12
Acta Medica Scandinavica. Vol. LXXX, fasc. IV-VI, 1933. From thr Fir51 Medicd Clinic Srrafirnrrlasiil.cttPt Stockholm. Proftwm I. IIolmgren Pseudo-diabetes Insipidus after Encephalitis Lethargica. BY GUNNAR WOHLFART. 1)iabetes insipidus is characterized, as is well known, in the first instancc l)y a persistent excessive polyuria although no foreign constituents can Iw demonstrated in the urine and although no genuine nephric disease is present. This disease picture has heen known for several hundred years. Kot until the end of the last cenlury ho\ievcr did we begin to I-ealiLe, that the conrept diahetes insipidus comprcihends several different diseases. Senator (1 876) l6 is probably the first \vho has realized this fact. He distinguished a variety of diahetes insipidus with primary Iiolyuria from a rarer variety with primary polydipsia and indicated that this later variety (ould lie thought to arise Iiy injury to thc nervous apparatuses, which transmit the sensation of thirst. The variety of diahetes Insipidus, wliicli is characterized hy primary polydipsia. is now generally called pseudo-diabetes insipidus. While the genuine dialwtes insipidus is characteriA by com- pulsory polyuria with urine of very lom specific gravily, conriderahly low concentratiou-capacity of the kidneys, and on acrcunt of the polyuria, a srcondary polydipsia, on the other hand tlie chief symptom of pseudo-diabetcs insipidus is, as mentioned above, a primary polydipsia with sequent secondary polyuria. In the latter disease picture the conceIitration-rapncity of tlie kidneys is normal. Submitted for publication March 13. 1933

Pseudo-diabetes Insipidus after Encephalitis Lethargica

Embed Size (px)

Citation preview

Page 1: Pseudo-diabetes Insipidus after Encephalitis Lethargica

Acta Medica Scandinavica. Vol. LXXX, fasc. IV-VI, 1933.

From thr Fir51 Medicd Clinic Srrafirnrrlasiil.cttPt Stockholm. Proftwm I . IIolmgren

Pseudo-diabetes Insipidus after Encephalitis Lethargica.

BY

GUNNAR WOHLFART.

1)iabetes insipidus is characterized, as is well known, in the first instancc l)y a persistent excessive polyuria although no foreign constituents can Iw demonstrated in the urine and although no genuine nephric disease is present. This disease picture has heen known for several hundred years. Kot until the end of t he last cenlury ho\ievcr did we begin to I-ealiLe, t h a t the conrept diahetes insipidus comprcihends several different diseases. Senator (1 876) l6 is probably the first \vho has realized this fact. H e distinguished a variety of diahetes insipidus with primary Iiolyuria from a rarer variety with primary polydipsia and indicated tha t this later variety (ould lie thought to arise Iiy injury to t hc nervous apparatuses, which transmit the sensation of thirst. The variety of diahetes Insipidus, wliicli is characterized hy primary polydipsia. is now generally called pseudo-diabetes insipidus.

While the genuine dialwtes insipidus is c h a r a c t e r i A by com- pulsory polyuria with urine of very lom specific gravily, conriderahly low concentratiou-capacity of the kidneys, and on acrcunt of t he polyuria, a srcondary polydipsia, on the other hand tlie chief symptom of pseudo-diabetcs insipidus is, as mentioned above, a primary polydipsia with sequent secondary polyuria. In t he latter disease picture the conceIitration-rapncity of tlie kidneys is normal.

Submitted for publication March 13. 1933

Page 2: Pseudo-diabetes Insipidus after Encephalitis Lethargica

P b E U D O - D I h B E T b b 1YSII’lI)IrS A r l r H I:

Even with restricted supply of fluid, a person with genuine tliahetes insipidus still excretes a great quantity of urine with low specific gravity. Through this the body suffers from loss of fluid, the blood becomes more concentrated and the hody loses in weight. On the other hand, a person, who suffers from pseudo-diabetes insipidus and abstains from taking fluid, immediately excretes urine of a higher specific gravity. ‘The dilution of the blood and the weight of the body remain practically unchanged.

I t was chiefly through the works of ‘Tallqvist and Erich Meyer that pseudo-diahetes insipidus rame to lie regarded as a disease, distinguished from t h e genuine diabetes insipidus.

