Neurophysiological Evidence of Auditory Channel
Anomalies in Developmental Dysphasia
Gerry A. Stefanatos, DPhil; Gary G. R. Green, DPhil, BM, BCh; Graham G. Ratcliff, DPhil
\s=b\ Steady-state auditory evoked re-
sponses to frequency-modulated tones
were obtained from normal children and
two groups of children with developmental
language disorders (developmental dys-
phasia). Children with predominantly ex-
pressive language impairment produced
responses not different from normal chil-
dren, while children with primary receptive
language impairment produced responses
that were markedly diminished, even ab-
sent. This occurred in recordings from
either cerebral hemisphere and at mean
frequency-modulation depths ranging
from \m=+-\20 to \m=+-\100Hz. Pathophysiology of
auditory mechanisms concerned with fre-
quency-modulation analysis are particu-
larly associated with receptive develop-
mental language impairment and may un-
derlie associated difficulties in speech
perception.
(Arch Neurol. 1989;46:871-875)
"Tievelopmental dysphasia refers to a
collection of disorders in children
characterized by severe retardation of
language development in the absence
of clear causal factors such as hearing
loss, gross neurological disability, in-
Accepted for publication February 6, 1989.
From the Neuropsychology Unit, Oxford (En-
gland) University Department of Clinical Neurol-
ogy, Radcliffe Infirmary, Oxford (Dr Stefanatos),
and the Department of Physiological Sciences,
The Medical School, University of Newcastle upon
Tyne, Newcastle, England (Dr Green); and the
Departments of Neurology, Psychiatry, and Psy-
chology, University of Pittsburgh (Pa) (Dr Rat-
cliff). Dr Stefanatos is now with the Medical Col-
lege of Pennsylvania, Philadelphia.
Reprint requests to the Division of Child Psy-
chiatry, Medical College of Pennsylvania, 3200
Henry Ave, Philadelphia, PA 19129 (Dr
Stefanatos).
Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/14/2015
tellectual subnormality, or psychiatric
disorder.1 Several studies directed at
uncovering a basis for the disorders
have shown that many of these chil¬
dren have particular difficulty in dis¬
criminating speech sounds distin¬
guished acoustically by rapidly chang¬
ing frequency structure,25 but the
nature of this problem and its rela¬
tionship to impaired language devel¬
opment is controversial. According to
one view, this apparent perceptual dif¬
ficulty is simply one manifestation of a
higher-order failure in the develop¬
ment of linguistic abilities concerned
with the phonological and syntactic
processing of speech and can thus be
regarded as a consequence of the lan¬
guage disorder.6·7 An alternative view,
however, suggests that the problem is
attributable to deficient auditory tem¬
poral processing since developmental
dysphasics are also impaired in the
perception of rapidly changing non-
speech sounds.1·810 Such a basic audi¬
tory problem, it has been argued, could
underlie their language impairment
by impeding the process by which lin¬
guistically important acoustic cues in
the speech signal are encoded. Clearly,
this question has important implica¬
tions for the understanding and treat¬
ment of the disorders.
The auditory hypothesis has been
criticized because, as a unitary expla¬
nation, it does not account well for the
diversity of manifestations of lan¬
guage impairment in developmental
dysphasia11 and because poor perfor¬
mance on behavioral measures of au¬
ditory temporal processing may, in-
some instances, be related to factors
other than language impairment since
deficits have also been observed in
clinical populations with normal lan¬
guage development.12 Moreover, there
appears to be no convincing corrobo¬
rative evidence available from neuro-
physiological studies employing corti¬
cal auditory evoked response tech¬
niques to support the view that
disturbances of auditory processing
systematically exist in developmental
dysphasia, let alone that an auditory
disorder is primary. Cortical auditory
evoked responses recorded at the ver¬
tex frequently show thresholds, ampli¬
tudes, and latencies that are within
normal limits,13·14 although abnormal
waveform morphology has been noted
over temporal areas of the left cerebral
hemisphere.15
A critical feature of the evoked re¬
sponse studies to date is that they have
uniformly employed acoustically
steady-state stimuli, such as pure-tone
bursts, and since the behavioral evi¬
dence suggests that the perceptual def¬
icits in dysphasics are related to pro¬
cessing rapidly changing frequency in¬
formation, these stimuli may not be
sufficiently sensitive or, indeed, neuro-
biologically appropriate probes. Ani¬
mal neurophysiological studies, for ex¬
ample, have demonstrated that a sig¬
nificant population of neurons in the
central auditory system are relatively
unconcerned with steady-state stimuli
such as pure tones but are pref¬
erentially activated by tones with
stimulus characteristics that are
temporally varying such as modula¬
tions in frequency.1618 Analogous fre¬
quency modulation—sensitive mecha¬
nisms have also been observed in the
human auditory system1921 and have
been distinguished from neurophysio¬
logical mechanisms selectively respon-
 sive to amplitude modulations in
sound.
