MRI findings in boys with specific language impairment

BRAIN

AND

41, 52-66 (1991)

LANGUAGE

MRI Findings in Boys with Specific Language Impairment ELENA PLANTE, LINDA SWISHER, AND REBECCA VANCE The Child Language Laboratory,

The University

of Arizona

AND STEVEN RAPCSAK Department of Neurology,

The University

of Arizona

Magnetic resonance imaging scans of specifically language-impaired (SLI) boys were examined to determine whether atypical cerebral findings could be documented in children whose primary deficits were in language skills. Clinical examination of the scansfailed to reveal any visually obvious lesions or abnormalities. In contrast, measurement of the scans revealed atypical perisylvian asymmetries in most of these subjects. The distribution of perisylvian asymmetries in SLI subjects was significantly different from the distribution in controls (p < .Ol). Measurement of other brain regions revealed that extraperisylvian areas were occasionally deviant in individual SLI subjects; but no one region was consistently deviant across the SLI group. Thus, only atypical perisylvian asymmetries were linked to the language disorder. These neuroanatomical findings suggest that a prenatal alteration of brain development underlies specific language impairment. 0 1991 Academic

Press. Inc.

The few available autopsy studies of individuals who had developmental disorders during life have documented that cerebral abnormalities cooccur with various forms of language impairment. Landau, Goldstein, and Kleffner (1960) described the case of a boy who had a severe receptive and expressive language disorder along with a number of other complicating Work at the Child Language Laboratory is partially supported by United States Department of Education Grant No. GOO8630088.Additional funding for this study was provided through the United States Air Force Laboratory Graduate Fellowship Program (F49620-86-C-0127) and Biomedical Research Support Grant S07RR07002. We thank Joachim Seeger, M.D., and the MRI staff at the University Medical Center, whose time and efforts greatly facilitated the MRI portion of this study. Address all correspondence and reprint requests to Elena Plante at The Child Language Laboratory, 33 East Ochoa Street, Tucson, AZ 85702. 52 0093-934x/91 $3.00 Copyright All rights

0 1991 by Academic Press, Inc. of reproduction in any form reserved.

SPECIFIC LANGUAGE

IMPAIRMENTS

53

factors. Most notable among these were possible malnutrition and cyanosis secondary to Taussig-Bing syndrome. Postmortem examination revealed bilateral cortical atrophy in the perisylvian region, extending from the central sulcus into the occipital lobes. Gyri in this region were abnormally small and increased in number relative to normal. Microscopic examination also revealed degeneration of the medial geniculate nuclei and cerebral peduncles. Given this child’s multiple handicaps, it is difficult to generalize these widespread neuroanatomical findings to other cases of developmental language disorder. A second case involved a 7-year-old girl who had marked expressive language deficits and attention deficit disorder with hyperactivity (Cohen, Campbell, & Yaghmai, 1989). The brain of this child showed an atypical symmetry of the plana temporale. Also noted was a small dysplastic gyrus on the left inferior surface of the frontal lobe where it borders the sylvian fissure. While this child’s brain showed fewer abnormalities than those described in the earlier autopsy study, the perisylvian areas were again found to be abnormal. Perisylvian abnormalities were also documented in an autopsy study of four males with developmental dyslexia (Galaburda, Sherman, Rosen, Aboitiz, & Geschwind, 1985). Two of these subjects reportedly had early “speech” difficulties and a third had a marked language impairment. Documentation concerning particular language deficits was unavailable. At autopsy, each of the four subjects had cortical ectopias, predominantly in the left perisylvian regions. All four subjects also had an atypical symmetry of the right and left plana temporale. This symmetry was the result of an atypically large right planum temporale paired with a left planum temporale that was average in size. Common to all these autopsy cases is that some form of atypical or abnormal findings was documented for the perisylvian regions. Given that damage to the left perisylvian region is associated with persistent acquired language disorders in adults (see Rubens, 1984 for a review), these findings are not surprising. The available autopsy studies do not include cases of a well-described language impairment uncomplicated by other medical conditions or additional behavioral disorders. Therefore, whether abnormal perisylvian findings are common to children whose only presenting complaint is a language impairment remains to be investigated. The availability of noninvasive imaging techniques allows for measurement of brain areas in living subjects selected to meet specific behavioral criteria. Of the available studies, two focus on subjects with a documented language disorder. In one study, regional cerebral volumes were obtained from magnetic resonance imaging (MRI) scans of four subjects with auditory agnosia, two of whom also showed some autistic-like behaviors (Filipek, Kennedy, Caviness, Klein, & Rapin, 1987). This rare disorder is typically associated with seizure activity (Deonna, Fletcher, & Voumard,

54

PLANTE ET AL.