Veil (18) was later ahle to prove that the cases of genuine diahctes insipidus could he divided into two separate groups, cliaraeteri& respectively hy hyperclrloraemia and hypochloraemia. The division of genuine diabetes insipidus into different diseases according t o other prjncjples has also been suggested.

With the classification of the original concept dial)elcs insipidus into different disease pictures i t has heen possible t o esamine them more thoroughly than previously, when apparently contradictory reports were received from different observers.

In spite of Senator’s prescient opinion, expressed as early a i 1876, (see above), pseudo-diabetes insipidus for a long lime was regarded as dependent on purely psychical factors. In modern monographs also on d i a l ~ t e s insipidus (for instance (;ilI)rrt-I)reyfus: Le Diahtte insipide. Paris 1931) this view is maintained. 1<. MotL- feldt (Studier over 1)iahetes insipidus. Oslo 19% I), helievcs the came of the disease to lie in changes i n the sgnipathctic iiervolis system.

During the last years a number of facts have, however, I)ecorne known, which favour the helief t h a t demon5tral)le organic cereliral changes rimy be the cause of thc*disease in question. Clinical and experimental experiences aigue in favour of the existcnce of a special thirst-centre in the brain. By certain pathological processes in this centre an ahnormal sensation of thirst is S L I ~ ~ O S ~ to arise, which ran give hirth to the picture of a pseudo-diabetes in4pitfus.

In the following will he reported a case of tlisease, which may assist the clearing up of the causes of pseudo-diahetes insipidus. The patient in question was trcated in 192t a t Professor Holm- glen’s Clinic a t Serafimerlasarettet in Stochholrn.

Page 3: Pseudo-diabetes Insipidus after Encephalitis Lethargica

456 1 ; 11 V N 4 It M. O H I , F A H ' T .

N. 1'. boru 1902, luiiikw-man. .iournal number io on August I s t h , 1823, discharged on October Ist,. 1!)24.

. I ~ m n ~ n e s i s . S o known heredity for t,iiberculosis or nervous disrases. A t the age 01 six a pleurisq-. At, the age of about eight-trn an opthalniic diseasc (phlyctenae) I whic,li

was cured after treatment with oyellow ointmrnt for the eyes)). Was troiiblrd during the period o f growth periodically b y inirstinal

(.a tarrh. I n 1!)10 during lumber-work a rather hard trauma to tlie vertcx. ])id

not f,iint, but got a bleeding wound on the vertex and bled also rather violentlg from the nose. Could already work the following day.

X-mas 1!)20 B slight hronchial c-,at:irrh. Does not know i f Iw had frver. Was out of bed all the t,ime.

On December 31 st 1920 the patient fell ill during great drowsiness with a violent pain on a point jiist over t l i ~ right wrist and in t h t s ri&t middlc ringer.

The patirnt then slept practically without intermission tliiring the first two weeks of' .January 1921. Could be awakened Tor meals and thix like. ])id not feel really ill. Had no positive headache, only a feeling that i t osaiigu in his hmd. The temperaturr, was not taken. Thr pain in thr right middle finger and in the forearni abated after ahout a day anti a night, hul the patient has since then tell a nuntbness rrniaining on the place ahovr t h r right wrist wlierr tht\ pain was felt a t his falling ill. T h e midillr finger quite recovered. During the first days of the illness the patient saw donblr. The diplopsia has since then never returned.

Uuring t,he period of sleep the patient also had spasins of a clonic kind here and there in the body, not distinctly localized to either side. Thc spasins have remained since then as detached ticlikr twitchings in thk face and in the shoulder musculation.

When tlie patient was fairly recovered, hc consulted a doctor who diag- nosed albumin in the urine and prescribed a stay i n hed and dietary. Thp Iiatic.nt did, however, not nurse himself after the prescriptions he had reccivtd, but already began to work two weeks afterwards. He soon hecame vt!ry weak and tired, got pains in the small of the back and became swollen undw the eyelids so that he took to liis bed again. The patient again con- sulted a doctor and during the following years he was treated for his nephriv disease partly in his home, partly a t different hospitals and nursinghornes.

During the autumn of 1921 the patient began t,o drink more water thar. previously. His water consumption gradually rose to very considerable quant.ities. Sometimes he vomited u p the water without, however, feeling ill. Somebody had said t,o him that it, was wholesome to drink much. The patient does not. know, if this happrrieti before or after liis water consumption had begun to increase.

On May 28th, 1924, the patient began his inilit.ary service and then came to be treated in the military hospital a t Pollefteh for twelve days.

