MEASLES ENCEPHALITIS

(1)

Evaluation

of

Treatment

with

Adrenocorticotropin

and

Adrenal

Corticosteroids

Samuel Karelitz, M.D., and Melvin Eisenberg, M.D.

Department of Pediatrics, Long Island Jewish Hospital, and Queens General Hospital, New York

ADDRESS: (S.K.) Long Island Jewish Hospital, 270-05 76th Avenue, New Hyde Park, Long Island,

New York.

MEASLES

ENCEPHALITIS

Psnxmics, May 1961

F

ORTY-TWO PATIENTS with measles

en-cephalitis were observed at the Queens

General Hospital from 1952-1958 and at the

Long Island Jewish Hospital from

1954-1959. All survived. The cases were reviewed

to evaluate the results of treatment, with

particular emphasis on the effects of

adreno-corticotnopin (ACTH) and adrenal

corti-costeroids, and to report the status of the

patient 2 to 7 years after discharge from

the hospital.

Earlier reports indicate a mortality of 10

to 15% and sequelae in an even larger

per-centage. Tyler1 reviewed 67 eases of

mea-sles encephalitis; 10 were patients who had

hemiplegia, probably due to cerebral

vas-eular pathology rather than encephalitis,

and 3 were excluded as likely cases of toxic

eneephalopathy. Of the remaining 54, 4

died in status epilepticus at the time of the

initial illness and 1 died 8 years later; 11

had severe residua. The mortality was

ap-proximately 9% and sequelae occurred in

223%. The use of ACTH or adrenal steroids

is not mentioned.

Only a few publications deal with the

re-suits of therapy with ACTH and

corticoster-oids. Allen2 and Applebaum and Abler3

related the survival of 10 and 17 consecutive

cases, respectively, and sequelae occurred

in only 1 of the 17 cases of the latter

au-thors. Swanson4 reported 24 cases; 7

re-ceived steroids and 6 of these developed

sequelae.

CASE MATERIAL

Most of the 42 eases in the present series

were observed personally by one or both of the

authors, the remainder were treated by other

members of the staffs of the two hospitals. No

fixed regimen of therapy was employed.

Never-theless there was considerable similarity in the

treatment, both as to choice and dosage of the

drugs. Six patients received almost the identical

regimen suggested by Allen.2

CLINICAL FEATURES

The disease was characterized by

head-ache, vomiting, fever, irritability, muscular

weakness, strange behavior, transient

star-ing episodes, rolling of the eyes, diplopia

and nystagmus, hallucinations,

disorienta-tion and lethargy. These were frequently

followed by coma and convulsions. In a

few, athetosis and myelitic symptoms

(

weakness of the extremities) developed.

The dominant findings upon admission

were : coma, convulsions, lethargy, athetosis,

pareses, ataxia, fever and respiratory

diffi-culties. At the time of admission, 23

pa-tients were in coma, 15 were lethargic and

30 were convulsing-indicating severe

dis-ease in most instances. No cases of

hemi-plegia or of toxic encephalitis, as described

by Tyler,1 were encountered. Encephalitis

was not encountered in any patient who had

measles modified by gamma-globulin.

The encephalitis became manifest from 1

to 7 days after appearance of the measles

rash in 41 eases and in 1 case after 10 days;

most frequently (27 out of 42) on the third,

fourth or fifth day (Table I). It is noteworthy

that in no instance did the disease occur

during the incubation or pre-eruptive phases

of measles.

More cases were observed in the years of

greater incidence of measles. The disease

(2)

l95 I 6 3 1 1 0 1

1953 1 0 1

1954 5 1 0 0 6

1955 1 1 1 0 1 0 4

1956 1 4 ‘2 1 0 8

1957 0 0 0 0 0 1 1

1958 1 0 3 2 2 1 1 0 10

c 2 3 18 8 5 3 0 1 42

Total (by 11.5011th)

TABLE III TABLE I

ONSET OF ENCEPHALITIS-DAYS AVrER

APPEARANCE OF RASH

Days 1 S 4 5 6 7 8 9 10

Case8 3 3 7 l2 7 3 6 0 0 1

May and June, the months of highest

in-cidence of measles in this area (Table II).

The encephalitis was most frequent

be-tween 5 and 10 years of age. This is in

keep-ing with the greatest incidence of measles in

our community. Only six patients were less

than 5 years of age (Table III).

