Some Effects of Severe Head Injury : A Follow-up Study of Children and Adolescents after Protracted Coma

Develop. hfed. Child Neirrol. 1963, 5, 471-482

Some Effects of Severe Head Injury A Follow-up Study of Children

and Adolescents after Protracted Coma

Frederick Richardson

Introduction THE patient who has survived a severe head injury but who has remained comatose for days or weeks, is an increasingly frequent problem in childhood and adoles- cence (Rickham 1961). The prognosis for each patient depends on the extent and nature of cerebral tissue damage, and Russell, in his classical study (1932), developed Symonds’ suggestion (1 928) that the duration of loss of consciousness should be used to indicate the degree of cerebral injury. Thirty years later, after a comprehensive review, Smith arrived at a similar but more refined conclusion, stating that ‘the length of the interval during which a patient with non-focal closed head injury is unable to record his experience is directly related to the degree of structural alteration’, and therefore to the ultimate prognosis for each patient (1961).

The interval during which the patient lacks the capacity to store the memory of current events (Russell 1932) has become known as the period of post-traumatic amnesia (PTA) and includes the period of

coma. Provided that other variables such as the differential effects of age are taken into account, the period of post-traumatic amnesia is the most reliable single index of the severity of cerebral injury (Russell and Smith 1961).

In a study of patients who survived post-traumatic coma for a week or more, Akerlund suggested that when unconsciousness lasted for more than a month, grave neurological defects and invalidism were to be anticipated (1959). As several children we had examined were in this category it was decided to study the intellectual and neurological sequelae which persisted in younger survivors of prolonged coma after severe head injury.

Case Material The group consisted of ten patients,

ranging in age from 5 to 18 years at the time of the accident, who could be classified as ‘very severe concussion : prolonged coma or stupor; post-traumatic amnesia over 7 days’ (Russell and Smith 1961). The period of coma ranged from 7 to 47 days, with a median of 28 days,

___. ~ -~

Based on a paper presented at the Neurological and Neurosurgical Symposium on ‘The Late Effects

This study was supported in part by a grant from the Mount Ararat Foundation, lnc. Address: Diagnostic and Evaluation Center for Handicapped Children, Department of Pediatrics,

of Head Injuries’, held at the Johns Hopkins Medical Institutions, April 1962.

Johns Hopkins Hospital, Baltimore 5 , Maryland.

47 1

TA

BL

E I

N

atur

e of

Acc

iden

t and

Gro

ss S

eque

lae

2 3

Cas

e N

o.

5 21

25

+ 8

Col

lisio

n. T

hrow

n fr

om r

ear

Rig

ht te

mpo

ral f

ract

ure.

5 28

28

+ 13

8 St

ruck

by

car.

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ilar f

ract

ure.

seat

. Mot

her

kille

d.

Bra

in la

cera

ted.

Dec

ereb

rate

.

Dec

ereb

rate

.

~~

__

_

1

__

__

__

__

__

5

1 7 1 35

1 56 1 24

11 Stru

ck b

y ca

r. T

hrow

n so

me

dist

ance

.

Year

s si

nce

inju

ry

104

Rig

ht f

ront

al l

acer

atio

n. N

o fr

actu

re.

Nat

ure

of a

ccid

ent

6 1 7

1 30 1 30+

1 3

11 Collis

ion.

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own

from

rea

r se

at.

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er

and

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d-

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illed

.

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hit

tree

. T

hrow

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ft.

from

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r se

at.

C4 a

nd C

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actu

re.

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skul

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e.

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d tr

aum

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7 1 11

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ht p

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tal

regi

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truc

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. -

__

_~

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sed

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ntal

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ture

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riet

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ract

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o su

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erat

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. N

o fr

actu

re.

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sed

left

fr

onto

pari

etal

fr

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re.

9 10

16

35

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3 C

ar o

vert

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d. T

hrow

n fr

om

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ht p

arie

tal f

ract

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fr

ont p

asse

nger

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.

18

7 a+

2 D

rive

r. Fr

actu

red

pelv

is.

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ht e

xtra

dura

l he

mat

oma.

~

__

__

__

_

Dec

ereb

rate

.

Neu

rolo

gica

l seq

uela

e

Park

inso

nian

fac

ies.

B

ilate

ral m

ild s

igns

. In

volu

ntar

y m

ovem

ents

.

Mod

erat

e le

ft h

emip

legi

a.

Bila

tera

l mild

ast

erog

nosi

s.

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etoi

d qu

adri

pleg

ia, s

ever

e dy

sart

hria

an

d dr

oolin

g.

