Changing Patterns of Childhood Aphasia Bryan T. Woods, MD, and Hans-Lukas Teuber, P h D

Acquired aphasia in children has been generally characterized as nonfluent, transient, and frequently due t o right hemisphere lesions. We studied 65 children with unilateral hemispheric brain lesions occurring after speech acquisition any time from the second through the fourteenth year. Of 34 patients with a left hemisphere lesion, 25 had an initial aphasic speech disturbance, while of 31 patients with a right hemisphere lesion, only 4 (including 2 lefthanders) showed any initial aphasia. All those who became aphasic before the age of 8 years eventually regained speech, but recovery time required ranged from less than a month to more than two years. One 5-year-old boy who recovered had initial jargon aphasia. Our review of the literature indicated that the conflict between our results and the traditional claim of frequent aphasia with right hemisphere lesions was only apparent; the great majority of crossed aphasias are concentrated in reports written before antibiotics were used, and many cases were associated with systemic bacterial infections. Woods BT, Teuber H-LChanging pattterns of childhood aphasia. Ann Neurol3:273-280, 1978

The standard doctrine about childhood aphasia seems to have emerged quite early after Broca's [6] initial description of the condition in the adult. Only seven years later, in 1868, Charcot's pupil Cotard [9] noted that there had been no subsequent failure to acquire language in several patients with infantile hemiplegia and complete atrophy of the left cerebral hemisphere. The implication seemed to be (and has remained) that i n some sense, either hemisphere can initially sustain language functions. This belief was soon enhanced by the numerous case reports of rapid recovery from acquired aphasia in children [8].In time a general principle has emerged based o n the view that up to a certain age, variously estimated to be from 9 to 11 years old [2 11, t h e assumption of language functions by the right hemisphere remains possible. A corollary observation contained in the early literature was that aphasia, when it does occur after very early hemispheric lesions, is not only relatively transitory but occurs with nearly equal frequency after lesions of the left or right hemisphere [121. Furthermore, it was generally believed that recovery from childhood aphasia is more rapid the earlier the lesion is sustained. Last, the claim was advanced (as early as Bernhardt's survey of 1885 [ 4 ] ) that childhood aphasias differ in kind from adult aphasia, being predominantly motor (or nonfluent), with a virtual absence of cases of jargon. These principles were restated with some modification by HCcaen [ 151, with a caveat (after Krashen [IS]) that only those right hemi-

From the Department of Neurology, Massachusetts General Hos-

sphere lesions incurred by age 5 years are likely to produce aphasia. O u r own observations are somewhat different. In t h e course of an ongoing study of neurological and behavioral sequelae of early brain lesions, we found aphasia much more directly tied to clinical evidence of left hemisphere lesions than the early literature led us to expect. Therefore, the purpose of this communication is twofold: to present observations on a small group of patients with early cerebral lesions and comment o n the incidence and nature of their language disorders relative to side and time of the lesion; and to review the earlier literature regarding childhood aphasias and point out that the currently accepted doctrine on this subject is largely supported by the earlier literature but contradicted by more recent reports, including the present series of observations.

Methods T h e patients described in this report were part of a large study of the late effects of unilateral nonprogressive cerebral lesions in childhood. Initially, the records of approximately 400 patients with congenital or acquired hemiparesis were reviewed by one of us (B. T. W.). Only those cases in which the clinical evidence in the record indicated involvement of a single cerebral hemisphere by a single, fixed lesion received further consideration. Excluded were most cases of hemiparesis due t o trauma, neoplasm, or infection of the central nervous system. Ultimately 50 of the acceptable cases were entered into the more detailed and protracted study, which included neurological and special neuro-

Accepted for publication Sept 28, 1977.