There were only two Negro children in

the 42 cases. This is striking and probably

significant because of the high percentage

of Negro children admitted to the Queens

General Hospital. That the disease occurs

rarely in Negroes was also reported by

Hoyne and Slotkowski. There were 23 males

and 19 females in the present series.

Convulsions associated with measles but

not caused by encephalitis were observed

in two children; one was 6 years old and

one was 4 years old, both with

tempera-tunes over 104#{176}F(40#{176}C).Tile cerebrospinal

fluid was normal in both instances and the

measles progressed without further

cvi-dence of central nervous system disease.

Both children had Koplik spots within the

next 24 hours and thereafter experienced

uneventful uncomplicated measles. The

convulsions were considered to be due to

fever and these patients were not included

in this series.

LABORATORY DATA

The cerebrospinal fluid revealed wide

variations in the cell count and the protein

and the sugar content. In 12 patients there

were less than 20 cells in the cerebrospinal

fluid and in 24 patients, between 51 and

650 cells. Lymphocytes predominated but

in one instance 60% of 160 cells were

poly-morphonuclear. The protein content was

less than 50 mg/100 ml in 15 patients and

between 50 and 197 mg/100 ml in 27.

Sugar in the fluid ranged from 48 to 197

mg/100 ml; it was 48 to 74 in 12 and 75 to

197 mg/100 ml in 26.

Of the 12 patients with cell counts in the

cerebrospinal fluid less than 20, 11 had

con-TABLE II

DATE OF OCCURRENCE OF CASES OF MEASLES ENCEPHALITIS

l’ear Jan. Feb. Mare/i April May .Jnne .Jnly Dec. Total

(by year)

AGE DISTRIBUTION OF CASES

Age(yr) 1 3 4 5 6 7 8 9 10 13 14 16 30 35

(3)

vulsions and 1 was in coma. Nine were

treated with steroids, but none prior to the

first cenebrospinal spinal fluid examination;

6 developed sequelae, 2 behavior defects,

1 headaches, 1 mental deterioration, 1

epi-lepsy and 1 paresis of the lower extremities.

All of the 6 children with less than 5 cells

in the cerebnospinal fluid were admitted on

the first or second day of encephalitis; 1

with only 4 cells in the fluid developed a

behavior disturbance; 1 with 3 cells had

mental deterioration and 1 with no cells

developed epilepsy; the other 3 seemed to

recover. Of the 6 patients with cell counts

in tile eenebrospinal fluid less than 5, the

proteins were 21, 34, 12, 49, 67 and 172 mgI

100 ml. Where the fluid contained from 6

to 19 cells, the proteins were 35, 12, 197,

76, 67 and 68 mg/100 ml. Thus there was no

consistent correlation between the number

of cells and the level of protein in the

eere-brospinal fluid, on between either of these

and tile severity and outcome of the illness.

The leukocyte count in the blood and the

percentage of polymorphonuclear cells

varied widely. In 17 patients the counts were

less than 10,000/mm3, 7 had 15,000 to

20,000, and 5 had more than 20,000/mm3.

The polymorphonuelear cells ranged from

40 to 93%, most often 60 to 83%. The two

children with pneumonia and the one with

tracheostomy had high counts, but others

with leukocytosis did not manifest

bac-tenial complications.

Electnoencephalographs obtained on the

fourth to the thirtieth days of illness

re-vealed diffuse pathology in 17 of 19

pa-tients. Many whose tracings were abnormal

were free of signs on symptoms at the time.

A child with schizophrenic behavior had

abnormal tracings on several occasions, the

last being 2 months after the onset of

ill-ness. A child with myelitie signs had a

non-mal tracing, as did one other child free of

central nervous system symptoms at the

time. Of the 19 who had

eleetroeneephalo-grams, 19 were treated with adrenal

eon-ticosteniods and/or ACTH and only 2 of

these had normal tracings.

TREATMENT

Intensive nursing and medical care was

given to all patients who required it.

Twenty-eight patients were placed in

oxy-gen tents because of cyanosis, irregular

res-piration or poor peripheral circulation.

Electrolyte imbalance was corrected with

appropriate fluids given intravenously. All

but a few were given antibiotics

intrave-nously or intramuscularly on admission and

orally thereafter, during the acute phase

of the disease. The drugs were continued

after the acute phase only for patients with

complications; 32 received penicillin daily

and 6 of these were also given

ch!oram-phenical, while 5 were given tetracycline.