Rea

ds, t

ypes

with

hea

d.

Mod

erat

e ri

ght h

emip

ares

is.

Dys

arth

ria.

R

ight

im

pair

- m

ent o

f st

ereo

gnos

is.

Mild

rig

ht h

emip

ares

is.

Now

pre

fers

lef

t ha

nd

for

fine

task

s.

Clu

msy

, but

no

over

t ne

urol

ogic

al s

igns

.

Seve

re ri

ght h

emip

ares

is.

Pyra

mid

al s

igns

on

left

.

No

neur

olog

ical

resi

dual

. Sp

eech

and

lan

guag

e di

ffic

ultie

s.

Seve

re

Park

inso

nism

. L

eft

hem

ibal

lism

us.

Res

iden

t ps

ychi

atri

c tr

eatm

ent.

Min

imal

neu

rolo

gica

l si

gns.

Sp

ecia

l hig

h sc

hool

.

and the duration of post-traumatic amnesia ranged from a minimum of 25 days to 65 days, with a median of 49 days (Table I). All patients were considered to have sustained acceleration concussion (as defined by Denny-Brown and Russell 1941) as their major insult, although three of the patients also sustained some focal brain injury in addition. Six of the patients had closed fractures of skull and three had lacerations of the brain at exploratory craniotomy. The duration of follow-up was at least 2 years in all cases (six have been followed for 2 to 4 years and four for 8-14 years). I saw and examined all the patients myself on the same occasion that their relatives were interviewed. The statements obtained were compared with the hospital records of the patients, in order to verify duration of coma and to determine the duration of post-traumatic amnesia (which had not been previously estimated). During a two-day period, neurological, psychological and social investigations were carried out and other necessary examinations completed. Several of the patients were re-examined over a period of some years.

Findings Residual Neurological Disability

In the period following the return of consciousness almost all patients had severe physical disabilities which gradually improved; in some cases neurological signs showed continuing improvement for more than three years, leaving in most cases some impairment of function to which the patient had adjusted (Table I). In only one case was the final outcome of the lesion such that the patient was not able to walk or care for himself. This was a severely dysarthric athetoid quadriplegic boy of eighteen, who was able to read a t a 12-year level and communicated entirely by typing with a peg strapped to his forehead (Table I, Case 3).

FREDERICK RICHARDSON

473

The presence of decerebrate rigidity in the acute stage in some patients did not mean that they had a worse prognosis than the other cases. The slow rate of improvement can be illustrated by two case histories :

Case 2 (age 5 years) The patient was the second child. There

was normal pregnancy and delivery. He had uneventful progress and was considered to be above average intelligence until aged 5 years, when the automobile, in which he was a rear-seat passenger, was struck on the side by another car when turning into a driveway. All passengers were ejected, the mother being killed. The patient was admitted to hospital in a state of decerebrate rigidity, and craniotomy of the right temporal region revealed exten- sive brain damage, the devitalised tissue being removed. On the sixth day the rigidity diminished and on the 21st day he recovered consciousness and was able to follow the examiner with his eyes. When transferred to an orthopaedic hospital on the 69th day, power had returned to the right arm but the other limbs were still extremely weak. He was discharged 54 months later in bilateral short leg braces and with a marked left hemiparesis.

Five years later (age 104 years) when the patient was making poor progress in a school for handicapped children a full scale Stanford Binet examination revealed an intelligence quotient of 100, but poor performance on digits forwards and backwards. The major neurological disability was a left hemiparesis of moderate degree with a small left hand and arm, impaired fine finger movements and moderate astereognosis for small objects, the left limb and hand rarely being used spon- taneously. The right upper limb was subjectively normal but many stereog- nostic errors occurred in the recognition

DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY. 1963, 5

474

of small objects. At this time the boy was difficult to manage in the home, in spite of all efforts by a sensitive and affectionate stepmother.

Eight years after the accident (age 13 years), the hemiparetic gait had improved and he was participating actively in school games with a desire to improve his physical performance. The small left upper limb and hand had good motor power but the deep tendon reflexes were still grossly exaggerated and fine finger movements were markedly impaired. Voluntary individual finger movements were not possible but a strong grip with all four fingers and thumb was achieved with normal release. Sensation appeared intact bilaterally to light touch, pin prick and vibration and no errors of recognition were made with small objects in either hand.