1982; Landau & Kleffner, 1957; Msall, Shapiro, & Balfour, Niedermeyer, & Capute, 1986; Rapin, Mattis, Rowan, & Golden, 1977; Wijndaele, Tyberghein, Wellens, De Wijngaert, Casaer, & Casteels-Van Daele, 1981; Worster-Drought, 1971). Compared with normal controls, two of these subjects had significantly reduced cerebral volumes as measured from MRI scans for the posterior, superior temporal lobes bilaterally. No differences were documented for any other cerebral region. A more common form of language disorder occurs in children who do not have additional deficits in cognitive, social-emotional, motoric, or sensory functioning. These children are referred to as specifically language impaired (SLI). The configuration of the cerebral hemispheres posterior to the sylvian fissure was examined in a group of SLI subjects (Jernigan, Tallal, & Hesselink, 1987). While the protocol did not include a measure restricted to the perisylvian areas, atypical cerebral configurations of the hemispheres posterior to the sylvian fissure were noted for some of the subjects. The present study was designed primarily to examine brain regions in a group of children whose language disorder was uncomplicated by other medical conditions or remarkable behavioral deficits. Boys were chosen as subjects because they are disproportionately represented in the language-impaired population (Silva, 1980; Stevenson & Richman, 1976). To further reduce heterogeneity within the study group, all subjects were required to have significant deficits in the comprehension or expression of language form (morphology or syntax). A vocabulary deficit alone did not qualify a child for study. Previous studies demonstrate perisylvian involvement in cases where language impairment is complicated by other medical or behavioral disorders. If perisylvian involvement is a correlate of impaired language, SLI boys will have atypical perisylvian areas. We hypothesize that involvement of the perisylvian area will produce atypical perisylvian asymmetries in SLI subjects. We reason that a process or agent that alters development of the brain, producing atypical perisylvian asymmetries, might also produce changes in extraperisylvian regions. To explore this possibility, selected regions of the frontal, temporal, parietal, and occipital lobe will also be measured to test for atypical volumes. All cerebral measures in SLI subjects will be compared with controls. METHOD Subjects. Eight boys between the ages of 4;2 (years;months) and 9;6 (M&r. = 5;2) participated as subjects in this study. They were recruited by soliciting referrals from professionals serving SLI children in the Tucson area. The first eight referrals who met the inclusion criteria and completed the protocol served as subjects. Each subject was required to be (a) male, (b) between the ages of 4 and 10 years, (c) monolingual English speakers, (d) sufficiently intelligible to permit adequate assessment of language skills, and (e) considered to have a language impairment and no other handicapping conditions by the referral source.

