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DOI: 10.1148/radiol.2293021746
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(Radiology 2003;229:651-658.)
© RSNA, 2003

Pediatric Imaging

Speech Delay in Children: A Functional MR Imaging Study1

Byron Bernal, MD and Nolan R. Altman, MD

1 From the Department of Radiology, Miami Childrens’ Hospital, 3100 SW 62nd Ave, Miami, FL 33155. From the 2002 RSNA scientific assembly. Received December 16, 2002; revision requested February 27, 2003; final revision received July 9; accepted July 16. Address correspondence to N.R.A. (e-mail: nolan.altman@mch.com).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To determine if children with speech delay who have been sedated have patterns of activation to passive language paradigms that are different than those of children with normal speech.

MATERIALS AND METHODS: Seventeen children with speech delay (age range, 2–7 years; mean, 4.0 years) and 35 age-matched children with normal speech (age range, 2–8 years; mean, 4.2 years) were evaluated. The subjects in the control group were selected from patients referred for conventional magnetic resonance (MR) imaging. All children had absence of auditory impairment or mental retardation, and MR findings indicated that brain structure was normal. Sedation was achieved with pentobarbital (3–5 mg/kg) or chloral hydrate (75 mg/kg). Functional MR imaging was performed with a single-shot echo-planar blood oxygen-level–dependent technique and a passive block paradigm, in which the child listened to his or her mother’s prerecorded voice. Statistical postprocessing of functional MR images was performed with the t test and cluster detection methods. Comparison between groups was performed depending on the type of data with a nonparametrical Mann-Whitney test, parametrical t test, or Fisher exact test.

RESULTS: Five (83%) of the six children older than 3 years with speech delay had lateralized activation of functional MR imaging signal in the right hemisphere. Ten (71%) of 14 age-matched patients with normal speech had activation in the left hemisphere when exposed to the same passive listening tasks. When these groups were compared, this difference was statistically significant. (P = .036). No statistically significant lateralization was seen across all age groups in children with activation.

CONCLUSION: Children older than 3 years with speech delay have activation in the right hemisphere more frequently than children older than 3 years with normal speech, who often have the expected finding of activation in the left hemisphere.

© RSNA, 2003

Index terms: Brain, growth and development • Brain, MR, 138.121413 • Magnetic resonance (MR), functional imaging, 138.121413 • Magnetic resonance (MR), in infants and children, 138.121413 • Speech


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Functional magnetic resonance (MR) imaging has been used extensively as a method for studying language in adults (1–7) and children (8–10). The vast majority of these examinations have been performed while patients are awake so that they can cooperate and perform the verbal tasks. Functional MR examinations have also been performed in sedated children by using verbal stimulation that elicited primary and secondary auditory cortex activation (11,12). Applications of functional MR imaging with sedation offer substantial potential for the assessment of language development and disorders in the pediatric patient.

Speech delay encompasses a broad spectrum of conditions with confusing nomenclature (13) and is classified as a communication disorder of childhood in subsections 315.31 and 315.32 of the Diagnostic and Statistical Manual of Mental Disorders DSM-IV (14). These disorders are characterized by a rate of acquisition of speech skills that is slower than normal.

Speech disorders are differentiated from language disorders. Speech refers to the articulation of sounds, and it is the part of language that deals with communication and cognition. Speech disorders may be due to isolated expressive problems, but comprehension always affects expression. The prevalence of speech delay in 6-year-old children in the United States is 3.8% (15). Speech delay is approximately 1.5 times more prevalent in boys (4.5%) than in girls (3.1%) and varies with communal, racial, and cultural backgrounds (15). Shriberg et al found that 11%–15% of children with persistent speech delay have language impairment, although only 5%–8% of children with language impairment have speech delay (15).

There is no clearly defined predictor for language and speech problems in school-aged children (13). Speech delay has many causes and names, including mixed expressive/receptive language disorder, expressive language disorder, developmental language delay, developmental language disorder, and developmental language impairment (16,17). In a patient with any of these disorders, motor skills are preserved, and the rest of the developmental milestones are acquired at an appropriate age. There are no overt abnormalities or underlying neurologic conditions. These children lend themselves to evaluation with sedation and passive paradigms because of the obvious difficulties of cooperating with task performance and remaining still for the examination.