On psychological examination using the Wechsler Intelligence Scale for Children, the verbal score was 116, performance 103, and full scale IQ 11 1. In all tests dependent on rote memory his performance was poor, the recall of digits forward being at a 7-10 year level and digits backwards at less than the 9-year level. Performance was variable in repeat- ing sentences and he failed some Binet items at an 11-year level. Similar scores on visual tasks were achieved on the Benton and Wechsler Coding Tests. Prob- lems with reading and spelling were being encountered in school but he was working hard and persevering in his efforts.

Case 4 (age 66 years) The patient was the firstborn child and

the product of a normal pregnancy and delivery. In the home and kindergarten his progress was uneventful and reported information suggested at least average mental a n d physical abi l i t ies were developing.

At the age of 6 years and 5 months he

was struck by an automobile and rendered deeply comatose. The automobile made 293 feet of skid marks prior to the impact and travelled a further six feet. The patient was knocked 32 feet from the point of impact. A closed fracture of the right frontoparietal region was found and at craniotomy marked generalised cerebral oedema was noted, but there was no evidence of intracranial bleeding. The child remained deeply comatose for 28-30 days and had intermittent high fever with several convulsions during the period. After seven weeks he uttered a few intel- ligible words and from then on showed rapid improvement in his mental abilities. Physically he remained severely disabled with a spastic quadriparesis and a fractured left femur which was in traction. After six months he was transferred t o an orthopaedic hospital and when discharged after 5 weeks of physical therapy, he was able to sit unsupported, but was too ataxic to be able to stand alone or walk except with support.

Neurological and psychological examinations at 7 years and 2 months (8 months after the accident) revealed a quadriparesis more marked in the lower limbs and ataxia of all four limbs but no other cerebellar signs. At this time his IQ was 40-50 and formal language testing revealed considerable perseveration.

Thirteen months after the accident, when aged 7 years 6 months, he was able to walk unaided in spite of a severe right hemiparesis. Neurological examination revealed a slight dysarthria and a right homonymous hemianopia but normal macular vision. On psychological examination the performance had improved to a 5-6 year level and although there was no difficulty in understanding spoken language occasional difficulty occurred in naming objects and pictures-e.g., when shown a chair he responded ‘table’ but with an auditory clue such as ‘what do


you sit on?’ he corrected his error. Word definitions proved difficult-e.g., ‘straw’ was defined as ‘big bad wolf can blow the house down’; tasks involving block patterns were all performed extremely poorly but showed improvement.

The EEG showed increased slow activity which was generalised with occasional non-focal spike discharges.

Twenty-two months after the accident (age 8 years 2 months) the boy was walking well with an unsteady gait and a mild dysarthria persisted. Psychological examination remained much the same (IQ 65-75); word definitions and ability to use the language expressively had improved, but non-verbal tasks demanding organisational ability remained very poor, as did rote memory performances. At re-examination four years after the accident, his signs were the same.

Intellectual Sequelae A major purpose of the study was to

determine the degree of intellectual recovery possible in young patients who had survived prolonged coma. In these cases, by careful attention to school records, previously measured intelligence quotients, milestones of development and parental observations, it was possible to estimate the pre-accident intelligence quotient to within 10 or 20 points (Table 11).

Tests for mental function consisted of standard intelligence test batteries, in addition to special standardised tests such as the Wechsler Intelligence Scale for Children, the Benton and a number of selected items including the Hiskey Block, Peabody Picture Vocabulary and the Stanford-Binet.

When given formally scored intelligence tests patients showed a loss of 10 to 30 points (Table 11). However in each patient there was a larger range of variation in measured abilities than usually found in a normal population. All patients per-

formed poorly when given tests dependent upon rote memory, such as items from the Stanford-Binet examination.

Performance and Behaviour at School and at Home

Reports from the school teachers were unanimous in describing academic difficulties not present before the accident; in two patients (Cases 8 and 10) academic difficulties had been present but to a lesser degree. The classroom problems encountered ranged from patients’ difficulties with reading and other complex tasks, to teachers’ complaints of distractibility, poor comprehension, concrete and perseverative performance. The variation in individual performances was such that any attempt to make a sophisticated analysis of academic problems encountered would be meaningless.

The behaviour of patients varied con- siderably both at home and in school and this was reflected in the attitudes of their peers which ranged from increased toler- ance and protection of the patient, to marked intolerance, baiting and teasing (Table 111). Russell (1932) commented that a complete change of character was not uncommon in young children after an injury, and in this series the parents remarked that their children behaved quite differently and that new personalities had emerged, often with characteristics less pleasing to the parents.

All these patients eventually returned to and remained in school, but the impression gained from the parents, teachers and other information received suggested that, to some extent, a sheltered and tolerant environment existed for most of them.