SPECIFIC LANGUAGE

IMPAIRMENTS

55

In addition, norm-referenced tests of nonverbal skills were required to be above - 1.00 SD for the child’s age level on tests of nonverbal skills, and below - 1.64 SD for age level on at least one of the several measures of morphosyntactic skills in the test battery described below. Background characteristics for each of these subjects are provided in Table 1. To corroborate the diagnosis of SLI by standardized testing, two certified speech-language pathologists independently reviewed each child’s case reports. These included therapy records, a medical history, and results of standardized testing, exclusive of those tests of morphosyntactic skills given as part of this study. The standardized tests administered as part of this study were selected according to preestablished criteria. They (a) cover the potential age range of the subjects, (b) have manuals that provide means and standard deviations so that z scores can be calculated (cf. McCauley & Swisher, 1984a), and (c) are also relatively strong psychometrically, compared with other available tests (cf. McCauley & Swisher, 1984b), or had demonstrated utility in identifying children diagnosed as SLI. All language tests in the battery are considered by the authors to be familiar to most speech-language pathologists in the United States. All standardized tests were administered and scored by a speech-language pathologist or a graduate student in speech-language pathology. Those who administered and scored the behavioral measures were unaware of the neuroanatomical findings for each subject. Interrater reliability for test scores was assessedon a point-to-point basis for all storable items on 50% of the tests given. Median reliability was 97% with a range of 75-100%. The results of behavioral testing are displayed in Table 2. Each subject passed a hearing screening prior to behavioral testing. A passing performance consisted of reliable responses to pure tones of 20 dB HL at 500, 1000, 2000, 4000 Hz (American National Standards Institution, 1969). The Kaufman Assessment Battery for Children (K-ABC) (Kaufman & Kaufman, 1983) and the Vinelund Adaptive Behavior Scales (Vineland) (Sparrow, Balla, & Cicchetti, 1984) were used to corroborate reported normal cognitive, social, and motoric functioning. The following tests were used to document significant difficulty with morphosyntactic skills: the Grammatical Closure subtest of the Illinois Test of Psycholinguistic Abilities (ITPA-GC) (Kirk, McCarthy, & Kirk, 1968), Northwestern Syntax Screening TestExpressive (NSST-E) (Lee, 1969), the Test of Auditory Comprehension of Language-Revised (TACL-R) (Carrow-Woodfolk, 1985), and the Token Test for Children (Token) (DiSimoni, 1978). For children above the age of 7;ll the Clinical Evaluation of Language FundamentalsRevised (CELF-R) (Semel, Wiig, & Secord, 1987) was administered. Speech and language tests, in addition to those assessing morphosyntactic skills, were administered to describe additional verbal skills. The Expressive One Word Picture Vocabulary Test (EOWPVT) (Gardner, 1979) and the Peabody Picture Vocabulary Test-Revised (PPVT-R) (Dunn & Dunn, 1981) were used to assess single-word vocabulary skills. The Templin-Darley Test of Articulution (Templin & Darley, 1968) was used to assesssingleword articulation skills. Language samples were collected for subjects ages 7;ll and below. The samples were obtained according to Lee (1974). After transcribing the language sample, trained graduate assistants analyzed them using Developmental Sentence Scoring procedures (Lee, 1974). Twenty percent of each child’s utterances were selected at random for reliability checks. Point-to-point reliability for the language transcriptions ranged from 81 to 99%; occurrence reliability for the analysis procedures ranged from 71 to 98% with a median reliability of 90%. Disagreements in scoring were resolved through joint review of the items in question. Twenty-one boys were referred for study. In order to establish a clear relation between neuroanatomy and specific language impairment, boys who did not meet our criteria for SLI as described above were excluded from the study. Six were excluded because their language skills were not significantly impaired. Four had other handicapping conditions (i.e., attention deficit disorder, mild hearing loss, low nonverbal cognitive skills) that would confound the interpretation of any brain-language relation. One was excluded because of

2 brothers, 4 halfbrothers (father’s)

Right

Ambidexterous

Handedness

1 sister

3 years

2 years

Age problem was noted

Family history Siblings

3

2

gen at birth

3 weeks pre-

mature, oxy-

3 weeks

premature

2

Birth order

Personal history Perinatal risk

1

BACKGROUND

2 brothers, 3 sisters

Right

1;6 years

5

Cesarian

3

CHARACTERISTICS

2 sisters (died as neonates), 2 halfbrothers (mother’s)

1 brother, 1 sister

Right

2 years

2;6 years Left

2

4

None reported

6

PARENTS

1 brother (3 miscarriages)

Right

3 years

1

Cesarian

AS REFQRTED BY THEIR

Subject

Induced labor, Cesarian

4

TABLE 1 SLI Bovs

OF

1 sister (1 miscarriage)

Right

1;6 years

1

None reported

7

-

2 sisters, 3 halfbrothers, 2 halfsisters (father’s)

Right

2 years

2

None reported

8

F-

$

3

None

None

Mother (fraternal)

Left handedness

Twins

Maternal cousins (fraternal), halfbrothers (identical)

Speech language, attention deficit (brothers and parents), mental retardation, cerebral palsy (halfbrothers)

Dyslexia Autism, attention deficit (cousins)

Developmental disabilities

Subject (fraternal)

Sister

activity (maternal uncle)

Hyper-

Sisters (fraternal)

None

Dyslexia (halfbrothers)

Maternal cousins (fraternal)

Father

None

None reported

None

None reported

None reported

None

Dyslexia (mother, maternal cousin, paternal uncle) , speech (sister)

half-brothers (fraternal)

Mother

Language (father, patemal uncle, and sister), speech (mother)

Y

2CA

E

2 B

K

2

F

5 ij

6 E

.

