing to associate the first two ofthese in a durable and enriching way with the third.

Barbizet also points out that memory proceeds partly fromfeeling, emotion, and instinct, a situation caricatured perhaps,as Russell puts it, in the intense sense of familiarity to be foundin deja vu phenomena of limbic origin. This is in keeping withthe outcome of feeding experiments, as a result of which thehippocampus has been equated 19 with a system whichoptimises reward and amplifies motivation. This suggestionis moreover supported by studies in reward by self-stimulationof the limbic system in rats with implanted electrodes.Z° Centralor diencephalic disorder of such motivational factors, however,is less likely to be due to lesions of the mammillary bodies thanto disease in adjacent hypothalamic grey matter 1° to whichBarbizet refers, and which in health does not require an intactneocortex to produce complex instinctive peripheral activity 10 21

e.g., genital readiness, gastric hunger contractions, or som-atic changes like those of endogenous (or so called " sham 1022)emotion. Such peripheral activity nevertheless does impingeon or enter full consciousness when the neocortex is intact, andonly then can it influence memory. The anatomical connectionbetween motivation and " memorising " is probably thereforefinally one between the limbic cortex and the cortex of thecerebral convexity.

Ide Hill, Kent.


Dr. C. L. SHARP, medical officer of health for Bedford(Public Health Department, Town Hall, Bedford), writes:

" I have been asked by the Regional Office for Europe ofthe World Health Organisation to write and present a reporton this subject to their meeting in Prague in 1964. The WorldHealth Organisation was good enough to arrange for me tovisit Czechoslovakia and Sweden to meet people carrying outprojects along these lines. I am, however, very anxious to befully informed about schemes in the United Kingdom eitheralready functioning or planned to go into operation in 1964,whether in general practice, as university projects, or by localauthorities. I will, of course, supply the information collectedto those helping in this way."19. Lancet, 1961, ii, 1243.20. Olds, J. Science, 1958, 127, 315.21. Michael, R. P. Medical News, Sept. 27, 1963, p. 8.22. Martin, J. P. Brain, 1950, 73, 453.

AppointmentsBAILEY, A. G., M.B. Manc., D.P.H. : senior medical officer, Brighton.BROWN, R. J. K., B.A., M.B. Cantab., M.R.C.P., D.c.H.: consultant physician,

children’s department, Middlesex Hospital, London.CATTERALL, R. D., M.R c.s., M.R.C.P.E. : consultant venereologist, Middlesex

Hospital, London.FRANKLIN, C. B., M.B. Birm., F.F.A. R.C.S.: consultant anaesthetist, West

Cumberland hospital group.JEPSON, MARION E., M.B., B.SC. Mane., D.P.H., D.C.H. : senior M.O. (maternity

and child welfare), Sheffield.KARNEY, P. L., M.B. Madras, D.P.H. : M.o.H., Woking.KENYON, J. R., CH.M., B.sc. Glasg., F.R.C.S.: consultant surgeon, St. Mary’s

Hospital and Paddington General Hospital, London.LOWTHER, C. P., M.B. Glasg., M.R.C.P.E., M.R.C.P. Glasg.: consultant physician,

Eastern General Hospital, Edinburgh.MACLEOB, H. M., M.B. Edin., M.R.C.P.E. : consultant physician, Longrrore

Hospital, Edinburgh.SPANTON, D. B., M.B. Lond., M.R.C.O.G., D.OBST.: consultant obstetrician and

gynxcologist, West Cumberland hospital group.SWINBURNE, L. M., M.B. Leeds, B.sc., M.R.C.P., D.C.H. : consultant in

pathology, Leeds A and B hospital groups.

Hospital for Sick Children, Great Ormond Street, London:MENZIES, 1. S., M.B., DIP.PATH. : registrar in chemical pathology.TIGHE, SHELAGH M., M.D. Sheff., M.R.C.P., D.C.H. : M.O., department of

dermatology.WOOD, C. B. S., M.A., M.B. Cantab., M.R.C.P., D.C.H. : house-physician.

Wessex Regional Hospital Board:BuRSTON, JOHN, M.D., B.sc. Lond.: consultant pathologist, Portsmouth

and Isle of Wight area pathological service.MELVILLE-THOMAS, D. G., M.B. Cantab., D.P.M. : consultant child psychia-

trist, Hampshire child-guidance service.SMITH, E. B. 0., M.B. Lond., D.P.M. : psychiatrist (s.H.M.o.), Herrison

hospital group.VALVIS, MARY, M.B., N.U.I., D.P.M. : psychiatrist (s.H.M.o.), Herriscn

group (St. Ann’s Hospital).