EEG Findings at Follow-up Examination Careful inquiry failed to reveal any

evidence of clinical or subclinical seizures in this small group of patients. Electro-

475

TA

BL

E I

1 C

hang

e in

Inte

llect

ual A

bilit

ies F

ollo

win

g Se

vere

Hea

d In

jury

Bef

ore

Ave

rage

(fat

her

a ph

ysic

ian)

Age

at

Day

s of

Ye

ars

sinc

e A

fter

IQ

90.

Rot

e m

emor

y po

or.

Wid

e sc

atte

r.

1 2

5 35

56

10

4

5 21

25

+ 8

~~~

3 4 5 K

5 28

28

+ 13

3

6: 28

53

4

7 35

56

23

_

__

~~

Est

imat

ed i

ntel

ligen

ce

Ave

rage

.

Hig

h av

erag

e.

Adv

ance

d gr

oup

in c

lass

.

IQ 65

-70.

W

ide

scat

ter.

Poo

r Sp

ecia

l cl

ass,

sec

ond

grad

e ro

te m

emor

y.

leve

l.

Low

ave

rage

(IQ

80-

89).

Con

- T

hird

gr

ade.

R

eads

w

ell.

Cre

te, p

erse

vera

tive.

V

ery

dist

ract

ible

. Im

prov

ing.

Pres

ent p

erfo

rman

ce

Slow

se

ctio

n ni

nth

grad

e.

Poor

at c

ompl

ex ta

sks.

6 7 8 9

Goo

d av

erag

e.

I 30

30

+ 3

11

41

65+

11

~~~

~~~

14

42

60

14

16

35

56

3 ~~

~

Ave

rage

. W

ide

scat

ter.

Poor

ro

te m

emor

y.

Ave

rage

.

Ave

rage

. Fif

th g

rade

.

Rea

ding

dif

ficu

lties

. Inc

reas

- in

g di

ffic

ulty

with

com

plex

ta

sks.

Low

av

erag

e. W

ide

scat

ter.

T

hird

gr

ade.

Po

or

read

er.

Poor

rot

e m

emor

y.

Poor

com

preh

ensi

on.

rote

mem

ory.

Rea

ds p

oorl

y.

Low

av

erag

e. S

catte

r. P

oor

Fini

shed

hi

gh

scho

ol. Re-

spon

sibl

e se

mi-

skill

ed jo

b.

Ave

rage

. L

ow a

vera

ge.

No

inte

lligi

ble

spee

ch. W

ide

scat

ter.

Ath

etoi

d qu

adri

pleg

ic. S

ixth

gr

ade

wor

k; i

mpr

ovin

g.

Low

ave

rage

. IQ

70-

80.

Con

cret

e. P

oor

rate

Sl

ow

eigh

th

grad

e.

Poor

R

epea

ted

four

th g

rade

. m

emor

y.

read

er. S

low

impr

ovem

ent.

IQ 1

IS. C

lass

lead

er.

IQ 8

0. V

ery

wid

e sc

atte

r.

Pers

ever

ativ

e.

Park

inso

nism

. E

xpel

led

two

scho

ols.

Ps

ychi

atri

c ca

re

in t

hird

sch

ool.

IQ 9

5-10

0.

Beh

avio

ur p

robl

ems.

IQ

70-

80.

Poor

com

preh

ensi

on.

Spec

ial h

igh-

scho

ol.

Impr

ovin

g. U

nrea

listic

fu

ture

goa

ls.

(* P

ost-

trau

mat

ic a

mne

sia

incl

udes

com

a.)

Beh

avio

ur a

nd p

erso

nalit

y E

EG

var

iatio

ns *

(N

o pa

tient

had

sei

zure

s)

21

28

25 +

28 +

~_

__

28

35

53

~_

__

56

30

41

30+

65 +

~~

Stro

ng m

otiv

atio

n. G

ood

adju

stm

ent

in jo

b.

Abn

orm

al.

Dif

fuse

slo

w a

ctiv

ity r

t te

mpo

ral

regi

on.

Del

ta s

low

act

ivity

who

le r

t he

mi-

sphe

re.

-

Cas

e N

o.

-

Age

at

inju

ry

(yea

r)

-

Yea

rs

sinc

e in

jury

1 5

35

I 56

1 0: Po

or m

otiv

atio

n. F

ew fr

iend

s. ‘

Pick

ed o

n’.

Gen

eral

abn

orm

al

slow

act

ivity

. O

ccas

iona

l sp

ikes

.

2 5

Plea

sant

. G

ood

mot

ivat

ion.

M

othe

r co

rn-

Abn

orm

al, d

isor

gani

sed.

Sei

zure

dis

char

ges

on

plai

ns o

f hi

s fo

rget

fuln

ess.

do

zing

. 8 13

+ 3

5 W

ell a

djus

ted

to q

uadr

iple

gia.

No

mot

ivat

ion.

N

o gr

oss

abno

rmal

ity.

Inst

abili

ty

of

alph

a fr

eque

ncy.

4 4

Ple

asqt

, w

ell-

man

nere

d.

Tri

es

hard

. Jm

- N

orm

al a

wak

e. D

iffu

se s

low

act

ivity

of

hype

r-

prov

ing.

ve

ntila

tion.

5 I

2: Pl

easa

nt.

Hyp

erac

tive.

Le

ss

relia

ble.

Pe

r-

1 Rt p

oste

rior

tem

pora

l the

ta a

ctiv

ity. N

o sp

ikes

. se

vere

s at s

choo

l.

6 W

ell-

beha

ved.

Qui

et. ‘

Prot

ecte

d’ b

y fr

iend

s.

Gro

ssly

abn

orm

al.

Gen

eral

sei

zure

dis

char

ges.

D

iffu

se a

bnor

mal

slo

w a

ctiv

ity.

3 11

I 11

I 8 14

42

I 6

0 1Q

~