0364-5 134/78/0003-0314$01.25 @ 1978 by the American Neurological Association

273

psychological examination, complete histories, and various experimental tests of language, perception, and complex motor skills. One important aspect of the detailed study of these 50 patients was the effect of the lesions on speech. W e were concerned with three aspects: first, the immediate effects of the lesion on speech in those patients with some previously acquired language; second, the course of language development, recovery subsequent to the lesion, or both; and third, the state of language at the time of the study. Data for the first two questions-immediate effects and subsequent course-had to be retrospective and historical, while answers to the question of current status could be obtained directly from the patients in the study by appropriate examinations and testing procedures. T h e present report is concerned only with historical data; the current language status of the patients will be the subject of a separate report. It was determined from the records, as well as from patient and family interviews, that 26 of the 50 patients already had acquired speech at the time alesion developed. We then realized that we could use historical data available from the records of other patients who had not participated in the full study for a variety of reasons (distance, loss to follow-up, lack of interest), but who had acquired speech before their lesion occurred and otherwise met the criteria for inclusion in the study. In this way we acquired an additional 39 patients for this aspect of the study. Table l shows the lateralization and presumed cause of the lesions in the 6 5 patients comprising both groups, those examined and those having record reviews only. There were 34 males and 31 females. O u r definition of aphasia was inclusive. If a child who was observed to be otherwise alert and responsive either failed to speak or spoke in a defective manner that experienced observers called aphasia, we classified that child as aphasic following the lesion. O u r data on recovery was similar; as soon as it was noted that the child spoke normally according

to ordinary clinical standards, we classified him or her as recovered. (The historical data on speech development in the patients who had not y e t acquired speech at the time of their lesions was so sketchy that we did not attempt to include that information in this report.) In the absence of autopsy verification, both cause and anatomical location of the lesion must remain somewhat imprecise, especially since CAT scanning was not available at the time of the study. Whenever possible, use was made of data from surgery, angiography, isotope brain scans and electroencephalography to supplement the clinical data. Basing our opinion on these data sources, we believe that all the vascular lesions involved at least a portion of one of the middle cerebral arteries; the other lesions were assumed, based on the presence of unilateral motor (and usually sensory) deficits, to involve at a minimum the posterior frontal (or frontoparietal) region. Patients with unequivocal evidence of bilateral dysfunction were excluded, as were those with a suspected subtentorial lesion.

Results T a b l e s 2 t h r o u g h 5 summarize t h e available clinical d a t a for all the patients, both those subsequently personally examined a n d t h o s e for whom only records w e r e available. The p a t i e n t g r o u p s are separated by the p r e s u m e d side of lesion a n d by w h e t h e r or n o t w e examined them. Two principal findings are revealed i n these tables. The first is t h e disparity b e t w e e n t h e effects of left a n d right h e m i s p h e r e lesions o n previously acquired speech. In t h e group of examined patients, 10 of t h e 15 with left h e m i s p h e r e lesions (Table 2) had e i t h e r transient or longer-lasting aphasic s p e e c h disturbances. I n contrast only 2 of t h e 11 patients with early

Table I. Presumed Cause of Lesions Side of Hemiparesis in Examined Patients Cause

Left

Cerebrovascular accident Thrombotic or idiopathic Embolic H ypotensive Transient ischemic attacks lntracerebral hemorrhage Seizures and hemiparesis Persistent hemiparesis Todd’s paralysis Resected tumor Trauma Infectious process Abscess Tuberculous meningitis with thrombosis

7

Annals of Neurology

No 3

Right

9

4

6

1

2

1 1

1 3

1

2 1

2

1

3 2 1

1

1

4

5

20

19

3

1 1

11

Vol 3

Left

1

Total

274

Right

Side of Hemiparesis from Record Reviews Only

March 1978

15

Table 2 . Occurrence and Duration of Aphasia in Patients with Right Hentiparesi.r and Previously Acquired Speech Who Were Examined b-y the Authu1a.r

Paricnt No.

Age at Lesion (yr)

Handedness

Sex

I

R

F

I 8/12

Persisrenr. severe

+, 5

2

R

F

2 3/12

Persistent. mild

A.

3

L

F

2 7/12

Pcrrirtent. mild

4

R

F

2 9/12

F

3 8/12

5

6

L

M

5 1/12

1

L

F

5 9/12

Durarion of Hemiparesis

Presence and Duration of Aphasia

Localnation Based on:

+

Tuberculous mcnmgris wrh CVA

L MCA rerrirory

It

L

CVA

L ICA rerrirorg

- , dyrdnhric

I

+

CVA

L MCA rerrrrory

Persisrenr. mild

+. 2 mn

t

+

L MCA terrirory

Persisrent. mild

-

’+

+

Tcrralogy o f Fallor; hemiparcrrs 1 I days afrer Blalock shunt R-sided wealnris afwr T&A: ? hypotension

Persisrenr. severe Perrrsrenr. mild

+. 30 nio

+

CVA

L MCA territory

t

2

)+

2 wk

+

6 4/12

Persisrent. modcrnre

+, > 5 mo

9

R

F

7 2/12

Perrrsrenr.