It has been suggested that frequency
modulation—sensitive mechanisms
subserve the analysis of frequency
transitions in temporally complex Mean
Modulation
sounds, including speech.2224 It seemed Depth, Hz
to us that dysfunction of these mecha¬
nisms may be a possible physiological
basis for the perceptual difficulties ob¬
served in children with developmental 1 kHz
dysphasia, and this may be detect¬ -

able through examination of cortical

evoked responses to frequency modu¬
lations in sound. We, therefore, exam¬
ined responses evoked by tones whose I-250 -1 Time, ms
frequency was modulated at 10 Hz, a
rate that falls within a range relevant
to the phonetic analysis of speech.24 EDD RDD
Since traditional transient cortical 1
evoked responses diminish greatly at Mean
Modulation
frequency-modulation rates greater Depth, Hz
than about 1 Hz, we employed a re¬
cently developed steady-state auditory
evoked response technique that allows
±20
s^W
the study of neural responses to tones
frequency modulated at more rapid
rates.25 We studied these responses in
developmentally dysphasic children :60
with and without severe receptive lan¬
guage impairment and in a group of
normal children.
SUBJECTS AND METHODS

Twelve children with developmental dys¬

phasia (ages 11 to 16 years) with normal
hearing thresholds and normal-range non¬
verbal intelligence (IQ, >85) were divided
into two equal groups on the basis of their
speech and language profiles. A group with
expressive developmental dysphasia con¬
sisted of children whose core symptom was
severe difficulty in producing spoken lan¬
guage. Their expressive language was syn¬
tactically impoverished and their phonemic
productions were marked by omissions,
distortions, and substitutions. Language
comprehension was relatively spared, with
problems becoming apparent predomi¬
nantly for long or complex sentences. Thus,
their expressive disabilities formed their
primary problems with language. A group
of children with receptive developmental
dysphasia displayed primary problems in
understanding language. They exhibited
marked difficulties in decoding the phono¬
logical and syntactic structure of language,
resulting in gross language comprehension
deficits, which, because of the developmen¬
tal nature, were associated with concomi¬
tant expressive language difficulties. These
groups would correspond to the mixed pho¬
nological-syntactic syndrome and verbal
auditory agnosia of Rapin and Allen,26 re¬
spectively. A group of 6 age-matched nor¬
mal control children, with no history of
neurological, audiological, or language dis¬
ability, were also tested for comparison
purposes.
The stimuli were continuous frequency-
modulated tones, generated by an audio
signal generator consisting of three inde-
±100
\S^>
Control
Condition
(No Response)
<^=^
Fig 1.—Top, Schematic diagram of the temporal characteristics of frequency change in the fre¬
quency-modulation stimuli. The tones vary in frequency around the carrier (1 kHz) in a sinusoidal
fashion 10 times per second, corresponding to the frequency-modulation rate. The size of these
frequency deviations (the modulation depth) varies sinusoidally 4 times a second, corresponding
to the depth-modulation waveform, and it is to this envelope that the responses are locked (indi¬
cated by the arrows and superimposed response). Note that the amplitude of the tone is constant;
it is the amplitude of the frequency change that is varying according to the depth modulation
waveform. Responses are approximately periodic, with a maximum frequency component at 4 Hz.