* * ‘1.66

* * -1.07

* *

-2.91

0.72

* *

0.40 -0.33

-0.13 -0.80

0.00 - 0.47

~ 1.15 - 2.41 -2.17 -0.33 0.00

-0.20 -0.93

-1.00 -2.78 - 0.66 -0.20 N.C.

-3.00 -5.10 -1.18 -0.95 N.C.

0.67

5;O

5

- 1.98

* *

-2.07 - 0.46

* * * *

- 1.82 -3.33 -2.71 - 1.75 - 1.05

-0.80 0.33 - 0.87 0.13 - 0.47 0.87 (All subjects passed)

* * * *

- 2.35 -5.10 -0.66 -0.52 - 1.00

0.07 0.33 -0.80

1.20 -0.47 -0.67

0.60

4;9

4

* * * *

1.40 0.73 0.47

-0.77

0.27

4;8

0.00

4;2

4;2

3

TESTING’

” All scores expressed as units of standard deviation (z-scores) from the normative sample mean. * Test was not administered because it was not appropriate for the child’s age. N.C:The test was discominued because the child failed to demohstrate knowledge of co

General functioning K-ABC Vineland Daily living Socialization Motor Hearing screening Morphosyntactic skills DSS NSST-E ITPA-GC TACL-R Token CELF-R Oral directions Formulated sentence Recalling sentence Sentence assembly Semantics PPVT-R EOWPVT CELF-R Word classes Semantic relations Articulation Templin-Darley

Age:

2

1

TABLE 2 RESULTS OF BEHAVIORAL

-0.53

* *

- 0.87 -0.80

- 1.68 -3.30 - 1.00 -0.52 ~ 1.58

1.07 0.20 0.20

1.11

5;2

6

e

-0.79 -0.50 -1.94 -0.79 - 1.08 - 1.63

th t&s&.

0.52

-0.67 -1.34

0.54 0.40

~

*

~~

-2.05 -0.68

0.00 0.33

-2.33 -0.68 -0.68 -1.00

* * * *

-1.64 -1.67 0.00 -1.34

0.66 -0.53 *

- 0.07

9;6

8

0.27 -0.33 *

-0.13

8;2

7

$

2

% 2

4

F

3

SPECIFIC LANGUAGE

IMPAIRMENTS

59

FIG. 1. Cerebral regions measured from MRI scans. a history of seizures, which are associated with acquired language disorders in children (c.f. Landau & Kleffner, 1957). Two potential subjects qualified for inclusion, but failed to complete the MRI portion of the study. Procedures. MRI scans were obtained using a Toshiba scanner (0.5 Tesla). Five-millimeter contiguous slices were obtained in the axial plane. Twenty axial slices, covering the full volume of the cerebrum, were obtained. The slice angle was standardized by aligning slices parallel to a line connecting the inferior edge of the frontal lobe with the inferior edge of the occipital lobe. This minimized measurement variability due to head tilt among subjects. Spin-echo sequence used a repetition time (TR) of 2800 with an echo time (TE) of 90. Subjects below age 8;0 were given a mild sedative (chloral hydrate) to facilitate their ability to remain still throughout the scan. Total scan time was 27 min. Scans from the eight SLI subjects were compared with eight control scans drawn from a bank of scans obtained on volunteers. The eight scans were selected at random from a group of scans that met the following criteria: Scans were from male volunteers who had no personal or familial history of language impairment, no medical conditions known to alter brain anatomy (e.g., stroke, trauma, or seizures), and had no medical reason to be scanned. Because the SLI subject group had a high rate of twinning in their family histories, volunteers with a family history for twinning were likewise excluded. The eight controls selected were all right handed. The scans were clinically evaluated as normal by a neuroradiologist who was not otherwise associated with this study. Prior to quantitative analysis, identifying information was removed from the scans to ensure that those measuring the scans were blind to each subject and control’s language status. Two groups of neuroanatomical measures were completed. The first involved the perisylvian area. As measured in this study, the perisylvian area in each hemisphere contains portions of the frontal and parietal operculae, superior temporal gyrus, and planum temporale. The perisylvian area is delineated by tracing a line from the posterior edge of the sylvian fissure to the edge of the cortex. The tracing follows the cortical edge forward to the inferior frontal gyrus. A straight line connects this point back to the starting point. The area contained within this outlined region is calculated. This procedure is completed on all slices in which a sylvian fissure can be identified in the left and right hemispheres, and the successive areas are summed to provide the total perisylvian area. A sagittal view of the perisylvian area is included in Fig. 1. In order to determine whether atypical perisylvian asymmetries characterize SLI boys, a measure of perisylvian asymmetry (right perisylvian

