nerve-energy as: "The total potential energy in the neurone available for use in the transmission of impulses."

This is sufficiently comprehensive to include both augmentor and inhibitory factors as well as cerebellar innervation.

Now if neuronic energy is real, the problem is to measure it. We ought not to say that this problem is insoluble, problems more difficult have been solved. The reality of neuronic energy need not depend on our discovering a quantitative method for it, because heat, light and electricity were all acknowledged as real before they were measured.

The definition just given is of potential energy, but potential energy as such cannot be measured. Energy is 'capacity for doing work,' but only the work or kinetic energy can be measured.

Clearly neuronic energy cannot be measured as potential. But just as heat is measured by a mass of water raised through a certain range of temperature, and light by its chemical effects, and electricity by its thermal, chemical or photic effects, so neuronic energy might be measured by some form of work done through its influence.

The most obvious index to use for efferent discharges is muscle. Is muscle a reliable index? Miss Buchanan of Oxford would doubt this, so would Professor Forbes of Harvard. But Horsley thought it was reliable, for in his paper with this title "A contribution towards the determination of the energy developed by a nerve-centre" (Brain, XXI, 1898)—he wrote: "It is an attempt to estimate quantitatively the work done by the central mechanisms of the central nervous system when these discharge their nerve-energy"; and again he said: "the work done by the muscle varies directly with the amount of the discharge from the

nerve-centre."

So that Horsley believed nerve-energy (1) was real, (2) that it was measurable, and (3) that muscle was reliable for measuring it.

The recent work at Utrecht would corroborate this last belief.

In conclusion,

one can but make some more or less random suggestions

in regard to possible methods of measuring neuronic energy.

(1) The most obvious method is simply to estimate quantitatively the muscular work done with some form of ergograph: this could, of course, be expressed as kilogramme-metres per unit mass of muscle per

unit time.

(2) During the performance of maximal voluntary work with the ergograph, distract the attention of the subject, and then measure the diminution of the work.

(3) The electrical maximal stimulation of all the fibres in the nerve to the biceps, for instance, is more powerful than the voluntary maximal contraction of the same muscle. Since the former is amenable to quantitative determination, we might have in this method a means of obtaining an equation.

(4) By means of a water manometer in the urinary bladder, determine the height of column before and after destruction of the tonic centre for the sphincter vesicae in the lumbar region of the spinal cord.

(5) Determine the force required to distend the sphincter ani before and after destruction of the cord.

(6) Determine the pressure necessary to block impulses descending the phrenic nerves, as in Lady Briscoe's experiments1.

(7) Measure the changes in conductance in the skin in the psychogalvanic phenomenon, during feeble and powerful innervation respectively 2.

(8) Investigate the variations in E.M.F. in the retina and in the visual centre according as the stimulus to the retina is made to vary in intensity. (9) Ascertain what pressure on the upper lip is required to inhibit the reflexigenous impulses for sneezing.

(10) Compare the times during which the breath can be held up to the 'breaking-point,' when the alveolar carbon dioxide is diminished to different degrees.

(11) In a certain conditioned reflex, the quantity of saliva is proportional to the loudness of a tuning-fork used as the stimulus: have we not here a quantitative method?

This discussion, properly speaking, would not be complete without some attempt being made to correlate neuronic energy with 'mental energy,' 'vital energy' and 'biotic energy.'

Inasmuch as biotic is merely the Greek for 'vital,' I do not see what we have gained by using the term 'biotic,' unless it be to get as far away as possible from the occult and miraculous associations with 'vitalism.' But clearly biotic energy cannot mean something other than vital, so that one of the two terms may be dropped as superfluous.

Biotic or vital energy is evidently a wider term than neuronic, for whereas neuronic contemplates only dynamic manifestations in the nervous system, biotic energy is co-extensive with the whole vital field.

1 Grace Briscoe, Journ. of Phys. LXI, No. 3, p. 353, June 1926.

2 Professor Macdowall of King's College, London, has shown that this phenomenon is a reflex vascular one. (Communication to British Association, Oxford, August 5, 1926.)

We cannot greatly err in calling neuronic energy a species of biotic energy, the biotic energy that manifests itself in neurones. A moribund invalid or a despondent melancholic has little biotic or neuronic energy; the eupeptic athlete has much.