+.>lmo

t

9/12

+.

1 mo

+ I/+ scan

reverr 7

i

-

M

M

Ango6

wk

R

R

Lesion Lncalizarion

Cause of Lrsion

A

10

EEG

Clin.

Surg.

I wk

+

+

+

Contusion. !mild CVA: earlier leaon

L cerebral warerrhed

L cerebral hemisphere

L ICA rerrrtory

+

Carotid clamped to trcir L MCA aneurysm CVA

+

t

CVA

L MCA territory

+

+

L MCA rerrirory

+

+

Srizures. hemiparcrib CVA

L MCA rerritory

+

CVA

L ICA rcrritory

+

+

Abscess, rurmrally drarned

L anterior

’I

+

C V A ; hisrory

’1MCA rerrirory

L ICA

territory

scan 11

12

13

14

15

R R

R

F

M

M

8 1/12 8 7/12

13 4/12

R

M

1 3 10112

R

M

I 5 2/12

Persisrenr. mild Pcrsirrenr. severr

+. persir-

Persisrent. severr Face weakness less than 3 mo Persisrenr. mild

+. persir-

rent

+

+. Pcrii5rrnr after 4 yr

+

W”1

-

-

t

fronral regton

oi mrgrmnr

C V A = cerebmvawcular xccidenr. T&A = tonrillectumy and adenoidectomy: MCA = middle curebrdl arrery: 1C.A = lnrernal r;imntid artery

right hemisphere lesions (Table 3 ) had any noticeable language difficulties following the lesions, and 1 of these 2 was known to be left-handed prior to the lesion. Similarly, with the larger unexamined group, 15 of the 19 children with early left-sided lesions (Table 4) showed an initial language disturbance, while only 2 of 20 with early right hemisphere lesions (Table 5 ) were so affected; again 1 of these 2 “crossed” aphasics had been noted to be left-handed before the lesion occurred. The second finding concerns the relationship between the age when the lesion occurred and the duration of subsequent aphasia. In 4 patients, all with left hemisphere lesions (Patients 11, 12, 13,43),clinically evident aphasiawas present up to the time of the study (an interval of more than four years). These 4 patients



were qed years years l 3 years and l 2 years months at the time the lesion occurred. The other 25 initially aphasic Patients ultimately recovered to the extent that they were no longer clinically aphasic. Nevertheless, the time re-

quired for recovery was variable and did not appear to show any linear relationship to age when the lesion occurred. For those who recovered, the duration of the language impairment ranged from less than aweek to two and one-half years (Patient 6, 5 years 1 month old at the time of the lesion). Also, the recovery time did not seem to be closely correlated with the severity of hemiparesis. An unexpected observation in this study involves the nature of the language disorders. For the most part, the aphasia in these patients seems to have been nonfluent. One particular instance, however, is difficult to describe in terms other than those involving “jargon.” W e summarize from the record of Patient 6: A boy was 5 years old when he had several seizures followed by weakness of the right Icg and “jabbering” speech sounds. After two days the weakness had progressed and involved the entire right side, T h e only speech consisred sounds such as “ga-ga” and “OOOO.” He failed to respond to some commands or to pick up named objects. Six days later, when

Woods and Teuber: Childhood Aphasia

275

Table 3 . Occurrence and Duration of Aphasia in Putients with Left Hemiparesis and Previously Acquired Speech Who Were Examined by the Authors ~~

Age ar Lesion (yr)

Parlent No

Handedness

Sex

Duracion of Hemiparesis

16

R

F

1 9/12

I'

R

F

1 11/12

IR

R

F

5 6/12

Persisrenr. severe Persistent. severe Persisrenr.