Tracheostomy was performed in two

in-stances because of inability to clear

pharyn-geal secretions. Adrenocortica! extract (4 to

12 ml) was administered to three patients

in collapse on admission. Convulsions were

controlled with intravenous use of

bar-biturates, usually sodium phenobarbital.

Three patients received injections of

gamma-globulin : one, 48 ml on the second

day; another, 10 ml daily for three doses

be-ginning on the second day of illness; and a

third, 12 ml on the fourth day.

Six had daily diminishing doses of ACTH

(40, 20, 10 and 5 units) and cortisone (300,

200, 150 and 100 or 75 mg on the fourth

day).

This regimen was adopted because

of tile dosage recommended by Allen.2

5ev-era! other patients were given 25 units of

ACTH on admission and every 6 hours

thereafter for 5 to 22 doses; several received

other corticosteroids, as indicated in Table

Iv, where tile results of therapy are also

shown.

COURSE AND RESULTS

All but three patients were admitted

witilin 24 hours after onset of the

eneephal-itis; treatment was started promptly.

Seque-lae were observed in 13. There were no

deaths. Improvement and recovery were

rapid in all who seemed to recover

eom-plete!y, slower in those who had residua at

(4)

TABLE IV

SEQUELAE VS. THERAPY WITH C0RTIc0TR0PINS AND/OR CORTICOSTEROIDS

Regimen

ACTH Corticosteroids

(units) (mg)

0IV 25q6hX16

l5IV

-25 q 61i X 18

40, 0, 10, 5 Solucort 100 IV IM Cort. 300, 150, 75

25 IV Cort. 300, 00, 100 40, 0, 10, IM Solucort 5 IV

80 IV Hydrocort. 100 IV

Hydrocort. 50 IV q 1h X 10

- Meticort. 60 daily 4 days

Solucort 100 IV Meticort. 0 q 61i X 10

Admission

Hosp. Age Di

No. (jp) e

405I 6 1956

4170 13 1956

6905 9 1958

67677 8 1958

6938 15 1958

53711 li:iz 1958

84005 9 1957

84316 7 1958

65500 9 1958

A9659 6 1953

A1056 7 1955

1096 35 1955

1099 6 1955

A10016 9 1954

A41908 7 1956

4096 7 1956

65018 5 1956

5008 115z 1958

6819 16 1958

401 Q 1945

Discharge Condition Meningeal signs Asymptomatic Asymptomatic Asymptomatic Asymptomatic Asymptomatic Memory loss Schizoid Paresis extreln. Regressed Behavior change Muscle spasm Behavior change Mental deter. Behavior change Mental deter. Asymptomatic Asymptomatic Asymptomatic Asymptomatic Asymptomatic Asymptomatic

25 q 6h X 5

Meticort. ;25 q 61i X 2d.

300-150-75

Solucort 100

300-150-75

Solucort 100

0 q 6h X 19

40 TM ‘25 l5q6hX12 -5q4hX16 -QOIV -5IMq6hX’2

-25q6Is X4 25q6liX28

15Iv

-50 q 61s X 4

0 IV 40 IV 40-20-10-5 40-0-10-5 10 IV Follow-up Age . Cond?tzon (yr) 9 Asymptomatic 16 Asymptomatic

1 1 Jumpy, restless,

nightmares, illness

H Emotional lability,

school problem,

attention poor

16 hearing loss 30%

3 Cranky, hyperreflexia

11 Epilepsy-schizoid, mental deteriora.

tion 9 Paresis, extremities

1 1 Personality change improved some

12 30% loss vision

No follow-up

10 Marked behavior change

14 Severe behavior change

I I Headaches

10 Nightmares, dizziness

No follow-up

(5)

ARTICLES

815

TABLE V

TIME REQUIRED FOR RECOVERY

Treatment

-Days

4 1 S ,5 6 7 8 9 10 12 14

UNTIL IMPROVED*

ACTH and/or steroids it 7 0 0 0 0 1 0 0 0 0 0

NoACTilorsteroids 1 7 6 4 0 0 0 0 0 0 0 0 0

UNTIL UEC0vEUED**

ACT!-! and or steroids 0 1 0 4 0 1 0 1 1 1 0 0

NoACTHorsteroids 0 1 0 4 3 1 5 3 0 0 1 0 0

*Improvement: (emergenCe from coma, cessation of convulsions, normal temperature, etc.).