60

PLANTE ET AL.

volume/left perisylvian volume) was calculated. Perfect symmetry produces a quotient of 1.OO.Quotients that reliably (p < .lO) reflect asymmetry are those that exceed measurement error by more than * 1.64 SE. Given a standard error of 0.03 for perisylvian asymmetries, quotients exceeding 1.05 are classified as R > L, while those less than 0.95 are classified L > R. All others are classified L = R. Only asymmetries of L > R are considered typical in that this is the most frequently occurring pattern in the general population (Chi, Dooling & Gilles, 1977a; Geschwind & Levitsky, 1968; Wada, Clarke, & Hamm, 1975; Witelson & Pallie, 1973). The perisylvian region will be examined further by comparing the proportional volumes of the right and the left perisylvian areas to those in control scans. This allows further description of the perisylvian areas. In order to determine whether widespread effects on the brain are apparent, additional neuroanatomical measures were developed. Like the measurement protocol for the perisylvian area, these measures were designed to follow anatomical landmarks that were readily visible across scans. Use of such landmarks increases the chance of detecting variations in neuroanatomy across individuals. A sagittal view of the regions measured is provided in Fig. 1. Detailed descriptions of measurement protocols for each neuroanatomical region are provided elsewhere (Plante, 1990). All regional measures are expressed as a proportion of total brain size to stabilize the values for differences in head sizes across subjects. Measurement reliability was assessed using a Pearson product-moment correlation for each anatomical region measured. Reliability was assessedfor 50% of the scans (selected at random). Acceptable reliability was defined as an ? value of .70 (r = .84) and above for a series of measures. The r values ranged from .85 to .99 with a mean of .92.

RESULTS Table 3 displays the results of the perisylvian measures. The distribution of perisylvian asymmetries in the SLI subjects was significantly different from the distribution in controls (t = 2.67, df = 14; p < .Ol). This group difference was also apparent when the data were analyzed on a subjectby-subject basis. Six of the eight SLI subjects had atypical perisylvian asymmetries (R = L and R > L), whereas only two of the eight controls had an atypical pattern (R = L). An examination of the proportional volume data for the left and right perisylvian areas indicates that the right perisylvian areas for the group of SLI subjects was significantly larger (t = 3.12, u’f = 14; p < .Ol) than this area in controls. No significant differences (t = 1.26, df = 14; NS) were detected for the size of the left perisylvian area between subjects and controls. This group pattern also held when SLI subjects were examined on an individual basis. For each SLI subject who had atypical perisylvian asymmetries, the asymmetry was comprised of an atypically large (z > 1.35) right perisylvian area paired with a left perisylvian area that was of the expected size (z < + 1.35). Table 4 contains the results of the extraperisylvian measures. An examination of the ranges for these proportional volumes demonstrates that there are marked differences in the amount of neuroanatomical variability for the SLI subjects and controls. This variability, as high as 4.45: 1 (subjects:controls), violates a basic assumption for using an ANOVA to compare these regions across the two groups. Mann-Whitney U tests

SPECIFIC LANGUAGE

61

IMPAIRMENTS

TABLE 3 PERISYLVIAN FINDINGS IN BOYS WITH SPECIFICLANGUAGE IMPAIRMENT AND IN CONTROLS

Asymmetry Quotient SLI subjects 1 2 3 4 5 6 7 8

1.04 0.83 0.98 1.09 0.91 1.15 1.10 1.01

Proportional volume” Type

R=L L>R R=L R>L L>R R>L R>L R=L

Right

2

Left

z

2.23 1.83 2.17 2.14 1.89 2.41 2.67 2.26

1.93 0.14 1.66 1.51 0.37 2.76 3.93 2.08

2.13 2.22 2.21 1.97 2.08 2.10 2.44 2.25

0.36 0.67 0.64 -0.19 0.19 0.26 1.41 0.78

Mean SD

1.01’ 0.11

(L = R)