The purpose of this study was to determine if children with speech delay have different patterns of activation to passive language paradigms compared with children with normal speech.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients
Fifty-seven children aged 2–8 years were sequentially selected from patients referred for MR imaging examinations. The sample size was the result of a period of recruitment between June 1999 and October 2002. We chose this period to maintain consistency of the hardware and software, which quickly becomes obsolete. This constraint ensured homogeneity throughout the entire process. The control group consisted of 36 of the 57 children who were referred for headaches, syncope, febrile seizures, or extracranial benign lesions. One patient was excluded because he was younger than the children with speech delay. This resulted in a control group of 35 children with a mean age of 4.2 years ± 1.4; 16 patients were boys (mean age, 3.75 years ± 1.12) and 19 were girls (mean age, 4.6 years ± 1.49). Nineteen of these children were included in a previous study (11). In the control group, the right hand was dominant in 24 subjects, the left hand was dominant in four, and the dominant hand was unknown in seven.

The group of patients with speech delay initially consisted of 21 of the 57 patients referred to our center for speech delay, which was diagnosed with a neurologic examination. Of the four patients excluded from the study, three developed autism, and in one, the data were corrupted and could not be salvaged. This resulted in a group of 17 patients with a mean age of 4.0 years ± 1.52; 11 were boys (mean age, 4.18 years ± 1.32) and six were girls (mean age, 3.8 ± 1.9). In the group of patients with speech delay, the right hand was dominant in 10 patients, the left hand was dominant in two, and the dominant hand was unknown in five.

Each group was separated into two age categories, as shown in Table 1. All children had normal audiograms and results of brainstem electric response audiometry, which ruled out hearing loss. In addition, all children underwent neurologic developmental screening examinations that were performed by the same neurologist (B.B.). The findings of a neurologic examination had to be normal for inclusion in the study. The neurologic examination consisted of general questions of family history, hand dominance, hearing loss, and learning disabilities. Patients were excluded if they had a history of exposure to ototoxic antibiotics, head injuries, intracranial infection, hearing loss, global developmental delay, or autism or if the results of brain MR imaging were abnormal. Our referral region has a large bilingual population. Determining that one of the parents spoke a foreign language at home defined a bilingual environment. Informed written consent was obtained from the parents, and the hospital’s institutional review board approved the study.


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  		TABLE 1. Age of Subjects and Patients

 
Imaging and Stimuli
Imaging was performed with a 1.5-T MR unit by using a birdcage quadrature-transmit-and-receive head coil that was designed for whole-brain imaging. Image acquisition and processing have been previously reported (11); however, a brief description follows. A series of 16 localizer images were obtained in the sagittal plane. Ten transverse section locations were selected parallel to a plane defined by a line between the basal aspects of the frontal and occipital lobes for MR and functional MR examinations. The MR images were obtained with T1-weighted spin-echo acquisitions (repetition time msec/echo time msec, 300/14; field of view, 240 mm; matrix, 256 x 256 pixels; section thickness, 6 mm; and section gap, 2 mm). Functional images with the same section thickness and gap were obtained with gradient-echo single-shot echo-planar acquisitions (3,750/60; flip angle, 60°; field of view, 240 mm; and matrix, 64 x 64 pixels). The experiment consisted of one run of 48 time-points (sets) of 10 images, with two extra sets at the beginning of the series, used to obtain the steady state of transverse magnetization. The 48 time-points were divided into six epochs, three off (baseline condition) and three on (activated condition). The experiment was started in the off epoch and switched epochs every 30 seconds. Thus, each section was imaged 48 times, which resulted in a total of 240 image pairs for comparison.

Functional MR imaging data were processed off-line with software (MEDx 3.4; Sensor Systems, Sterling, Va.) functioning with a Linux (Red Hat, Raleigh, NC) platform at a workstation (Intel, Santa Clara, Calif). Time-point images were first analyzed to detect motion, comparing the center of intensities of the total of images acquired by using the intensity-weighted method module provided with the computer software. The images were spatially smoothed with a gaussian kernel of full-width-at-half-maximum of 7 x 7 x 10 mm for the x, y, and z axes, respectively, to reduce noise in the images. Intensity normalization was applied to normalize the signal of each voxel and remove the effects of signal drift.