**Apparent complete recovery: (complete disappearance of signs of the disease).

Patients hot accounted for had sequelae at tune of discharge from hospital.

t Number of cases.

(

Table \7). Emergence from coma or

leth-argy, cessation of convulsions and return of

temperature to normal occurred in most

in-stances in 24 to 72 hours after admission to

the hospital.

Of the 13 patients with sequelae on

dis-charge from the hospital, 9 were treated

with steroids and/or ACTH, 4 were not.

One child who received a single dose of 25

units of ACTH on admission continued to

have muscle spasticity after 14 days. The

inclusion of this case in the treated group

may be questioned because of the limited

amount of therapy. Of tile other 8 patients

\Vitil sequelae, who received ACTH and/on

corticosteroids in larger amounts, 3

de-veloped behavior defects, 3 mental

de-terioration, 1 schizophrenia and epilepsy

and 1 paresis of the extremities. Of the 4

patients with seque!ae, who received neither

steroids nor ACTH, 3 had behavior

dis-turbances and 1 mental deterioration.

FOLLOW-UP

Follow-up examinations were attempted

from 2 to 7 years after discharge from the

hospital. Twenty families responded; 18

children were examined and their parents

were interviewed. The parents of two other

children supplied information about their

progress. Fourteen of the children seen on

follow-up had been treated with ACTH

and/or corticosteroids, and six without

these drugs. The children were evaluated

by a group consisting of a social service

case worker, two third-year resident

pedia-tnicians and the authors. Social histories

and complete physical, neurologic and

fun-duscopie examination were performed. The

results are revealed in Table V. Several of

the patients had had psychologic and

psy-chiatnic evaluation while attending child

guidance or psychiatric clinics. Follow-up

psyehologie testing of patients, such as was

employed by Meyer and Byers6 in

pa-tients with measles encephalitis, was not

possible.

Of the steroid-treated group, 1 with

sequelae on discharge was normal at

fol-low-up, 6 with sequelae had the same or

other complications on follow-up, 1

be-lieved to he well on discharge was well

later but 5 others considered well on

dis-change developed late sequelae. Therefore,

of the 14 steroid-treated children seen at

follow-up, 7 originally had had

compliea-tions and 7 did not; at follow-up, 12

re-vealed sequelae and only 2 did not. Three

of those wilo were found to have developed

sequelae were among the six patients

treated with a regimen similar to that used

by Allen.2

Two of the non-treated patients, who

were considered normal on discharge,

de-veloped changes later; 2 of the 4 with

(6)

follow-up while the other 2 remained

affected. Thus, of the 22 non-treated

chil-dren, 4 had sequelae on discharge while 4

of the 6 seen at follow-up had evidence of

sequelae.

Sequelae observed at follow-up varied

frequently in type or severity or both from

those observed on discharge from the

hos-pital. Three patients had developed

epi-lepsy. The onset of epilepsy occurred 1

month to 23 years after discharge from the

hospital. None had family histories of

epi-lepsy. One, the child who received only

one dose of 25 units of ACTH, was

ob-served to have developed a visual deficit in

one eye, and another had a 30% hearing

loss; these changes may have been present

and missed at the time of discharge. One

patient continued to have paresis of the

lower extremities, but it was less severe

2 years after discharge from the hospital.

Seven patients had moderate to severe

emo-tional disturbance; all were under

psycho-therapy

at the time of follow-up examina-tion.

One 14-year-old girl, who was first in her

class prior to encephalitis at 9 years of age,

was now at the lowest level. Two others had

considerable loss of intellectual ability. Two

were noted to have hallucinations, with

temperatures of 101#{176}to 102#{176}F;previously

this was not observed even with

tempera-tures of 104#{176}F.

DISCUSSION

The outstanding observation in this study

is the survival of 42 consecutive cases of

measles encephalitis. Except for identical

results presented by Steinhardt at a

con-ference,7 our experience is at variance with

earlier reports. Close examination of the

variables involved is therefore mandatory.

The likelihood that conditions other than

measles caused the encephalitis must be

rejected on the basis of clinical and

labora-tory evidence. All patients included in this

study presented characteristic Koplik

spots and measles rash prior to the onset

of encephalopathy. While no attempts to

isolate rubeok virus from the cerebrospinal

fluid were made, occasional efforts to

iso-late other viral agents from such fluids were

unsuccessful.