1924. \!'as a d m i t t 4

lrnnietiiately afterwards he has bocn able to drink again.

Page 4: Pseudo-diabetes Insipidus after Encephalitis Lethargica

I’S E U D 0 -D I A B E TE S I N S I P I D Ll S A F TE R E N C E I’ €I A L1 T I S LET H A Rb IC A. 4.57 Here it was proved by control measurements that the patient had urine quantities between 18 and 22 ?IL litres per day. Further aa defect on one lung)) was observed and the patient was discharged from military service. On . Idy 8th, 1921 the patient was submitted to an examination of the lungs at, i j s t r rmn’s Sanatorium (Dr. Tiirnell). The report runs: ))Signs of a non- malignant tuberculosis on the right lungs. He was recommended t,reatment a t Serafimerlasareltet in Stocliliolni for examination of kidneys and n w - vous system.

Was admitted to I h r First Medical Clinic at Srrafimerlasarettet on

E‘t, stutus ut the admission: General st,atc. ol health good. Strongly built, man. Flesh ordinary. Skin coloiir normal. On the right shotildpr and over sternum a slight pityriasis vcrsicolor.

August 13th 192-1.

Thyroid glarid: Not enlarged. Heart : No comment. Llloorl-pressure: 11.5 > i.5 c,m IIg. fmigns: On the right side somewhat smaliw rcspiration movements.

Right supraclavicular fossa niore sunken than the left,. Slight, dullment in right supraclavicular fossa. Respiration sound o v w right apex piilrnonis of broncho-vesicular type. Nowhere any murmur is heard.

X-ray exaniinalion of the lungs: ))The lungs show signs of bronchitis. k o changes characteristic of tubcrcu1osis.o (Lysholm).

A b d o m n : KO comment. i\.ewe s ta tus : S k u l l : I n the middle line an exceptionally projcct,ing Iirot,uberant.ia

cocipitalis externa. For the rest no deformat ion of skull or spinal column and no sensitiveness t,o percussion.

X-ray examination of the skull: Sella turcica measures lrorii tlic front to the back 11 mm. vertically 9 mm. No excavation. Smooth, wt,ll-defined c:ontours. Normal roentgenogram. (Lysholm).

Psyche: Gives his account clearly though soincwhat slowly. His memory of the past relatively somewhat I)et,ter than that of thr present. Obvioiislg j)rolonged reaction t,init>. Stat(’ of mind quiet and c hccrlul,

,Ypeec/i: No comment. Cruniol tierves: I-VI no comment.. K. VIII: The patient shows a stiff mimicry. Can make certain niiiiiical

movements, although with great hesitation. 13y extreme or unusual movements with the miniical musculation, clonic twitchings a p p a r . The eyes are filled with tears, the mouth seems rather to be somewhat dry.

Jtereogriosis no c’ommrn t .

N . VIII---XII: no comment. For the rest the total examination ol the nervous system sho\vetl notliiny

remarkable except a slight t!iminution of the sensitiveness to the touch and possibly also to temperature on the dorsal side 01 the right forearm within an area or about a section of two centimetres, just proxiinally o l the ulnar styloid process 29 - Aclu med. Scnndinau. Vol . L X X X .

Page 5: Pseudo-diabetes Insipidus after Encephalitis Lethargica

458 (; I T h N A I< W O €1 LF .4 RT.

Lu/trbar puncture: Initial pressure 14 cni. After the removal of 5 cirP

3onne’s and Pandy’s wartions were negative. Cells: Three mononiiclear and fourteen red corpiiscclt% per cubic milli-

n l c,erebrospinal liquid the final pressure was 12 cin.

metres . Wnsserwann’s reaction in cerebrospinal liquid and blood neg a t’ 1ve.

Urine: Yellow clear, amphotoric reaction. Specific gravit,y 1,008. Hellrr’s, Alnien’s and Schlesinger’s reactions iwgativr.

Specifig i l ravi ty of

the urine

Excretion of urine and watersupply 111 tilips

IXagrani of urine quantities, water supply and specific gravity of urine during two weeks of the slay in hospit.al.