Presence and Durauvn nf Aphasia

~~

~

hralizarion Rased on:

Surg.

-

-, slurring of speech +, 4 wk

Anlpv~.

FEG

Clin.

Cause ot Leaion

Lesion localization

+

+

+

CVA

R MLA rrrrirory

+

+

+

CVA

R ICA

+

+

Gunshot wound. .22

R rurubral h u n -

+

CVA

R ICA rerrrrory

+

CVA

R ICA rrrrirory

+

CVA

R MCA

+

+

CVA

R MCA terrirow

+

+

R rrmpvro-

+

+

AVM. b u r p cally resected CVA

+

+

Ependymnma. excised

R tronrotemporal

AVM wirh hemnrrhqr

R frontal r e g o n

,L.voru

trrrirnry

sphrre. frontal cntry. OCClP. exit

19

R

M

20

R

21

R

22

23

5 6/12

Pcrrirrmr. mild

F

5 loll2

F

6 6/12

L

F

7 11/12

R

M

8 2/I2

Irno Perrirrenr, severe Persistent, severe Persrrtcnr,

t

t

~

-

?+

+. 5 wk

+ +

-

scvurc

24

R

M

10 10/12

25

R

F

14 0112

R

26 CVA

M

= cerebrovascular acrdenr;

14 0112

Persistent. moderare Persirrenr. mild

+

-

t

+

Persistent, mild

+

t

+

-

AVM = arreriovenour malformation; MCA

= middle

cerebral arrery. ICA

=

ierrirory

parieral lobe

R MCA

rurrirurg

prrasaglrral regmn

intrrnal cdrotid artery.

Table 4 . Occurrence and Duration of Aphasia in Patients with Right Hemiparesis and Prwiously Acquired Speech. Datu from Rerords Only ~~

Age at Lesion

handed^

Patient No.

"ell

Sex

27

R

M

(VI)

14/12

Durauon of Herniparesir

Pr?Se"Ce and Duration of Aphasia

3 mo

+, approx.

Localiz~tionBased on. Lesion Surg.

Anpjog.

EEG

Clin

Cause nl Lesion

Localliarion

+

Seizures. he mi^

L hemisphere

paresis

R mo

zn

M

I loll2

- wk

+, 2 wk

+

29

M

2 0112

4 wk

+. 4 wk

+

30

F

2 10/12

< 2 wk

-

+

M

R

32

M

3 4/12 4 0/12

33

M

12/12

31

L hemisphere

Seizures. hemlparesis Trauma Trauma

L hemi5phrrr

L MCA rrrrmrry

< 3 mo

i

Perrmenr. mild Perstrrenr

+. 3 wk

+ +

+,>3mo

+

Seizures, hemiparrair

L hemrrphrre

1 mo

+, > I wk

+ +/+

+ +

CVA CVA

L MCA rerrirvry

+. 2 wk

+

Ruprured AVM

L thalamus and basal ganglia

+

Hemophiliac; inrracerebral hemorrhage

L hemisohere

+

Trauma

L paricrwccipiral

*

CVA CVA Trauma. cnn[recoup

L hemisphere L hemisphere L hemisphere

Cysric astro-

L rempnral lobe

34

R

F

4 3/12

5

35

R

M

4 7/12

Persistent, mild

F

5 3/12

Died 2 wk h e r hemp

36

CVA, chicken PUX CVA; terralogy of Fallor

L hemirphrrc

L I C A rerritnry

scan

+

~

aurop

37

M

5 4/12

4 mo

38

F

6 4/12

Persistent

+.

F

6 4/12

Persistent ', > 1 mn > 6 wk

+. < 5 yr

Perrlrrenr. mild

+, < 9 mo

10 mo

t

IOhK

R

39 40 41 42

M

R 4/12

M

10 11/12

F

1 I 0/I2

/.