The children were administered a sedative by a radiologist (N.R.A.). Pentobarbital was administered with a single bolus dose of 3–7 mg/kg in all but one patient. Chloral hydrate was administered orally at a dose of 75 mg/kg in the one remaining patient. All subjects received 6% O2 by face mask for the length of the procedure. The MR imaging examination was performed first and the functional MR imaging examination followed if the patient remained in a state of sedation. This resulted in performance of the functional MR examination 45–90 minutes after the onset of sedation. The auditory stimulus was delivered through generic headphones that were connected by insulated tubing to a pair of generic 40-W speakers located inside an aluminum box placed close to the magnet. The stimulus was a recording of the child’s mother speaking familiar and endearing words; recalling relatives, pets, and events; and singing familiar songs. Mothers were encouraged to use intonation and infant-directed prosody, according to the theory of "motherese" (18,19). The speech was recorded in an isolated room for 2 minutes, and the mothers were instructed to speak at a normal volume. The volume was then adjusted by the examiner, who used a digital equalizer range spectrum display to maintain similar volume levels among subjects and across groups.

Statistical Analysis
For functional MR data analysis, parametrical statistical maps were obtained in each series by using an unpaired t test and computing the differences of the intensities between the test (on) and control (off) epochs. The initial off epoch was made one time point longer to take into account the hemodynamic response lag.

Two methods were used to determine the activation maps. We will call the first method first level analysis. In this method, we looked at the individual areas of activation with a voxel-by-voxel statistical analysis of the intensities. For the z-score maps yielded by the t test, activation was defined as positive in voxels, where uncorrected P values were less than .0005 (z-score threshold, 3.28). This method has been used by other authors with even lower values to limit false-positive results (20,21), and it has been a standard procedure in positron emission tomographic examinations (22). Additional criteria of positive activation include clusters of more than 4 voxels in extent located in the cortex.

In the second level analysis, we looked at groups of activation, and this analysis was performed by using cluster detection techniques that allow comparison between the patient groups and determination of localization of the center of the clusters. This procedure follows the method of Forman et al (20) by using either a z score of 3.0 and {alpha} < .1 or a z score of 2.33 and {alpha} = .05. This restricts the false-positive results for an 11-voxel cluster to a range between .05 and .01 (18).

The midline location in the x axis was manually determined by a radiologist (N.R.A.) from the first echo-planar image of each subject obtained at the level of the third ventricle to correct for off-midline displacement among subjects. This process allowed localization and lateralization of the clusters. A ratio of activation was determined by dividing the number of voxels activated by the number of total voxels. This controlled for differences in head size among subjects when groups were compared.

Areas of activation were assigned to a lobe by consensus on the basis of first level analysis and anatomic localization by superimposing the functional MR images on T1-weighted MR images of the same patient at the same location. In each patient, the lateralization index was defined as the total voxels activated in the left hemisphere minus the total voxels activated in the right hemisphere, divided by the total voxels activated in both hemispheres, and multiplied by 100 (23–25). Midline voxels were excluded within 4 voxels of the midline to avoid any uncertainty close to the midline. Negative values correspond to right hemisphere localization and positive values correspond to left hemisphere localization, with a tolerance of 10%. Lateralization and extent of the activation were statistically analyzed in groups and subgroups. Automatized functional MR imaging group analysis was attempted with the FSL module of MEDx; however, this attempt was unsuccessful. This was due to difficulties in coregistration to a normalized template.