Bottom, Examples from each group of evoked responses to frequency-modulated tones with ± 20,
± 60, and ± 100 Hz mean modulation depth recorded from the left and right cerebral hemisphere.
For the control condition responses, subjects listened to a 1-kHz pure tone. These represent "no
response" since no frequency modulations occur in this stimulus. NL indicates normal language;
EDD, expressive developmental dysphasia; and RDD, receptive developmental dysphasia.
pendent waveform generators and a four- late the depth of a 10-Hz sine wave. The re¬
quadrant multiplier.27 The tones generated sultant waveform was then used to
were composed of three component wave¬ frequency modulate a 1-kHz pure-tone car¬
forms combined to form a 1-kHz tone, fre¬ rier. The depth modulation waveform
quency modulated at a rate of 10 Hz, where therefore defines the envelope of the fre¬
the depth of modulation varied sinusoidally quency modulation (Fig 1). In this experi¬
between a pure tone and a fully frequency- ment, the mean modulation depth was var¬
modulated one, four times a second. This ied by ±20, ±60, and ±100 Hz to compose
was accomplished by using a 4-Hz sinusoi¬ three experimental conditions. Mean mod¬
dal waveform, termed the "depth modula¬ ulation depth is defined as half the maxi¬
tion waveform," to 100% amplitude modu- mum deviation in frequency around the

Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/14/2015


>
a.
1 -
J L
Control
Fig 2. Histograms represent the mean response magnitudes for each group at each modulation depth examined: NL indi¬
cates normal language; EDD, expressive developmental dysphasia; and RDD, receptive developmental dysphasia. The as¬
—
sociated error bars represent the SD of the phase of responses at the various frequency-modulation depths.
carrier (1 kHz). The average evoked re¬
sponse to these stimuli has the same fre¬
quency as the depth modulation waveform
(4 Hz) and is time locked to its envelope.25
The responses are contingent on the analy¬
sis of the instantaneous frequency changes
of the tones. Accordingly, a continuous tone
without the frequency changes does not
produce a significant response at 4 Hz.
Differential recordings from the left and
right cerebral hemispheres were obtained
with chlorided silver disk electrodes, placed
on F3 and F4 of Jasper,28 each referred to
their respective ipsilateral mastoid, with a
common ground on the forehead. These
sites span primary auditory cortical areas
and have previously been used with normal
adult subjects.29 Signals from each side of
the head were amplified (system gain,
25 X 10"), and band-pass filtered between 2
and 10 Hz, before entering the analog-
to-digital converter of a minicomputer (In¬
tertechnique Multi-20). Trigger pulses,
used to initiate the acquisition of 250-milli-
second samples of electroencephalographic
activity by the computer, were locked to the
depth modulation waveform and thus oc¬
curred every 250 milliseconds. Acquisitions
containing artifact (>50 u\) were rejected.
Response acquisition occurred continu¬
ously, so the averaging epoch was also 250
milliseconds. Eight hundred acquisitions
were summed to produce an average evoked
response and three responses were obtained
for each frequency-modulation depth. To
obtain artifact levels, a control condition
was introduced in which responses were
also obtained using a 1-kHz continuous
pure-tone stimulus and the same sampling
parameters. All stimuli were delivered bin-
aurally at 60 dB above audiometrie thresh¬
olds through a pair of calibrated head-
Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/14/2015
±20 ±60
Mean Modulation Depth,
phones with a flat frequency response over
the frequency region tested.
RESULTS
Representative responses for each
group, for each modulation depth, are
represented in Fig 1. It can be seen that
in the control condition using the pure-
tone stimulus, responses were flat and
without consistent or substantial spec¬
tral peaks. There did not, therefore,
appear to be phase locking of the elec¬
troencephalogram to the sampling pe¬
riod. Since these potentials represent
the averaged activity of the electroen¬
cephalogram when no frequency mod¬
ulations are present in the stimulus,
they can be regarded as a "no
response" condition. Responses to the
frequency modulated tones in the nor¬
mal group and expressive developmen¬
tal dysphasic group are similar to
those obtained in normal adults, ap¬
proximating sinusoids with a fre¬
quency of 4 Hz and with consistent
phase characteristics. Responses of
the receptive developmental dysphasic
group, however, deviated markedly
from this pattern: their responses did
not have the characteristically large
4-Hz frequency component or a con¬
sistent phase of that component. In¬
deed, their responses to the frequency-
modulated tones were much like the
control responses of each group. This
suggests that the frequency-modu¬
lated tones used herein did not evoke a
detectable response in these children.