~~~

Frus

trat

ed a

nd a

nger

s ea

sily

. But

det

erm

ined

D

iffu

se l

ow v

olta

ge s

low

act

ivity

. N

o lo

cali-

an

d im

prov

ing.

sa

tion.

9 16

35

I 56

3

Agg

ress

ive,

off

ensi

ve.

Dan

gero

usly

vi

olen

t. D

isor

gani

sed.

N

o se

izur

e di

scha

rges

. D

e-

Unr

ealis

tic. I

mpr

ovin

g.

pres

sed

It he

mis

pher

e vo

ltage

s.

10

7

18

-

I 2

~~

Poor

mot

ivat

ion.

Fr

ustr

ated

, co

ncei

ted,

un-

D

iffu

se s

low

act

ivity

with

dep

ress

ed h

emis

pher

e vo

ltage

s. N

o se

izur

e di

scha

rges

. I

real

istic

.

* 18

elec

trod

es:

‘10-

20 e

lect

rode

sys

tem

of

the

Inte

rnat

iona

l Fe

dera

tion.


encephalograms were made in all patients and showed variations outside the accepted range of normal for the patients’ age (Table 111). As was to be expected, there was no simple correlation between the degree of electroencephalographic abnormality and the patients’ behaviour or intellectual performance-e.g., case 6, who, without medication, was reported to be pleasant, quiet, well-behaved, liked and protected by his friends and teacher. In this patient, a recording during spontaneous sleep was grossly abnormal with generalised seizure discharges and diffuse abnormal slow activity. In contrast, case 2, for two years following the accident, was aggressive, offensive, dangerously violent and unrealistic, as described in the heterogenous cases of post-traumatic psy- chosis by Meyer (1904). The electroencephalogram showed an awake, spontaneous dozing and sleep record of normal low voltage patterns, occasional low voltage slow activity and depression of the left hemisphere voltages, but no seizure discharges (Table 111).

The absence of specific localisation or abnormality in the electroencephalograms appears to be compatible with severe acceleration concussion and was of no particular diagnostic or prognostic value in this group seen so many years after the initial injury. Although Silverman (1962) suggested that during the acute stage of a head injury, good correlation exists between the degree of injury and the abnormality in the electroencephalogram, he also found that striking EEG abnormality may appear to result from negligible injury; in contrast, Rickham (1961) noted that of 30 cases of severe head injury in children 5 had normal electroencephalograms throughout the illness. The value of the EEG in the acute stage of a cerebral insult has been summarized by Williams (1945). The wide variation in the electroencephalographic findings, years after

severe acceleration concussion, suggests that other factors are of greater importance in determining the prognosis of injury than the electroencephalogram.

Discussion The children and adolescents killed or

maimed in automobile and other accidents accounts for an increasing proportion of the total morbidity and mortality in this age-group during recent years (Cornell University 1961). Rickham (1961) observed that, during a four-year period, out of 5,000 admissions to the general surgical (non-orthopaedic) wards in Liverpool, 2,567 were due to head injuries. In 1962 about 5,000 people in the British Isles and 41,000 in the United States died after automobile accidents alone-an 8 per cent increase over 1961. It has been estimated that for every death there are six seriously injured survivors. Yet, relatively few hospitals have a comprehensive or syste- matic method of case recording, such as that devised by Symonds at the Military Hospital in Oxford (Russell and Smith 1961), and careful long-term follow-up studies are rare (Hjern and Nylander 1962).