Statistical analyses of the independent variables were performed, and the subjects in the control group were compared to the group of patients with speech delay. Subgroups based on age and sex were also analyzed. Dependent variables analyzed were activation ratio, lateralization index, number of subjects with a positive lateralization index, number of subjects showing activation, presence of activation, and location of activation. The Mann-Whitney test, parametrical t test, and Fisher exact test were used in the calculation of statistics. P values less than .05 indicated a significant difference. Statistical software (SAS/STAT; SAS Institute, Cary, NC) was used.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
Individual results for subjects are shown in Tables 2 and 3. Twenty-five (71%) of 35 patients in the control group and 11 (65%) of 17 patients in the group with speech delay showed activation at the first level analysis. Figure 1 shows the distribution of activation in the different lobes. Activation followed similar profiles between the groups, except in the temporal lobes. Activation occurred more often in the left temporal lobe in 13 (52%) of 25 patients in the control group. Activation occurred more often in the right temporal lobe in seven (64%) of 11 patients with speech delay (Fig 2).


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  		TABLE 2. Patient Data and Functional MR Imaging Results

 

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  		TABLE 3. Statistical Results

 


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  		Figure 1. Graph shows regions of activation in patients with normal speech (black bars) and speech delay (gray bars). Notice the predominance of temporal and frontal lobe activation and the difference between left and right temporal lobes between the groups. LO = left occipital, RO = right occipital, LT = left temporal, RT = right temporal, LF = left frontal, RF = right frontal, LP = left parietal, RP = right parietal.

 


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  		Figure 2. Auditory passive paradigms in a 5-year-old boy with speech delay (left) and a 5-year-old boy with normal speech (right). Colored areas of activation are depicted over transverse T1-weighted MR (300/14) images. Intensity is indicated by colors. Yellow indicates the highest intensity; green, high intensity; blue, low intensity; and purple, lowest intensity. The image of the patient with speech delay demonstrates activation in the right temporal lobe, whereas the image of the subject with normal speech demonstrates activation in the left.

 
The mean lateralization index number was positive (left sided) in the control group (27.83) and negative (right sided) in the group of patients with speech delay (-24.0), but a large SD (79.12 and 73.79, respectively) diminished the significance of the differences (P = .075, Mann-Whitney test). There was, however, significant association between the lateralization index number and the subgroups of children older than 3 years. In the control subgroup, 10 of 14 subjects older than 3 years had a positive lateralization index number, whereas one of six patients older than 3 years with speech delay had a positive lateralization index number (P = .04, Fisher exact test) (Fig 3). This indicated with statistical significance that children with speech delay have activation in the right hemisphere, and age-matched children with normal speech have activation in the left hemisphere.



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  		Figure 3. Graph shows number of patients over 3 years of age in the control group and in the speech delay group with left (black bars) or right (gray bars) hemisphere dominance, assigned by lateralization index sign (positive for left hemisphere dominance, and negative for right hemisphere dominance). The differences are statistically significant (P = .036, Fisher exact test).

 
There was no significant difference in the number of subjects with activation in each group, as 22 (63%) subjects in the control group and nine (53%) patients with speech delay (P = .19, Fisher exact test) had activation. There was, however, a trend, in which seven of 22 children with normal speech had more frequent activation than six (60%) of 10 patients with speech delay (P = .2, first level analysis). No differences were observed when comparing the activation ratios between groups (P = .77 Mann-Whitney test). No statistically significant difference in the number of patients with activation was observed when comparing the younger to older age groups in 14 (64%) of 22 subjects in the control group and in six (60%) of 10 patients with speech delay (P = .3, Fisher exact test). Activation ratios showed no differences between the younger and older subgroups (P = .96, Mann-Whitney test). There was a trend for girls to have greater activation ratios than boys in the control group but not in the group of patients with speech delay (P = .07 and P = .52, respectively). The rate of bilingualism was slightly more prevalent in the patients with speech delay than in the subjects in the control group (88% vs 71%, respectively), but this difference was not statistically significant (P = .2, Fisher exact test).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
REFERENCES
 
Children with speech delay do not differ significantly from children with normal speech, either in their ability to demonstrate activation and patterns or ratios of activation or in the lateralization index when all groups are combined. When children older than 3 years are considered, however, a significant difference appears in the frequency of lateralization of the activation. Children with speech delay have lateralization in the right hemisphere, and children with normal speech have lateralization in the left.

Previous studies have shown linguistic discrimination is present in infants as young as 2 months (26,27). Other studies have indicated that there is well-established left hemisphere dominance for simple auditory tasks in young children (28).