Tile pathogenesis of measles encephalitis

remains an enigma. Analysis of the

avail-able studies does not permit a definite

con-elusion. The isolation of rubeola virus from

the central nervous system in 19428 still

awaits corroboration. The failure of large

doses of gamma-globulin to alter the disease

may serve as negative evidence for this

theory as such amounts of gamma-globulin

do modify measles, even when given in tile

prodromal period. The theory that measles

activates a latent virus in tile host, which

is responsible for the brain involvement,9

has not been established. Another

hypoth-esis ascribes the observed changes in

measles encephalitis to a hypersensitivity

reaction. This theory is based on the

similar-ity of this measles complication to tile

en-cephalitides accompanying vaccinia,

van-ola and rubella,bO as well as to tile reactions

observed with rabies and pertussis vaccines.

The observations of others1’3 concerning

comparable central nervous system

involve-ment when experimental animals were

sen-sitized with homologous and heterologous

brain homogenates further support the

hy-persensitivity theory as the most likely

cx-planation.

The acceptance of this latter theory

oc-easioned tile use of adrenal steroids and

ACTH in an effort to interrupt the

sensi-tization sequence. While excellent clinical

results have been claimed by some authors,

the findings of others indicated that

conclu-sions based on a comparatively small

num-ben of patients may be misleading, e.g., 6

of 7 treated patients in Swanson’s series

developed sequelae.

Since no deaths occurred in either the

treated or the untreated cases in our series,

the effect of ACTH and steroid hormones

cannot be evaluated with respect to

stir-vival. It is not likely that the severity of the

encephalitis in the individual influenced our

decision to treat because both groups were

severly involved; 16 patients with

(7)

20 treated individuals, while 14 with

con-vulsions and 12 ill coma were among tile

untreated group of 22. Treatment with

these drugs was probably dependent on the

availability and popularity of the drugs at

the time. Thus, steroids and/or ACTH were

administered to only 2 of 19 patients from

1952 to 1954, while 18 of 23 were treated

between 1955 and 1958.

Analysis of our data concerning tile

bene-fits of tile hormone therapy seems

dis-counaging. Three of tile treated patients

with sequelae were admitted on or after

the third day of encephalitis with an

tin-avoidable delay in hormone therapy.

Treat-Iflellt ‘as initiated on the tenth day for

tile paretic patient, while the child with

prolonged spasticity and one with mental

deterioration were first seen on tile third

day of the complication. Animal

expeni-ments’ 14 suggest that in sensitization

cx-peniments irreversible changes are present

silontly after the initial symptoms of

enceph-alitis appear, and that these changes are

minimized only if ACTH on conticosteroids

are administered prior to sensitization.

Therefore it is questionable whether

de-lay in treatment with ACTH on

cortico-steroids resulted ill a loss of possible

bene-ficial effects.

The follow-up investigation revealed that

the status OIl discharge from tile hospital

was a poor indication of the patient’s

fu-tune. While 12 on possibly 13 patients with

sequelae were observed among tile entire

series of 42 on discharge from tile hospital,

16 of the 20 seen at follow-up had residua.

It is important to reiterate that few of those

with sequelae on discharge seemed veli at

the time of follow-up, while more of those

whose discharge examination indicated

complete recovery developed changes later.

Our experience offers no evidence that

we were able to reverse the central nervous

system changes. The data indicate further

that treatment with the amounts of ACTH

and adrenal hormones recorded in Table

V did not favorably influence tile course

of convalescence. In fact, it seems that

those treated with ACTH and/on steroids,

even those treated with the regimen

rec-ommended by Allen,2 fared poorly. Only

6 patients treated without ACTH or

corti-costenoids appeared for follow-up

examina-tion, and the finding of sequelae in 4 of

them suggests that more of this group

might have developed late complications.

Therefore, tile difference in the results

be-tween those treated with and those treated

without ACTH and/on corticosteroids

rnigilt have been of smaller magnitude.

Even if this is taken into account, the

over-all results of treatment raises serious doubts

as to tile advisability of the use of these

drugs in tile management of measles

en-cephalitis.