The duration of post-traumatic amnesia is more difficult to establish in children than in adults, and in this series it was assumed to approximate to the time taken for the patient to regain full orientation and cognizance of people and surround- ings. As some estimates depended upon the observations of unsophisticated ob- servers, unable to discriminate between automatic and cognitive behaviour, the period of post-traumatic amnesia may have been of longer duration than re- corded in Table I.

Organic Changes in the Brain Following Acceleration Concussion

The remarkable stress to which the brain is subjected by its own inertia in trauma of the acceleration concussion

478


type, has been estimated to be as much as 350 g., or 11,250 ft./sec.2 if the patient falls 30 feet on a hard surface (Russell and Smith 1961). If no fracture occurs, the effects of this force may be further increased by the elastic rebound of the skull in an opposite or tangential direction to that of the brain mass. Thus, the clinical effects of such trauma are quite different either to those encountered in crushing injuries of the stationary skull (compres- sion concussion) or the majority of penetrating head wounds from small missiles in which the patient may remain fully conscious (Denny-Brown and Russell 1941, Symonds 1962). The appearance of the brain at the time of the impact, photographed with high speed cinematog- raphy by Pudenz and Shelden (1946), revealed that ‘blows on the head cause swirling rotary movements of the brain within the cranial cavity’. This classical study confirmed Russell’s concept of the mechanism of concussion, that ‘the whole of the brain tissue undergoes mechanical agitation’ (1932), and enhanced Hol- bourn’s experiments on linear acceleration and rotation (1943, 1945), which suggested that the non-uniformity of white and grey matter causes specially large strains with shearing near the junction between the white and grey matter.

The human pathological confirmation needed has been demonstrated by Strich (1961), who found widespread diffuse degeneration of the cerebral white matter in patients dying 5-24 months after severe closed head injuries; she also gave ample histological evidence supporting the belief that nerve fibres are torn or stretched at the time of the accident by rotational forces (Strich 1956).*

The importance of focal injury to the brain and the relationship of the brain- stem to unconsciousness and concussion put forward by Jefferson (1944), has been brilliantly discussed by Symonds (1962), who clarified the present state of know- ledge concerning the Jacksonian-like levels of recovery of cerebral function which may exist following concussion.

The difference of opinion which still exists concerning the late prognosis of severe acceleration concussion in childhood, may be due to a less than adequate application of the PTA scale suggested by Russell and Smith (1961). Hjern and Nylander (1962), unlike Akerlund (1959), found no correlation between the duration of unconsciousness and the severity of the sequelae in twenty-two patients of whom 9 had severe sequelae, but the material presented is inadequate for independent detailed analysis. Moore and Reusch (1944) found that all patients with per- sisting gross intellectual deficit for six months had suffered a period of confusion lasting longer than nineteen days but commented that six months is not an adequate period to determine adequately the late effects of severe head injury.

Psychological Sequelae and their Organic Basis

In the present series of young patients, although mental and physical activities had been resumed to a remarkable degree in most cases, the moderate loss of formally measured IQ points did not represent the crippling effects of the injury on the child and the family. The majority of the families were painfully aware of the patient’s loss of previously sound abilities and accompanying changes in

* Strich describes one patient who died from drowning two years after his accident; after discharge from hospital several attempts were made to return the boy to school but the combination of anti-social behaviour, poor concentration and residual physical disabilities made this very difficult. Similar but more violent problems occurred for 2f years with case 9 of this series who initially required resident psychiatric treatment after being expelled from two residential schools, but who is now able to remain at home and

attend some school courses.

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character but discounted them thankfully. All patients experienced difficulty with

items dependent on rote memory, which in turn adversely affected their test scores. Difficulties of this nature have been noted previously in conditions other than post- concussional states (Tooth 1946), and may be seen in patients with dysfunction ranging from severe reading disabilities to the sequelae typical of mild cerebro- vascular accidents (Mark 1962).

Horn (1952) suggested that memory is stored in neuronal protein, and Dixon (1962) has put forward the hypothesis that interference with the process of memory occurring after concussion may depend on the brain’s ability to restore specific macromolecular configurations of neuronal protein in the surviving neurones.