+

mild Bmca'r

+. > 6 wk

+ +

+

t

cyroma. reSC'ICd

43 44

M

12 4/12

Perszrrrnr

M

13 3/12

Transient

45

F

14 6/12

5 wk

+, persistent ~

t , 5 wk

+CAT

+

CVA

+

Coarctation nf aorta; TlAs

t

L MCA rerritnry L hemrrpherr

Trauma -

CVA

276

=

cerebrnvascular accident, AVM = artenovennus malformation; TIA

Annals of Neurology

Vol 3 No 3

= rraniienr

March 1978

irchemlc atrack; MCA = middle cerebral anery

L fronrvrempvral remnn

Table 5 . Occurrence and Duration of Aphasia in Patients with Left Hemiparesis and Previous(y Acquired Speech, Data from Records Only Patient

No

HandednKSS

46

R

47 48

R

Age at

Sex

Lesion (yr)

Duration o f Hemipareris

F F

I 11/12 2 0/12

Persistent

M

2 G/12

< 24 hr

Presence and Duration of Aphma

Lvcallzarion Based nn Angog

Surg

+/+

> 4 wk

scan

EEG

Clrn

Cause of Lesion

Levon Lncaluatron

+

+

Thrombotic CVA

R MCA territory

+

+

Trauma

R fronre parietal region

+

? TIAr,

R hemisphere

-, ?confused baby talk

Seizures and Torid’s par& ysls

so

F

3 8/12 4 0/12

51

M

4 0/12

? Persistent

I2

M

4 8/12

4 ark

49

L

F

Persistent Persistent

s3

F

4 11/12

< 2 wk

54

F

5 0112

Persistcnt

55

M

5 71 I 2

56

F

h0/12

Severe. duration > 1 ark

M

6 G/12

F

7

57 58

L

2/12



Persistent Persistent

t

t

+, 4

days

+ +

Thrombotic CVA

R MCA and ACA

Seizures. hemiparesis

R MCA territory

Ependymoma. rerecred

R parietal reeon

Trauma. rntracerebral hemorrhage

R pnsrerior

Embolic CVA after viral myocarditis

R MCA territory

Seizures. hemiparesis CVA. trauma

R hemisphere

t

Seizures, hcmiparesis

R hemisphere

t

Emholir CVA Trauma. severe contuiion

R MCA territory R frontal,

+

t

+ I

-

+I+ PEG

-.arrhria SI. dys+. 5

+

+

+

+

I yr

-

+

+

i

frontal regwn

R hemisphere

anrerinr temporal regions

59

M

7 3/12

< 24 hr

+

+

Seizures. Todd’s paralysis

R hemisphere

GO 61

M M

7 5/12 & 11/12

< 3wk < 2 days

+ +

62 63

M M

1 1 3/ I2

13 6/12

Persistent Persirrent. mild

Trauma Seizures. Todd’s paralysis Thrombotic CVA Ruptured AVM

R hemisphere

t

64

F

13 6/12

Perrrsrrnr

I n , subarachn o d hcmorrhGge

R frontal lobe

G>

M

14 4/12

Persistent

Hemorrhage, mycotic aneurysm

R hemisphere

CVA = cerebrovascular accident; TIA = transient ischemic artack; AVM anterior cerebral artery. PEG = pneumoencephalogam

t

+

+

+

+

+ t

= arteriovenous malformation,

asked to “blow out the light,” he stuck out his tongue. At this time the neurologist noted that the patient “jabbers away with unintelligible sounds. At times he seems to realize that this is not clear and at other times he doesn’t.’’ H e obeyed simple commands but ignored more complex ones. Six weeks after the lesion appeared, a speech pathologist noted: “he still jabbers all the time as though you should understand him. Uses more words now, especially the names of objects.” Nine months after the lesion occurred, speech was said to have recovered and to be adequate for his age, but he retained only a three-digit span forward. After two and one-half years he was noted still to have considerable nominal aphasia. By the time he was 995 years old, he “had agreat deal of trouble recognizing letters. Could not read two-digit numbers correctly.” When examined at the age of 21, he still had severe right hemiparesis but was not clinically aphasic. He did have difficulty reading aloud, naming to category, naming from definition, spelling, and comprehending spelled words. H e made four Token Test sentence errors out of a possible total error score of 62, thus producing an essentially normal record.



R hemisphere R MCA territory R paricral lobe

ITP = idiopathic rhrombacyropenir purpun; MCA = middle crrebrnl artery; ACA

=

If the observations of two different trained individuals caring for the patient are to be credited, this appears to be an example of jargon aphasia in a 5-year-old boy.