2.20 0.27

1.80 1.22

2.18 0.14

0.52 0.48

Controls Mean SD

0.90 0.06

O- > RI

1.80 0.22

0.00 1.00

2.02 0.29

0.00 1.00

” Percentage of total brain volume. ’ In comparison to the control group. ’ Significantly different (p < .Ol).

failed to reveal any significant (p < .05) differences between SLI subjects and controls for any of the extraperisylvian regions. Nonsignificant findings occurred despite the fact that five of the SLI subjects had regions which were significantly deviant (z > 2 1.96; p < .05) compared with the group of control subjects. An examination of the proportional volume values for individual SLI subjects suggests that values for some of these areas may prove to be bimodally distributed in a larger sample of SLI boys. DISCUSSION The neuroanatomical results in this sample of boys with SLI demonstrate that atypical perisylvian findings occurred at rates that are above chance (p < .Ol). Six of the eight SLI boys had atypical perisylvian asymmetries. In each case, atypical perisylvian asymmetries resulted because the right perisylvian area was larger than expected (p < .Ol), while the left was of the expected size. Similar findings have been described for one perisylvian structure, the planum temporale, in subjects with developmental disorders that include some form of impaired language (Cohen et al., 1988; Galaburda et al., 198.5).The present findings indicate that previous reports of atypical perisylvian areas in individuals with developmental disorders that include impaired language generalize to children whose

1.64 1.52

1.35 1.29

0.81 0.73

1.12 0.99

1.09 0.99

1.24 1.14

4.69 5.26

1.86 1.95

1.70 1.46

0.66 0.66

1.70 1.48

0.50 0.44

1.70 1.48

3.43 4.25

1.74 1.34

1.06 1.21

1.23 1.09

1.20 1.03

1.52 1.44

3.96 3.89

3

1.71 1.95

2

VOLUMES

TABLE 4

4.42 4.83

1.32 1.37

0.59 0.33

1.97 1.85

1.20 1.20

2.10 1.76

2.24 2.26

4

4.46 4.48

1.65 1.24

1.03 1.05

0.94 0.86

0.76 0.77

1.79 1.56

1.72 1.95

5

4.75 4.76

1.59 1.72

0.63 0.60

1.33 1.41

0.55 0.80

1.26 1.02

1.44 1.43

6

SLI boys

4.82 4.99

1.75 1.40

1.24 1.32

1.12 1.16

1.03 1.02

1.33 1.20

1.75 1.59

7

FOR BOYS WITH SPECWIC LANGUAGE

Bolded values correspond to 2-scores of greater than + / - 1.96 (p < .05).

Superior frontal Right Left Middle frontal Right Left Inferior frontal Right Left Superior temporal Right Left Middle temporal Right Left Supramarginal/angular Right Left Occipital Right Left