We do not conclusively demonstrate differences in hemisphere activation index between the groups due to the limited sample size that cannot compensate for the large variance observed. There is, however, a clear trend and a significant difference in the distribution of frequency of the subjects’ lateralization in the older subgroup. The right hemisphere dominance that is seen in older children with speech delay needs to be further studied with a larger sample size in children who are conscious and children who are sedated. To our knowledge, this is the first functional MR imaging study conducted in patients with speech delay. Previous investigators have used positron emission tomography in children with developmental dysphasia. A dichotic listening task revealed that children with developmental dysphasia differed from children with normal speech who had Duchenne muscular dystrophy in that they had increased metabolism in the right hemisphere in the Broca region (29). Altered hemispheric asymmetries have also been described in patients with speech delay, as compared with patients with normal speech, by using event-related potentials (30).

Increased frequency of right hemisphere activation in children older than 3 years with speech delay may be caused by increased activation in the right hemisphere or decreased in activation in the left hemisphere. Lack of activation in the left hemisphere may be caused by an inability to settle and process language or the release of an inhibitory factor in the left hemisphere. Alternatively, the right hemisphere could be more involved because of the preponderance of affective prosody, which appears to be a function of the right hemisphere (31). If activation of the left hemisphere is truly decreased, the right hemisphere dominance, which is based on the lateralization index, could be considered an epiphenomenon. Studies have also demonstrated a particular excitatory state of the left hemisphere associated with acceleration of vocabulary acquisition in children younger than 22 months (32). This state may be delayed or lacking in the children with speech delay.

Patients with speech delay have difficulty transferring information from the left to the right hemisphere, which suggests a dysfunction in the corpus callosum (33). This may be because information originates in the right hemisphere and the maturation of the right hemispheric fiber crossing network is delayed (34).

The implications of this lateralized pattern of response to auditory stimulus in children with speech delay is unknown. Neurophysiologic studies have been performed with evoked potentials in children during the first few years of life in an attempt to establish the validity of a variety of factors in predicting long-term outcomes of language development (35). Molfese and colleagues studied whether general hemispheric differences or specific lateralized discrimination abilities could be used to identify children who would develop poor language skills. Event-related potentials were conducted longitudinally in 16 (36) and 54 infants (37) during the first 3 years of life. Event-related potentials were recorded from the left and right temporal areas every 6 months in response to a synthetic speech stimulus. Molfese and Molfese (36) found that electrophysiologic data recorded at birth could identify children who would perform better or worse on language tasks 3 years later. They found the best predictor of success was left-lateralized discrimination between consonants either alone or in combination with different vowel sounds. Accordingly, we believe that early differences in brain activation, as demonstrated on functional MR imaging studies with auditory passive tasks containing phonemes, words, and sentences, may identify and predict children who may have speech delay.

There are several potential pitfalls in our study. Bilingualism is prevalent in our community. This has been implicated as a cause of speech delay, but its effect may be overestimated (38). A study of the same community from which our sample was taken shows that the exposure of Hispanic children to English does not harm development of language (39). Other investigators have found a mild delay in the onset of language when two languages are learned concurrently; however, these children catch up by the age they begin reading (40). In our study, there were slightly more bilingual households represented in the group of patients with speech delay than in the group of patients with normal speech, but this difference was not statistically significant (P = .21, Fisher exact test).

Sedation is a necessary issue to consider. Language must be evaluated in infants and young children while the speech process is developing. Since most language is developed by 4 years of age, sedation is necessary in most patients if a functional MR examination is to be successful. Use of auditory functional MR imaging in sedated children has been reported previously (11,12). Results of studies conducted in monkeys also confirm the responsiveness of the primary and secondary auditory cortical areas, despite the effects of sedation (41).

Our stimulus of the mother’s voice—which includes endearing words, familiar names, and favorite songs—is a powerful paradigm in young children (24,25), even if the patient is sedated (11). Auditory activation has also been obtained by using plain tones in newborns who are not sedated (42).