Discussion The present study suggests several conclusions somewhat at variance with the standard teaching on aphasia in children. First, the study indicates that crossed aphasias (i.e., aphasia after right hemisphere lesions) may not be more frequent in children than in adults. (It must be recalled that clear determination of handedness is difficult with young children, especially in retrospect, so that the number of left-handers among the crossed aphasics is a minimal estimate.) Second, although recovery from aphasia is more likely to occur after early than after later lesions (i.e., in our sample, before the age of 8 years), the time it takes for recovery of language is not well correlated with the time of onset of the trouble. Third, though it may still be true

Woods and Teuber: Childhood Aphasia

277

that childhood aphasia tends to be predominantly nonfluent in kind, there can be exceptions, such as the case of jargon aphasia in a 5-year-old boy. It needs to be noted, however, that our observations of primarily nonfluent aphasia after early lesions may have been influenced by our reliance on hemiparesis as the neurological criterion for inclusion in the sample. O u r results prompted us to review the literature o n childhood aphasia primarily because of the wellknown insistence of earlier authors that the two cerebral hemispheres might at first be about equally potent for mediating speech, a proposition that at times takes the form of a claim for an initial sharing in language activities by the two hemispheres [25]. In contrast, results like ours would be expected from the more recent observations of an actual inherent anatomical asymmetry between the two hemispheres in the normal state, as shown by autopsy data in adults [ 131 and infants [31, 321 and by radiological evidence [ 2 0 ] . Recent electroencephalographic studies [26] as well as older studies with intracarotid amobarbital sodium [5] also point to an inherent functional asymmetry. A fairly extensive survey of the early literature on aphasias after childhood lesions suggests, in fact, a curious difference between the observations reported before and after the introduction of antibiotics and mass immunization (Tables 6, 7). Before the 1930s (Table 6), fully one-third of the total number of childhood aphasias reported were claimed to have followed

Author Clarus, 1874 [8] von Heine" Gaudard" Wallenberg' Lovett" Osier Freud, 1897 [12] Sachs, 1895 [271 Taylor, 1905 [301 Ford and Schaffer, 1927 [ l l ]

Total Patients

No. ADhasic

Total Patients

No. Aohasic

12

1

16

14

?

0

rl

5

5

0

7

5

?

1 (1)"JJ ?

11

7

13

15

15

?

5 (4)"

?

?

0

?

32

?

2

>

20

109 (5)"

28

3 (1)"

28

25

6

2 (1)"

17

15

21 t 7 P

249 ( 5 ) "

Left Hemisphere Lesions

Total

No.

Aphasic

Patients

Aphasic

5

?

9

5 25 66 13

2 8 17

7 55

94

4

13

?

1

?

4 25 45 3 12

12

3

23

7

>

7

?

10

?

124

?

2 00

>

1

?

3

318

'Cited in Freud 1121.

278 Annals of Neurology

Guttman, 1942 [14] LeFevre, 1950 [I91 Fisher and Friedman, 1958 [ l o ] Byers and McLean, 1962 [71 Basser, 1962 131 McCarthy, 1963 [231 Alajouanine and L'Hermitte, 1965 [21 Aicardi and co-workers, 1069 [I1 Isler, 1071r [17] Hecaen, 1976 [15]