1

PROFQRTIONAL

4.78 5.13

1.66 1.67

1.79 1.32

2.00 1.60

0.67 0.62

1.54 1.30

1.90 1.97

8

IMPAIRMENT

4.41 4.68

1.55 1.40

1.01 0.90

1.41 1.31

0.84 0.88

1.62 1.23

1.81 1.88

Mean

SD

0.49 0.46

0.18 0.22

0.43 0.40

0.44 0.63

0.24 0.25

0.30 0.38

0.26 0.29

AND CONTROLS

4.17 4.37

1.27 1.24

1.05 1.08

1.52 1.77

0.89 0.87

1.41 1.38

1.87 1.77

Mean

SD

0.70 0.59

0.24 0.21

0.12 0.16

0.29 0.27

0.12 0.20

0.44 0.43

0.50 0.50

Controls

SPECIFIC LANGUAGE

IMPAIRMENTS

63

deficit is relatively restricted to language. Overall, it appears that an atypical perisylvian configuration may be a neuroanatomical marker common to a range of disorders that include poor language skills. If so, it appears that the perisylvian areas are as important to normal language functioning in the developing brain as they are to the mature brain. This association is explored further in the companion paper (Plante, 1991). The results of other neuroanatomical measures suggest that widespread, bilateral involvement was present in the subjects. There were individual differences, however, in the extraperisylvian areas that were atypical across subjects. Thus, no statistically significant differences occurred between the SLI subjects and controls for any one extraperisylvian area. The type of atypical findings across both the present and previous studies suggests that an alteration of the normal course of brain development occurred, as opposed to damage that occurred following normal prenatal development. The finding of atypically large right perisylvian areas provides converging evidence for an effect that alters development. Brain development is characterized by an overproliferation of neurons that migrate out to the cerebral surface. The number of neurons are later reduced during a period of programmed cell death. A finding of atypically large cerebral volumes suggests a failure of regressive events which occur late relative to the prenatal developmental course of the affected region. The present finding that the left perisylvian area was of the expected size does not necessarily indicate that its development followed a normal course. An agent first acting during the period of cell generation may have limited cell birth or migration. This effect can be mitigated if the agent also acts to limit the normal period of cell death. The combination of effects would not produce an effect that is detectable within the limits of MRI. This interpretation, in the case of the findings for the perisylvian areas, is consistent with previous documentation that perisylvian structures including the superior temporal gyrus and the planum temporale develop earlier in the right than in the left hemisphere (Chi et al., 1977a). Thus, one agent could result in a large right perisylvian area and a normally sized left. In humans, cerebral asymmetries appear during the third prenatal trimester (Chi, Dooling, & Gilles, 1977b; Witelson & Pallie, 1973). The distribution of these asymmetries in fetuses, infants, and adults is constant (Chi et al., 1977b; Wada et al., 1975; Witelson & Pallie, 1973). Thus, atypical asymmetries will occur if some factor alters the pattern of cerebral development during the prenatal period. Gonadal hormones have been suggested as one explanation for the cooccurrence of altered brain development and impaired language skills (cf. Geschwind & Behan, 1982). Experimental manipulations of either endogenous or exogenous hormone levels alter neuronal volumes in the developing brain (Diamond, Dowling, & Johnson, 1981; Dodson, Shryne,

64

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& Gorski, 1988, Gorski, Gordon, Shryne, & Southam, 1978; Jacobson, Csernus, Shryne, & Gorski, 1981; Pappas, Diamond, & Johnson, 1978; Pfaff, 1966; Sandhu, Cook, & Diamond, 1986). Hormonally induced changes can be sufficiently large and widespread to alter the typical pattern of hemispheric asymmetries (Diamond et al., 1981; Pappas et al., 1978; Sandhu et al., 1986). The action of gonadal hormones in utero may also account for aspects of the familial background common in this sample of SLI boys. One signal of a hormonal role is the surprisingly consistent finding of dizygotic twinning in their families. Dizygotic twinning has been associated with high levels of gonadotrophic hormones (Milham, 1964). The presence of dizygotic twinning suggests that ambient conditions existed which increased the likelihood that these boys were exposed to high levels of gonadal hormones in utero. The same ambient conditions would also place other siblings at risk for developmental disorders commonly associated with impaired language. Such conditions would also explain the prevalence of language and learning disorders among the siblings of these SLI boys. The prevalence of such disorders in the families of our SLI subjects is not unusual; language and learning difficulties appear to occur at high rates in the families of SLI children, suggesting that the disorder has a heritable component (Neils & Aram, 1986; Tallal, Ross, & Curtiss, 1989; Tomblin, 1989). The familial constellations of impaired language and atypical brain configurations are explored in the companion paper (Plante, 1991). The atypical neuroanatomy observed in this study indicates that specific language impairment is, in fact, a “developmental language disorder.” Not only were language behaviors which develop over time affected in this sample of children, but also an alteration of the normal course of brain development appears to have occurred. Neither damage that occurred after normal brain development nor caregiving practices could account for the present findings. REFERENCES American National Standards Institution. 1969. Specifcufion for audiometers. ANSI S3.61969. New York: American National Standards Institute, Inc. Bloch, G. .I., & Gorski, R. A. 1988. Cytoarchitectonic analysis of the SDN-POA of the intact and gonadectomized rat. Journal of Comparative Neurology, 275, 604-612. Carrow-Woodfolk, E. 1985. Test of Auditory Comprehension of Language-Revised Allen TX: DLM Teaching Resources. Chi, J. C., Dooling, E. C., & Gilles, F. H. 1977a. Gyral development of the human brain. Annals of Neurology, 1, 86-93. Chi, J. G., Dooling, E. C., & Gilles, F. H. 1977b. Left-right asymmetries of the temporal speech areas of the human fetus. Archives of Neurology, 34, 346-348. Cohen, M., Campbell, R., & Yaghmai. 1989. Neuropathological abnormalities in developmental dysphasia. Annals of Neurology, 25, 567-570.

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