nl
+ 180°
Hi EDD
RDD
er
180°
Hz
For purposes of statistical analysis,
the magnitude of the 4-Hz component
was computed from the Fast Fourier
Transform of each response and sub¬
jected to a three-way ANOVA (group
by cerebral hemisphere by frequency-
modulation depth). The analysis con¬
firmed the highly significant differ¬
ence between groups (f[2,15] 62.64,
=
< .001), which was readily apparent
from visual inspection. There was also
a significant effect of frequency-modu¬
lation depth (f[2,39] 8.54,
= < .01)
and a significant group by fre¬
quency-modulation depth interaction
(f[4,30] =4.16, < .05). The main effect
of cerebral hemisphere was not signif¬
icant. Comparing the means defined by
the interaction, t tests indicated that
subjects in the group with receptive
developmental dysphasia had exceed¬
ingly small mean response magni¬
tudes, compared with both the normal
group and the group with expressive
developmental dysphasia, across all
modulation depths examined. The
enormous gap between the profiles of
the mean response magnitudes of the
receptive developmental dysphasic
group and the normal and expressive
dysphasic group is depicted in the his¬
tograms in Fig 2. The effect of modu¬
lation depth can be seen in the decreas¬
ing pattern of means from ±20 to
±100 Hz. There were no significant
differences between the normal group
and the group with expressive devel¬
opmental dysphasia at any modulation
 depth. The group by frequency-modu¬
lation depth interaction is clearly seen
as the different rates of decline of re¬
sponse magnitude in the three groups
across the three frequency modulation
depths. In the normal group, the re¬
sponses at ±20 Hz are significantly
greater than at ±60 or ±100 Hz
(P < .01 for both), while in the expres¬
sive developmental dysphasic group
the responses at ± 20 and ± 60 Hz were
significantly greater than responses at
±100 Hz (P<.05 and .01, respec¬
tively). In the group with receptive de¬
velopmental dysphasia, response mag¬
nitudes were consistently small and
did not vary significantly as a function
of frequency-modulation depth.
Means and SDs of the phase of the
4-Hz component of responses to each
modulation depth for each group are
also depicted along side the histo¬
grams in Fig 2. It can be seen that the
phase of responses in the normal and
expressive dysphasic groups are simi¬
lar and consistent. The phase of re¬
sponses in the receptive group, how¬
ever, are extremely variable. Again,
this is consistent with the interpreta¬
tion that children with receptive de¬
velopmental dysphasia show no de¬
tectable response to the frequency-
modulated tones used in this study.
COMMENT
The observed effects are not due to
the periodicity of the depth modula¬
tion waveform. In a separate study,30
with the same groups, responses were
obtained to a 1-kHz pure tone 100%
amplitude modulated by a 4-Hz sinu¬
soid. This stimulus was employed be¬
cause the envelope defined by the stim¬
ulus and the response it produces are
the same frequency as the envelope
and response elicited by the frequency-
modulated tones used herein. There
were no significant differences among
the three groups using such stimuli. It
appears that envelope periodicity per
se does not account for the poor re¬
sponses to the frequency-modulated
tones of the group with receptive de¬
velopmental dysphasia. Rather, it
seems that the crucial factor is the
composition of the envelope, that is,
whether or not it is defined by rapid
changes in frequency. There does not,
therefore, appear to be a general inhi¬
bition of rapid auditory processing,
resulting in generally poor steady-
state auditory evoked responses, but
rather poor responses specifically to
rapid frequency modulations in sound.