Sedirricnt: Solit,ary rrd arid white corpusclrs. Solitary granulous r y l i nders.

l iwing the first days of the stag in hospital the patient reccJivPd unsiiltrtl I’ood, but, was allowed to drink as much as he wished. The liquid quantity supplictl varied during these days between 8,330 c.m3 and 11.575 cnP per 2-1 hours. ‘I’he nrinc quantities vnried between 7,200 c1n3 and 1 0 3 ( ) 0 ~ ) w I B per 24 hours. See further dingrani which illustrates the patient‘s drink, crine quantititas and spccilic gravity of urinc dnring the period froni .luglist 15th to .diigust. 28th incliisivr.

On Augast 18th :I water t c s t was made \\liich gave the following wsult: (One litre ua t r r was supplic~d a t ’i o’clock a. ni. .\Ucr this the pntirwt rweived no water u n t i l aftcar i o’clock p. in.)

Page 6: Pseudo-diabetes Insipidus after Encephalitis Lethargica

P S E U D O - D I A B E T E S I N S I P I D U S AFTER E N C E P H A L I T I S L E T H A R C I C A . 459

Time.

8 a. m. 0

10

11

12 noon. 1 p. m . 3

5

7

Urine quantity. 100 cm3 260 1)

230 * 1 4 0 d

50 B

<50 1)

130 1)

90 P

xo 1)

Spec. grav. 1.013

1.004

1.006

1.009

1.010

1 .014

1.015

1.023

1.022

Nitrogen g/lit. i . 1 4

._

12.18

Table of the water test.

‘i’lre henioglohin content of the blood and the numher of red corpuscles were practically the same before and after the water test.

The result of the water test is interesting and not easy to explain. The patient excreted, after the supply of one litre of water a t 7 a. m., during the first three hours not more than 590 cm3 altogether. The specific gravity, however, sank to 0.004. During the rest of the day, when the patient received no further supply of water, the specific gravity rose t o about normal height. I t might have been expected that he would have excreted a quantity, about as great as the one he used to excrete during the course of three hours, thus a litre or more. For it seems impossible to explain the decreased diuresis by a deweased supply of water, when one litre in three hours corresponds approximately to t.he qualltity which the patient himself is accustonied to drink. At any mse w e can not, from the result of the water test, conclude that l.here is any defeat in the kidneys’ capacit.y of rlilution and concentration.

In consequence of the water test the patient’s drink was reshicted on August 19th to 2,000 cm3 and on August 22nd to 1,500 c d . The patient well endured the restricted supply of water. On August 24th the supplied water quantity was reduced to 1,000 cm3. This quantity proved, Iiowcve~*, to be somewhat scanty. On certain days the patient exceeded i t , sometimes by as much as 300 cm3. See further diagram.

Day notes i n the journal on September 2nd. ))Says he is feeling better from the restriction of water. :it meals, however, he finds it hard to swallow his fond.,

August 30th :i salt test was nratlc: (Aft,er emptying the bladder a t 8 o’clock a. m . 10 g common salt plus 200 cm3 w a k r were immediately t,aken. I h r i n g t.lre course of t h e day he rcceived another 800 cm3 wa!er and the ordinary food.)

Page 7: Pseudo-diabetes Insipidus after Encephalitis Lethargica

G O N N A R W O H L F A It T . 460

Time

Aug. 30th 8 a. m. 9

10 11 12 noon.

1 p. n1. 3 5 5

lirine quantity 50 cm3 6 u 80 90 70 60

110 5 0

100

Spcc. gravity

1.02; 1.022 1.022 1.021. 1.024 1.023 1.025 1.02x 1.029

G . coninion salt. 0 . 1 i 0.70 ll.65 0.93 (1.88 (1.85 1 . 5 2 0.78 0.95

. Aug. 31st G a. m. 25u 1.030 2.00

910 cmY 9.6;

Table of the common salt t r s t .

The? salt test, too, proves that no genuine diabetes insipidus is prese,nt. During the course of 22 hours 9.5 g common salt was excreted. If we calculate tha t , sirnultanrously with tlie extra quantity of common salt (10 g) thew have been administered 3-5 g, which are included in tlie diet wit,hout salt, we may probably be justified in inlerpret,ing the salt tcst, as indicating a slight salt retention.

During the continued stay in hospital the urine sometimes gave Heller’s reaction slightly positive. Ln the sediment, were found, on solitary occasions, red corpuscles. With regard to the anamnesis and status the patient must thus be considered to suffer from R slight chronic nephritis. This can possibly explain the result of the salt test.