Subjective symptoms noted by those who came into contact with the majority of the patients included anxiety, irritability, difficulty in sustaining mental concentration, impaired memory and excessive liability to fatigue. Although these are symptoms of a psychological kind this does not mean they have no physical basis (Symonds 1962) and they are commonly exhibited in the younger age-groups, where the question of compensation may exist only for overt injury. Psychological symptoms following brain injury due to trauma or infection are often unjustly attributed almost entirely to the patient’s premorbid personality (e.g., Denker 1958); if the patient’s pre-morbid personality is less than ideal, a cerebral insult is unlikely to be beneficial (Richardson and Battaglia 1962, Nyhan and Richardson 1963).

Efsects of Present-day Treatment on Sur-

difficult to obtain, the number of vegetative survivors in childhood may be increasing as a result of improved methods of treatment. Walker (1960) regarded young patients as the most rewarding candidates for tracheostomy and hypothermia and, as it is not possible to make finer discriminations in the treatment of the decerebrate comatose child, the increasing preservation of less severely injured children at one end of the scale is likely to be accompanied by more vegetative survivors at the other end. This is implied by Rickham (1 96 l), who noted that of 18 deeply unconscious patients treated by cooling, 3 were still comatose after 16, 12 and 5 months respectively and one who recovered consciousness after 9 weeks is likely to be a burden to the family or community for life. However, in contrast, Hendrick (1959) reported no vegetative survivors in 18 children with decerebrate rigidity treated with hypothermia, of whom 8 succumbed during treatment.

Addendum This study dealt with accidents and

trauma of exceptional severity and should not be regarded as in any way prejudicial to the potential benefits of passenger and driver seat-belts. The continuing studies of Cornell University show that ejection from the automobile (as occurred with some of the above patients) has a pro- foundly deleterious effect on the injury sustained, and that a child seated in the rear seat of an automobile is much less likely to sustain severe or lethal injury than in any other position, particularly if protected by a seat-belt.

viva1 and Sequelae Acknowledgements: The author is grateful for

The numerous reports of survivors of the assistance received from his colleagues, Dr. severe head trauma suggest that from the Edward Hopkins and Dr. Lewis Armistead, in

the early examination of these patients, to Dr. third decade onwards, the number of Curtis Marshall for the electroencephalograms vegetative survivors increase as an effect and to Dr. W. Ritchie Russell and Dr. Aaron

Smith for their encouragement to publish the of age. Although accurate information is case-material.

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SUMMARY Ten children and adolescents who had sustained severe cerebral trauma of the accelera-

tion concussion type, causing protracted coma (median 28 days) and post-traumatic amnesia (median 49 days), were examined 2 to 133 years after their injury.

In this small group of patients, who do not represent a statistical sample of a head injury population, rehabilitation into school and the community was to some extent possible in all cases and depended on the degree of residual neurological and psychological dysfunction. Protracted coma after severe acceleration concussion is likely to be followed by defects of memory which interfere with the patient’s academic and social adjustment; the moderate loss of points on formal intelligence tests in no way represents the long- term crippling effects of the injury on the patient and his family.

Within the limitations of this study the degree of recovery in individual patients supports previous observations that patients surviving severe head injury in the first two decades of life have a better potential for recovery than older patients.

RESUME Quelques conshquences des blessures graves de In t6te

On a examint 2 a 133 ans aprks leur accident 10 enfants et adolescents qui avaient subi un traumatisme cCrebral grave du type commotion dQe l’accklbration, suivi d’un coma prolong6 (28 jours en moyenne) et d’une amnksie post-traumatique (49 jours en moyenne).

Dans ce petit groupe de patients, sans valeur statistique pour reprtsenter une population d’accidentks de la tCte, chacun des patients a pu Stre reassimilk dans l’Ccole et dans la communaut6 avec plus ou moins de succCs selon l’importance de ses stquelles neurologiques et psychologiques. Un coma prolong6 conskutif une commotion grave diie a l’acct- ICration est vraisemblablement suivi par des dtfauts de mkmoire qui interferent avec l’adaptation acadkmique et sociale du patient; une perte de points modCrte au cours des tests d’intelligence conventionnels ne reprtsente en aucune faGon les constquences long terme des infirmitks dQes a l’accident sur le patient et sur sa famille.

Dans les limites de cette ttude on peut dire que le degrk de gukrison de chacun des patients est en accord avec des observations preckdentes selon lesquelles les patients qui survivent a une blessure grave de la tCte avant 20 ans ont un plus grand potentiel de gutrison que les plus igCs.