Total Patients

~~~

No.

172

Author

Left Hemisphere Lesions

"Left-handed. "This patient (No. 22) was also included in the current study. 'Figures based o n data from 82 case repons appended by the author.

?

Total

Right Hemisphere Lesions

Total

Table 6. Incidence of Acquired Aphasia in Childhood after Lateralized Lesion.\: The Earlier Experience Right Hemisphere Lesions

Table 7 . Incidence of Acquired Aphasia i n Childhood: The Recent Experience

Vol 3 No 3 March 1978

right hemisphere involvement [8, 11, 1 2 , 2 7 , 3 0 ] . T h e more recent experience (Table 7), starting with Guttman [ 141, however, is more in keeping with our findings [ l ,2 , 7 , 1 0 , 1 5 , 1 7 , 1 9 , 2 3 ] : less than 10% of the childhood aphasias seemed to occur after right hemisphere lesions, and if known left-handers are excluded, then the proportion drops to 596. An apparent exception is the much-quoted study by Basser [3]. A review of that report indicates that a number of his patients sustained their lesions in the late 1930s or early 1940s. It is possible, therefore, that his results and most of the similar early ones reflect the much higher incidence of bilateral pathological damage in patients who did not have the benefit of antibiotics o r other modern treatment. Moreover, in the older series, aphasias and hemiplegias were frequently listed as complications of systemic infectious illness. Infections accounted for one-third of all cases in which a cause could be determined [ 12,301, with scarlet fever, pertussis, measles, congenital syphilis, bacterial

pneumonia, and diphtheria being the leading offenders. Neuropathological studies have shown [11, 161 that such systemic infections, if severe and untreated, will produce not only focal cortical lesions, causing hemiplegia, but also diffuse encephalopathy extending throughout both cerebral hemispheres. It may well be, then, that many of the young aphasic, hemiplegic patients in the earlier series had, in addition, a diffuse bilateral encephalopathy. In contrast, in modern series of acquired hemiplegia and aphasia, the lesions tend to be focal thrombotic vascular lesions whose cause in most instances is not known [7, 17, 281. It is true that many of these vascular lesions occur in the setting of an acute viral illness, but as Lyon and co-workers [22] pointed out, careful management of fluids and electrolytes may (and now usually does) prevent the development of diffuse toxic encephalopathies. In any case, in recent years such encephalopathies have become much less common. In conclusion, both a reassessment of the literature concerning childhood aphasia and our own observations serve to underscore an early onset of hemispheric specialization for language. Our results, which contradict the hypothesis that both hemispheres initially play an active role in speech, should be considered in conjunction with recent findings on atypical speech representation (as seen by means of the Wada technique [24]) which suggest that an early left hemisphere lesion needs to be critically placed in the classic language zone before a latent potential for language can be released on the right. Moreover, one should refer to our supplemental observations on the groups of children with early right hemiparesis in whom strong indications were found for some persistent, if subtle, impairment in a series of nonlanguage tasks. Our interpretation of these results (from patients in the present group) is that a price must be paid for the apparent escape of language, and this price is borne by certain nonlanguage capacities [29, 331. But regardless of one’s acceptance or rejection of this interpretation, the initial equipotentiality of the two cerebral hemispheres and the plasticity of the human brain in the face of early postnatal lesions may have been overestimated. The view expressed by Clarus in 1874 [8] seems, except for the last clause, surprisingly appropriate a century later: “After all, one assumes nowadays that there is a language center in both cerebral hemispheres, but that the one on the left develops preferentially because the convolutions of the left hemisphere are formed earlier and more strongly, as a result of a richer blood supply.” Dr Woods’ work was supported in part by NINDS Special Fellowship Grant 2 F11 NS2370-02 NSRB, National Institutes of Health; in part by Grant RR-88from the General Clinical Research

Centers Program of the Division of Research Resources, National Institutes of Health; and in pan by Grant 72-4-1 from the Alfred P. Sloan Foundation. Presented in part at the 102nd Annual Meeting of the American Neurological Association, Chicago, IL, June 20, 1977.