The patient was discharged as recovered on October lst, 1 !Q4. He still suffered. however, from thirst, and this has continued during

the following years.’ The water cluantit,y tak6.n per 24 hours has varied considerably. At present (December 1932) it amounts, according to tlie patient’s own statement, to 7-8 litres.

Since 1924 other post-encephalitic disturbances of a typical kind have also been developed, chiefly pcrceivable after 1929. The power of motion of the extremities is lessened, the coordination of the eye-inuscles is disturbed in certain respects, the faculty of speech is reduced etc. Psyctiical defect,s are also present, especial1,v want of poww of initiative and of perseverance.

There can IK 110 doubt that , in the case reported ahovc, ~ v e have a patient with post-encephalitic disturbances. The acute falling ill in the mw-year of 1921 with a lethargic period of two weelcs as well as the pathological changes appearing during the last years are characteristic of encephalitis lethargica.

Rather soon he began to drink more water.

1 The following information has beeii given in writing, partly by the patient hiinself, partly hy tlie pastor of Stugun’s parish.

Page 8: Pseudo-diabetes Insipidus after Encephalitis Lethargica

PbI I D O - D I A B E TES I N S I P I D U 5 A F T E R E N C E P H A I ITIS L E T H A R L I C A 461

The intercsting fact is that , ahot 3/! of a year after the acute encephalitis there now appears an excessive polydipsia, which, judging from all circumstances, must he regarded as primary, viz. as a manifestation of a pseudo-diabetes insipidus.

Encephalitis letliargica is indeed cliaracterizetl pathologically- anatomically by sporadic nests in the gray su1)stance of the central nervous system, especially in the brain-axis around the third and fourth ventriclcs. Professor I. €Iolmgren suggested in 1928 (8), with especial regard to the case of disease related above t h a t pseudo-diabetes insipidus is due to injuries in about the same part of the h a i n as in the case of the genuine form of the disease. )>%We in the genuine form a diuresis centre in the hain-ground must be injuried, the ahovementioned case of pseudo-diabetes insipidus postulates the existence of a thirst-centre in the same part of the brain, \xliich should be injuried in the said case.))

Cases of polydipsia and polyuria after encephalitis letliargica are relatively not uncommon. In the literature we have, a t present, a t least a l ~ o u t thirty such cases reported. The majority are to be regarded as cases of genuine diabetes insipidus. With respect t o the general conception of diabetes insipidus as being due to a patho- logical process which is localized t o the hypophysis and the hypo- thalamus, it can not be surprising tha t an enccplialitis lethargica may give risc t o this disease picture.

In a small ~iumlier of cases has arisen, instead of this, after encephalitis letliargica, a primary polydipsia, a pseudo-diabetes insipidus, as i n the case reported above from the First Medical Clinic a t Serafimerlasarettet.

In the literature I have only been able to find three certain cases of post-encep!ialitic primary polydipsia, viz Biffis’ (1922), (4) Bcringer’s and Gyorgy’s (1923) (2, 3) and Moreira’s case (1924), (12) of mhich Beringer-Gyorgy’s case has been tliouroughly investigated as regards the supply and excretion of water, the separation of common salt and nitrogen, the specific gravity and reaction of the urine etc. Further were determined the conditions with common salt loads, supply of theocin and pituglandol etc.

In all these Ihree cases the polydipsia has appeared in children

The thcn assistant physician a t Serafimerlasarettet Dr. Albert Grbnberg tlrmonstrated the case i n the autumn o f 1924 in the Swedish Association for Irilerrial Medicinc.

Page 9: Pseudo-diabetes Insipidus after Encephalitis Lethargica

462 L 11 N N A R W O L H F A 117

of 12- 11 years of age. The urine quantity &as in Riffis’ case a t most 3-1 litres, in the other two cases 13- I5 litres. In Beringer- Gyorgy’s case the polydipsia appeared 3 years after an acute ence- phalitis with a lethargic stadium of six weeks. In connection with the sctting-in of the polydipsia an rarlier existing, double ptosis disappeared in this patient. In the other two cases in the literature the polydipsia set in shortly after the outbreak of the acute ence- phahlis.

From this short survey i t appears tha t tlie age a t the setting-in of the polydipsia in the patient described in this paper is somewhat higher than in the cases pchlished before. The measured urine quantities are greater than in any earlier case. That tlie polydipsia does not appear until after about 3/! of a year after the cncephalitis proves t h a t the long interval of time in Bcringer-Gyorgy’s case does not imply anything very remarkable. Besides, as is well known, other post-encephalitic complications can appear, a still longer time after the first, acute setting-in of the encephalitis.