The most likely explanation for tile

sur-viva! of the patients in our series may rest

with tile intensive supl)Ortive thera)y

ac-corded to all children, treated and

un-treated alike. These included connection of

dehydration and electrolyte imbalance,

early tracheostomy to avoid respiratory

phanyngeal distress, treatment or

preven-tion of bacterial complications with

ade-quate antibiotic therapy. Oxygen

ad-ministration for cyanosis, impaired

cireula-tion or respiratory difficulty, the use of

anti-convulsant drugs ‘hen indicated, and

ade-quate nursing and medical attention are

very important.

SUMMARY AND CONCLUSIONS

The histories of 42 patients with measles

encephalitis were reviewed to evaluate tile

treatment, in particular to determine

whe-then adrenal corticostenoids or

adrenocorti-cotropin were helpful, beyond the results

with usual supportive therapy.

There were no fatalities, but 13 patients

had central nervous system sequelae on

dis-charge; 9 of these had been treated with,

and 4 without ACTH and/or corticosteroids.

Re-examination of 20 of the 42 cases 2 to

7 years after discharge from the hospital

revealed that of 14 children treated during

the acute phase of encephalitis with ACTH

and/or corticosteroids, 12 had central

nerv-oils system sequelae, while only 6 of these

(8)

dis-charge. Four of 6 untreated patients among

the 20 followed-up had central nervous

sys-tem sequelae, as compared to 4 of 22 at the

time of discharge from the hospital.

The patient’s condition on discharge from

the hospital did not accurately indicate the

future course; some sequelae became

mani-fest later, others disappeared, some became

milder and others worse.

Adrenal corticosteroids and ACTH

ad-ministered to these patients did not prevent

central nervous system complications.

The advisability of the use of these

hor-mones in the management of measles

en-cephalitis is questioned.

The survival of 42 consecutive patients

in-dicates that some fatalities ma be

pre-vented by constant supervision and

in-tensive supportive therapy.

REFERENCES

1. Tyler, R. H. : Neurological complications

of rubeola (measles). Medicine, 36: 147,

1947.

2. Allen,

J.

E. : Treatment of measles encepha-litis with adrenal steroids. PEDIATRICS,

20:47, 1957.

3. Applebaum, E., and Abler, C. : Treatment

of measles encephalitis with

cortico-tropin. Amer.

J.

Dis. Child., 92:147,

1956.

4. Swanson, B. E. : Measles

meningoericepha-litis. Amer.

J.

Dis. Child., 92:272, 1956.

5. Hoyne, A. L., and Slotkowski, E. L. :

Fre-quency of encephalitis as a complication

of measles. Amer.

J.

Dis. Child., 73:554,

1947.

6. Meyer, E., and Byers, R. K. : Measles

en-cephalitis. Amer.

J.

1952.

7. Steinhardt, A. : Report of Pediatric

Confer-ence, June 19, 1958, Meadowbrook

Hos-pital, East Meadow, New York

(unpub-lished).

8. Schaffer, M. F., Rake, G., and Hodes,

H. L. : Isolation of virus from a patient

with fatal encephalitis complicating

measles. Amer.

J.

1942.

9. Greenfield,

J.

G.: The pathology of measles

encephalomyelitis. Brain, 52: 171, 1929.

10. Finley, K. H. : Pathogenesis of encephalitis

occurring with vaccination, variola, and

measles. Arch. Neurol., 39:1047, 1938.

11. Rivers, T. M.: Relation of filtrable viruses

to disease of the nervous system. Arch.

Neurol., 28:757, 1932.

12. Kabat, E. A., Wolfe, A., and Bezer, H. E.:

The rapid production of acute

dissemi-iiated encephalomyelitis in rhesus

mon-keys by injection of heterologous and

homologous brain tissue with adjuvants.

J.

Exp. Med., 85:117, 1947; effect of

cortisone. j. Immun., 68:265, 1952.

13. Morgan, I. M. : Allergic encephalomyelitis

ill monkeys in response to injection of

normal monkey nervous tissue.

J.

Exp.

Med., 85:131, 1947.

14. Movei, A. W., et a!.: Action of

adrenocorti-cotropin hormone (ACTH) in

expenimen-tal allergic encephalomyelitis of the

guinea pig. Proc. Soc. Exp. Biol. Med.,

75:387, 1950.

15. Karelitz, S., and Eisenberg, M. :

Adreno-corticotropin and corticosteroids in

measles encephalitis; an evaluation.

(9)

1961;27;811

Pediatrics

Samuel Karelitz and Melvin Eisenberg

Adrenal Corticosteroids