We thank D r Randolph Byers and Dr Charles Barlow of the Children’s Hospital Medical Center. We would most of all like to thank the patients and their families.

References 1. Aicardi J. Ansili J, Chevrie JJ: Acute hemiplegia in infancy and childhood. D e v Med Child Neurol 11:162-173, 1969 F Acquired aphasia in children. Brain 88:635-662, 1965 3. Basser LS:Hemiplegia of early onset and the faculty of speech with special reference to the effects of hemispherectomy. Brain 85:427-460, 1962 4. Bernhardt M: Ueber die spastische Cerebralparalysie im E n desalter (Hemiplegia spastical infantilis) nebst einem Excurse iiber “Aphasie bei Kindern.” Virchows Arch Pathol Anat 102:26-80, I885 5. Branch C, Milner B, Rasmussen T: Intracarotid Sodium Amytal for the lateralization of cerebral speech dominance. J Neurosurg 21:399-405, 1364 6. Broca P: Sur le siige de la faculti de language articule avec deux observations d’aphimie (pene de parole). Paris, 1861 7. Byers RK,McLean WT: Etiology and course of certain hemiplegias with aphasias in childhood. Pediarrics 29:376383,1962 8. Clarus A: fjber Aphasie bei Kindern. Jahresb Kinderheilkd 7:369-400, 1874 9. Cotard J: Etude sur I’atrophie panielle du cerveau. Thiw de Paris, 1868 10. Fisher RG, Friedman KR:Carotid m e r y thrombosis in persons fifteen years ofage or younger. JAMA 170:1918-1919,1958 11. Ford FR, Schaffer AJ: Etiology of infantile acquired hemiplegia. Arch Neurol Psychiatry 18:323-347, 1927 12. Freud S: Infantile Cerebral Pardysis (Infantile Cerebrallihmung, 1897). Translated by LA Russin. Coral Gables, FL, University of Miami, 1968 13. Geschwind N , Levitsky W: Human brain left-right asymmetries in temporal speech regions. Science 161:186-187, 1968 14. Guttman E: Aphasia in children. Brain 65:205-219, 1942 15. Hicaen H: Acquired aphasiain children and the ontogenesis of hemispheric functional specialization. Brain Lang 3:114-134, 1976 16. Ingram I T S : Paediatric Aspects of Cerebral Palsy. Edinburgh, E & S Livingstone, 1961 17. Isler W: Acute Hemiplegias and Hemisyndromes in Childhood. Clinics in Developmental Medicine, No. 41/42. Philadelphia, JB Lippincott, 1971 18. Krashen S: Lateralination, language learning, and the critical period. h g Learn 23:63-74, 1973 19. LeFevre AF: Contribuipo para o escudo da psicopatologia da afasia em criancas. Arq Neuropsiquiatr 8:345-393, 1950 20. LeMay M, Culebras A: Human brain: morphologic differences in the hemispheres demonstrable by carotid angiography. N Engl J Med 287:168-170, 1972 21. Lenneberg EH: Biological Foundations of Language. New York,John Wiley, 1967 22. Lyon G, Dodge PR, Adams RD: T h e acute encephalopathies of obscure origin in infantsand children. Brain 84680-708,1961 23. McCarchy JJ: Neurological theory and research on aphasia, in Osgood CE, Miron MS (eds): Approaches to the Study of Aphasia. Urbana, IL, University of Illinois Press, 1963 2 . Alajouanine TH, LHermitte

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24. Milner B: Hemispheric specialization, scope, and limits, in Schmitt FO, Worden FG (eds): The Neurosciences; Third Study Program. Cambridge, MA, The MIT Press, 1974 25. Mingazzini G: Uberden heurigen Stand der Aphasielehrr. Klin Wochenschr 4: 1289-1294, 1925 26. Molfese DL, Freeman RB, Palermo DS: The ontology of brain lateralization for speech and non-speech stimuli. Brain Lang 2:356-368,1975 27. Sachs B: The Nervous Diseases of Children. New York, William Wood, 1895. 532. 28. ShillitoJ: Carotid arteritis: acause of hemiplegiain childhood.J Neurosurg 21:540-551, 1964 29. Sperry RW: Lateral specialization in the surgically separated

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30.

31. 32.

33.

hemispheres, in Schmitt FO, Worden FG (rds): The Neurosciences; Third Study Program, Cambridge, MA, The MIT Press, 1974 Taylor J: Paralysis and Other Diseases of the Nervous System in Childhood and Early Life. London, Churchill, 1905 Wada J , Clark R, Hamm A: Cerebral hemispheric asymmetry in humans. Arch Neurol 32:239-246, 1975 Witelson SF, Pallie W: Left hemisphere specialization for language in the newborn: neuroanatomical evidence of asymmetry. Brain 96:641-646, 1973 Woods BT, Teuber H-L: Early onset of complementary specialization of cerebral hemispheres in man. Trans Am Neurol Assoc 98:113-117, 1973

Changing patterns of childhood aphasia.

Changing Patterns of Childhood Aphasia Bryan T. Woods, MD, and Hans-Lukas Teuber, P h D Acquired aphasia in children has been generally characterized...
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