Concerning the further progress of the discase only scanty information is found in earlier literature.

In Hiffis’ case the polydipsia seemed a t first to be incurable hut later on i t gradually sulnided, so tha t the urine quantities became normal.

A t the time of tlie investigation no other post-encephalitic complications had appeared.

In the case observed a t Serafimerlasarettet in Stockholm the polydipsia is, as mentioned before, still excessive twelve years after the acute encephalitis and must, 1 think, be regarded as incurable.

In this case also a typical Parkinsonismus is now present. In tlie literature are also described a number of cases of poly-

dipsia after encephalitis, wliere i t is unfortunately impossible, to decide on account of the scanty information, whether genuine or pseudo-diabetes has been present. Tliese puhlications will not here be further erttered upon. Besides, there are cases reported which arc possibly to be taken as comhinations of genuine and of pseudo- diahetes insipidus.

The question as to the real nature of pseudo-dia1)etes insipidus is illustrated, in an interesting way, by a case, newly published by Mainzer.

Page 10: Pseudo-diabetes Insipidus after Encephalitis Lethargica

P S E I ' D O - D I A A L T E S I U S I P I D b 5 A F T E R E I'll 4 L l T I S L E T H A R L I C A 463

The case was a man of 37 years who received a serious concussion of thc h a i n in a motor hicycle accident in April 1330. Immediately after the return of consciousness a strong sensation of thirst. At first he drank up to R ? litres a day. Was admitted to hospital in Noveniher 1030, where i t was stated tha t a typical pseudo-diabetes insipidus was present with urine quantities of 10-15 litres a day. The patient is said to have aggravated his troubles in erder to get a higher accident com pensation.

The casc was explained by Mainzcr as due to psychical canses i n connection with the sIiocI\ of tlic trauma.

I t seems howevcr more pro1)ahlc that an injury t o the thirst centre may have arisen a t tlic trauma, which injury has given rise to a pseudo-dial)etrs insipidus, analogously with the conditions of postenccphalitic primary polydipsia.

That tranmas to the skull can cause genuine dial)etrs insipidus has loiig 1)cen known.

411 intcrpretation analogous with the one maintained in this p a p has l)een advanced by A4dlersl)erg and Porges 1930 (1) with respect to the disease picture iq a case of primary polydipsia with signs of chronic hydrocephalus. These authors believe, tha t the polvdipaia in their case m a r e . . . durch einen Reizzustand dcs scnsorisclicn 1)urstzentrums erklarhar)).

binally it may l x mentioned tha t i t has heen possihle l o produce, in an experimental way too, a pseudo-diahetes insipidus.

Curtis ( 3 ) succeeded, in 1921, during experiments with dogs in producing a polyuria of longer or shorter duration through puncture i n tuhcr cincrcum.

In onc case the polyuria lasted for one month. When 11w dog if1

question was suhjectcd to water restriction and received food rich in salt, the kidneys proved t o possess a normal faculty of concentra- tion. 'Thus Ciirtis t o all appeareances seems to have succeeded in producing an experimental pseudo-dial)etes insipidus. The section of tlie dog showed, hesides thc lesion in thc hypothalamus, also atropliy in the pars nervosa of the hypophysis.

The idea expressed by I . Holmgren in 10'28 tha t pseudo-diabctrs insipidus depends on changes in a )kliirst centre)) of the brain, seenis l o he strongly supported hy the C R S ~ S of disease mentioned above and by the animal-esperiinents. As has heen said, in 1930, Adlersherg and Porges have touched on the same line of thought.

Page 11: Pseudo-diabetes Insipidus after Encephalitis Lethargica

464 I . 1 Y h A I{ W 0 I4 L F A R T .

'Tlic investigators who have occupied themselves with the physiology and pathology of the feeling of thirst (for instance Erich hleyer, (10. 11) L. I<. Miiller, (14) Veil (18) and others) seem to agree tha t wch a brain centre must exist and that i t may be localized to the diencephalon and more closely t o the hypothala- mus, where other important vegetative centres are also situated.

The defiiiitive evidence for the correctness of the theory can of course not I)e' o1)tained until after microscopic exaniination of lrrains from persons which have suffered from pseudo-diahetes insipidus.