ZUSAMMENFASSUNG Einige Nachwirkungen schwerer Kopfverletzungen

Zehn Kinder und Jugendliche, die schwere Zerebralverletzungen in Form von besch- leunigter Konkussion mit andauerndem Koma (Durchschnittsdauer 28 Tage) und post- traumatischer Amnesie (Durchschnittsdauer 49 Tage) erlitten hatten, wurden 2 bis 13+ Jahre nach der Verletzung untersucht.

Bei dieser kleinen Patientengruppe, d‘e nicht ein statistisches Beispiel der Bevolkerung mit Kopfverletzungen darstellt, war bis zu gewissen Grenzen, die Rehabilitation in Schu en und Gemeinden in allen Fallen moglich, obwohl sie von dem Ausmass der restlichen neurologischen und psychologischen Funktionsstorungen abhing. Anhaltendes Koma, das der schweren beschleunigten Konkussion folgt, fiihrt oft zu Gedachtnisstorungen, die dem Patienten die Schul- und Sozialanpassung erschweren; eine massige Reduzierung

48 1


von Punkten im formellen Intelligenz-Test deutet in keiner Weise auf die dauernden Schadenwirkungen der Verletzung auf den Patienten, sowohl wie auf dessen Familie.

Wenn man die Begrenzungen dieser Untersuchungsserie berucksichtigt, so bestatigt diese, dass Patienten die schwere Kopfverletzungen wahrend der ersten 20 Lebensjahre iiberleben, bessere Genesungschancen haben, als solche die einer hoheren Altersgruppe angehoren.

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University. Cornell Aeronautical Laboratory, Inc. P.O. Box 255, Buffalo 21, New York. Dencker, S. J. (1958) ‘A follow-up study of 128 closed head injuries in twins using co-twins as controls.’

Acta Psychiat. Neurol., 13, Suppl. 123. Denny-Brown, D. (1942) ‘The sequelae of war head injuries.’ New Engl. J. Med., 227, 771. - Russell, W. R. (1941) ‘Experimental cerebral concussion.’ Brain, 64, 93. Dixon, K. C. (1962) ‘The amnesia of cerebral concussion.’Lancet, ii, 1359. Hendrick, E. B. (1959) ‘The use of hypothermia in severe head injuries in childhood.’ Arch. Surg., 79, 362. Hjern, B., Nylander, I. (1962) ‘Late prognosis of severe head injuries in childhood.’ Arch. Dis. Childh.,

Holbourn, A. H. S. (1943) ‘Mechanics of head injuries.’Lancet, ii, 438. - (1945) ‘The mechanics of brain injuries.’ Brit. med. Bull., 3, 147. Horn, G. (1952) ‘The neurological basis of thought.’ Mermaid (University of Birmingham), 18, 17. Jefferson, G. (1944) ‘The nature of concussion.’ Brit. rned. J . , i, 1. Mark, H . Personal communication. Meyer, A. (1904) ‘The anatomical facts and clinical varieties of traumatic insanity.’ Amer. J . Znsan., 60, 374 Moore, B. E., Ruesch, J. (1944) ‘Prolonged disturbances of consciousness following head injury.’ New

Nyhan, W. L., Richardson, F. (1963) ‘Complications of meningitis.’ Ann. Rev. Med., 14, 243. (Annual

Pudenz, R. H., Shelden, C. H . (1946) ‘The lucite calvarium. A method for direct observation of the brain.

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Rickham, P. P. (1961) ‘Head injuries in childhood.’ Helv. chir. Acta, 28, 560. Russell, W. R. (1932) ‘Cerebral involvement in head injury.’ Brain, 55, 549. - Smith, A. (1961) ‘Post-traumatic amnesia in head injury.’ Arch. Neurol. (Chic.), 5,4 . Silverman, D. (1962) ‘Electroencephalographic study of acute head injury in children.’ Neurology, 12, 273; Smith, A. (1961) ‘Duration of impaired consciousness as an index of severity in closed head injuries.

Strich, S. J. (1956) ‘Diffuse degeneration of the cerebral white matter in severe dementia following head

- (1961) ‘Shearing of nerve fibres as a cause of brain damage due to head injury.’ Lancet, ii, 443. Symonds, C. P. (1928) ‘Observations on the differential diagnosis and treatment of cerebral states con-

- (1962) ‘Concussion and its sequelae.’ Lancet, i, 1. Tooth, G. (1947) ‘On the use of mental tests for the measurement of disability after head injury.’ J.Neuro1.

Walker, A. E., Black, P. (1960) ‘Heroic treatment of acute head injuries. A critical analysis of the results.

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Documents

Some Effects of Severe Head Injury : A Follow-up Study of Children and Adolescents after Protracted Coma