Patients sedated with pentobarbital have a 20% reduction in the rate of cerebral blood flow (43). To date, we are unaware of any studies that have been performed in humans to assess the metabolic impact of pentobarbital on normal brain metabolism. Previous studies in small mammals sedated with pentobarbital demonstrate that the regional metabolic rate of glucose does not change with stimulation during the generation of primary evoked cortical potentials in the somatosensory cortex (44). The expected decrease of activation from the sedative effect has been discussed previously (11). The effect of the sedative diminishing the proportion of cortical response to a given stimulus has an important statistical impact over the global signal-to-noise ratio, although reduction of patient movement and a pure rest state may partially negate this.

The statistical power of the functional MR imaging analysis may be affected by sedation. Sedation may make it difficult to assess activation when conservative thresholds are used. The investigator must be careful to avoid false-positive and false-negative results. Bonferroni and Resel correction for multiple comparisons may be too stringent, as clusters of activation may be deleted that are in expected locations, or with extent, symmetry, and intracluster distribution of intensities that are certainly not random. This phenomenon has plagued other researchers performing functional MR examinations in adults and is of the utmost importance in functional MR examinations of children. We are in agreement with Gaillard et al (45) that lowering the threshold below standards for adults will enable the discovery of areas of true activation.

Several investigators who use functional MR examinations to assess language localization in adults and children with epilepsy report having examined individual data at different thresholds (22,46,47). These authors describe reliable activation maps obtained at lower thresholds that match group activation maps established in normal populations at higher thresholds and that have been subsequently confirmed, either with an intracarotid sodium amobarbital procedure or with an electrocortical stimulation.

To justify the use of an uncorrected P value, we adopted a cluster-size threshold approach that depends less on the z score and more on the way the activated voxels are grouped, according to the method described by Forman et al (20). This approach provides a tool to compensate for the lack of multiple comparisons of our first level of pixel-by-pixel analysis maintaining the P values within an accepted standard range (.01 < P < .05).

The lateralization index number was used to determine hemisphere dominance. In 14 control subjects and four patients with speech delay, the lateralization index number was either 100 or -100, revealing the effect of the threshold used for the group analysis. Even with relatively low z scores, the {alpha} value (set to limit the false-positive results) was enough to cancel all clusters but those with the maximum extent. Thus, the lateralization index number becomes more of a qualitative than a quantitative measure. This effect of the z-score threshold on the lateralization index number has been observed and discussed previously (48). The percentage obtained with the lateralization index number does not give a reliable quantification of lateralization, but it does allow objective determination of the dominant hemisphere. The exclusion of midline voxels from the analysis adds power to these findings.

Last, our age-matched patients with normal speech development were patients who were referred to our institution for imaging. This creates bias in this population; however, our inclusion criteria are strict, and for obvious ethical reasons this is as close to a normal population as we could expect to get in a study that includes sedated children.

In conclusion, we demonstrate that the brains of children with speech delay are different from the brains of children with normal speech. By using a passive paradigm in sedated children, we showed that the brains in children with normal speech tended to lateralize to the left hemisphere as the child aged. Children with speech delay had an increase in the frequency of right hemisphere activation. This may be due to processing differences, plasticity, or immaturity. There is a trend toward less frequency of activation in children with speech delay. This may suggest these children are less receptive to speech. Functional MR imaging may play an important role in the early diagnosis in these children. The role of functional MR imaging in the monitoring of intervention and treatment needs to be evaluated with further investigations. The findings of this study suggest new alternatives for further investigation of cognitive processes in infants and children. Complete understanding of language development in early stages may help in the diagnosis, counseling, and treatment of patients with disorders that affect cognitive functions that define us as uniquely human.


   FOOTNOTES
 
Author contributions: Guarantors of integrity of entire study, N.R.A., B.B.; study concepts and design, B.B., N.R.A.; literature research, B.B., N.R.A.; clinical studies, N.R.A., B.B.; experimental studies, B.B., N.R.A.; data acquisition, B.B.; data analysis/interpretation, B.B., N.R.A.; statistical analysis, B.B.; manuscript preparation, definition of intellectual content, editing, revision/review, and final version approval, N.R.A., B.B.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 

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A. J. O. Whitehouse and D. V. M. Bishop
Cerebral dominance for language function in adults with specific language impairment or autism
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