Unless neuronic energy is a reality, the clinical conception of neurasthenia is meaningless.

In the present state of the psychological chaos involving this subject, it would not be profitable to attempt to relate neuronic energy with mental energy-important as this relationship must be.

THE SEQUELAE OF ENCEPHALITIS LETHARGICA1

By F. C. SHRUBSALL.

TOWARDS the end of the War and during the years which followed considerable anxiety arose from the appearance in epidemic form of an apparently new disease of the central nervous system. The onset was sometimes sudden with fever, stupor, alternating with nocturnal delirium, hallucinations and confusion, marked weakness, difficulties in speech and spasmodic twitchings of the face and limbs. Severe cases lay with complete lack of expression though evincing irritability when aroused. In some the phase lasted only a day or two, in others it persisted for weeks. Sometimes there were few localising symptoms, but more often there were squints, double vision, or paralyses of the muscles of the face, gullet or tongue. Death followed often from progressive paralysis of the respiratory mechanism. In those who recovered, the duration of acute illness varied from a few days to six to eight weeks. In some the onset was more gradual with general lassitude, headache, dryness of the throat and occasional vomiting or diarrhoea, usually accompanied by double vision and somnolence. Later it appeared that following the acute phase there were residual symptoms or sequelae in the form of partial paralysis, states of tremor, shaking palsies, character changes, mental hebetude, failure of intellectual development or even acute mental disorder.

The first cases were observed in France behind the Verdun front in 1915-16 and about a year later several were described in Vienna with the characteristic features of stupor and ophthalmoplegia.

In this country the first cases were noted towards the end of 1917 and in March and April of 1918 many cases of stupor or lethargy associated with ocular symptoms were noted and from the resemblance to clinical descriptions of botulism it was at first thought that infected food might be the cause. Soon however the separate nature of the disease was established, and it became popularly known as 'sleepy

1 A paper read before the Medical Section of the British Psychological Society, April 27, 1927.

sickness,' a name which has the disadvantage of a certain confusion with negro lethargy or 'sleeping sickness,' an entirely different disease. The two having as a common factor the part of the brain stem affected by quite different morbid agencies. After a time it too became evident that sequelae whether of the nature of motor disturbances or of conduct disturbances might follow very slight and indeed completely overlooked initial illness. The disease was made notifiable in England in 1919, and since that time in London efforts have been made to follow up all cases with considerable success, particularly in the case of children, the greater number of whom could be kept in touch through the agency of the Children's Care Organisation in the schools under the County Council.

During the seven years ending December 1925 there were notified in London 1560 cases, of which 235 on further investigation seemed not to be genuine examples. Of the remaining 1325 actual cases 338 were under 16 years of age and 937 over that age; of these 495 or over 37 per cent. proved fatal. The case mortality in different years ranged from 30 to 45 per cent., and this does not indicate the whole story, for in several cases death was recorded as due to some other condition, while during the period about 100 deaths were registered as due to encephalitis lethargica although the patients had never been notified during life as suffering from that disease. Of the survivors, or presumed survivors, 116 could not be traced in the year 1925; 375 or 28 per cent. were apparently perfectly well; 61 or 4-6 per cent. suffered from slight sequelae which definitely interfered with their occupation or education and 180 or 14-3 per cent. were totally incapacitated. Of those whose incapacity

was considerable

or total, in 54 or 4 per cent. this was due to Parkin

sonism, and in 114 or 8-6 per cent. to disorders of conduct. The seriousness of a disorder which is characterized by a death-rate of 37 per cent., serious incapacity in 22 per cent., and apparently complete recovery in

only 28 per that sequelae may come on even a year or two after absence of all

cent. cannot be gainsaid, and the position is the worse in

symptoms.

The figures for notified cases in London reveal that in the earlier years of life there is a greater case incidence in males, but a higher mortality in females. This no doubt serves to explain the greater number of cases both of physical incapacity and conduct disorder among postencephalitics of the male sex, a point of importance when the question of provision of accommodation for their care is considered. Like many other disorders epidemic encephalitis is most fatal at the two extremes

of age.