Whether all cases of pseudo-diabetes insipidus depend upon pathological changes of a thirst centre in t h ~ hypothalamus is of course impossible to decide. There may 1)e reasons to recollect tha t the cerehrum quite certainly plays an important r61e for the genesis of a sensation of thirst. The feeling of thirst can IN made to disappear through an act of will, at least for a short time, and on the other hand it can be produced 1,y an idea. Thus pathological processes in the higher centres of the brain ought theoretically t o be able l o produce a pathological feeling of thirst which gives the picture of pseudo-diahetes insipidus.

Summary.

1. Description of a case of pseudodiabetes insipidus aftcr

2. The disease is explained as depending upon cncephalitic

3 . A short summary of the literature 011 this subject.

encephalitis lelhargica.

changes in the ethirsl centre)) of the brain.

Literature.

1 . .~dlersl)t.rg-Poi,gcs: Beolxchtungen bri Iliahrlrs insipidus. Wirii. mcti. Wschr. 1930. I . 2. Deringer: Polydipsie und Encephalitis epidemica. %s 1. Neurol. u . Psych. B. 86. 1923. 3 . Beringer-Gyorgy: Polydipsie niicli Encephalitis epidemica. Iilin. Wschr. 1923. 11. 4 . Biffis: Studi sill diabetcl insipido. I'oliclinico? sez. med. 13. 29. 1!322. 5. Ciwtis: Thr production of experimental diabetes insipidus. A r ~ h . of internal med. €3. 34 , lW4. 6. Gilbert-Dreyfus: Le DiabGte insipid?. Paris 1931. i. Orduberg: E t t fall av polydipsi efter encephalit. Sr. fiir. f . inv. med. liirh. 8v . lakartidn. 1926. 8. Holmgren, 1srar.l: Diskussionsytt.raride om el t fall nv diabetes insipidus.

Page 12: Pseudo-diabetes Insipidus after Encephalitis Lethargica

1’s E L L) (1- D I A B E T E S I N SIP1 D U 5 A F TE R E N C E P H A 1.1 T I S I. E TH 4 RI; 1C A. 465 Sv. fijr. f . inv. nird. fijrli. 1028. 9. Mainzer: Diabetes insipidus odrr neuro- l i s c h Polydipsie? Ein (jutachten. k k d . I<lin. I ! l : i l . I. 10. Meyer. Erich: Ziir Pathologie und Physiologie dcs Durstcs. Schr. t l . wiss. ( i e s . in Strass- burg. 13. 33 . 1:)l8. 11 . MtiyPr, Erich: Diahctes insipidus. Hb . d . norm. 11. path. I’hys. 11. I S . 1926. 12. Moreira: Cn caso tlr polidipsia por encc- f’alite epiddmica. L i s h a riled. H . X-9, 192 I . ( (hrman reporl, in Kongress- Z b l . f . dic ges. inn. hled. 13. 39). 13. Motzfrlilt: Studier over Diabetes insipidus. Oslo 1!)24. 1-4. Miiller, L. R . : i ibrr tien 1)urst und iibci~clir Durst- c ~ m ~ ~ f i n d u n g . Dpuische mrd. Wschr. 1!)20. 13. ;\ronritfinbriic*h: Pathologic und Pharmakoloqir des Wasserhauslialtes c~inschliesslicli t)deni lind En t - ziindurig. IIb. d. norm. 11. path. Phys. B. 1 7 , 1020. 16. Sen:rl,or: Diabetes insipidus. Xiemssens Hb . (1. spez. Path. 11. Tlictr. B. 13, 1876. l i . Siebeck: Physiologie des Wasserhaiishaltes. Ilb. t J . norm. u. path. Phys. 13. 17. 1926- 1 8 . Veil: Uber interniediiire Vorglngc. Iwi Diahrtes insipidus. Riochern. %cit,schr. 91, 1 I ) l R . 19. Wohlfart: Tiirstens fysiologi och patologi, en kort Bversikt. Meti. for. tidskr. 1933.

Addition to the proof.

111 a work (Broers: Experimentwlr Diabetes insipidus. Pi,oefschrift. Utrrcht 1932.) recmtly (May, 1933) put on file a t the library of Karolinska Institutet, Stockholm is shown, among other things, that primary polydipsia (:an arisc from puncturc in tuber cinercuni. A line of thought analogous with t h e one maintained in this paper, is also Iliscussed.