Our analysis indicates that central
auditory mechanisms concerned with
the analysis of rapid frequency modu¬
lations in sound are grossly abnormal
Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/14/2015
only in children with receptive devel¬
opmental dysphasia. These children
might therefore be expected to experi¬
ence prominent auditory perceptual
difficulties when required to process
rapid frequency changes, and their
problems with speech may be only one
manifestation of this problem. Their
difficulties may be particularly evident
or severe in the perception of speech
sounds characterized by rapid formant
frequency transitions5 because these
transitions often provide essential
cues for discrimination,3133 whereas
the discrimination of many other en¬
vironmental sounds can often be ac¬
complished by using other acoustic
cues that may be neurally encoded
more adequately. Indirect support
that children with receptive develop¬
mental dysphasia do have more gen¬
eral problems with frequency modula¬
tion analysis may be evidenced by
their particularly poor performance on
nonverbal tasks that implicitly require
the analysis of frequency modulations.
It is possible, for example, that re¬
ported deficits in their ability to dis¬
criminate the temporal order of rap¬
idly presented tones differing in fre¬
quency may lie, in part, in a frequency-
modulation analysis deficit in this
group, although, since this is a complex
task, other factors may also determine
performance. Such tasks place de¬
mands on a number of abilities includ¬
ing attention, memory, associative
learning, and sequential response pro¬
gramming, among others. This may
contribute to the nonspecificity noted
earlier of such tasks to developmental
language disorders.12
Several studies have suggested that
auditory perceptual deficits in children
with developmental dysphasia are
epiphenomena of linguistic or cogni¬
tive processing deficits. Cromer,6 for
example, has reported that children
with receptive developmental dyspha¬
sia are unable to abstract the hierar¬
chical structure of language and has
suggested that this deficit reflects a
cognitive-linguistic impairment that
can readily explain some of their ap¬
parent auditory processing deficits,
well as their problems with the recep¬
tion of speech. By contrast, our data
suggest that an auditory deficit that
occurs at the level of coding of sensory
information, preceding the cognitive
and linguistic processing of speech, is
fundamental in this group and con¬
tributes significantly to the emergence
of language deficits by impeding the
perception of linguistically important
acoustic features in speech. The pri¬
macy of the auditory disorder in these
cases is also suggested by psycholin-
guistic studies that have shown that
linguistic deficits analogous to those
postulated by Cromer to underlie re¬
ceptive developmental dysphasia can
be observed in the linguistic perfor¬
mance of the profoundly deaf.34 Clearly
then, these linguistic deficits alone are
not indicative of primary receptive
language impairment, since such dif¬
ficulties can arise as secondary conse¬
quences of peripheral auditory dys¬
function.
These results contrast with previous
cortical evoked potential studies,
which have not found remarkable dif¬
ferences in the amplitude or latency of
transient cortical evoked responses in
children with developmental dyspha¬
sia when compared with normal chil¬
dren or when subgroups are examined.
These investigations have illustrated
that transient cortical responses are of
somewhat limited utility in the differ¬
ential diagnosis of receptive develop¬
mental dysphasia, largely restricted to
excluding hearing impairment and
gross central auditory dysfunction as
causes of the language disorder. The
abnormal steady-state evoked re¬
sponses to frequency-modulated tones
were observed in receptive develop¬
mental dysphasics without exception.
Consequently, this measure may pro¬
vide a useful adjunct method of screen¬
ing young children when there is some
suspicion of primary receptive lan¬
guage impairment.
It is significant that abnormal re¬
sponses were observed in the receptive
developmental dysphasic group in re¬
cordings from either cerebral hemi¬
sphere. This would suggest that the
underlying pathophysiology is imped¬
ing the elaboration of responses bilat¬
erally, but the level of the dysfunction
remains difficult to specify. Arlinger et
al35 have determined through magnet¬
ic-field recordings that the neural gen¬
erators of cortical responses to fre¬
quency modulations are localized in
the temporal lobes, and it seems possi¬
ble that bitemporal pathophysiology
may underlie the observed pattern.
This would be concordant with a single
as postmortem study36 of a child with
"congenital aphasia" and severe recep¬
tive language impairment that re¬
vealed gross degeneration of the insula
and temporal opercula bilaterally, ex¬
tending down to and including the me¬
dial geniculate bodies. Both auditory
nerves were apparently histologically
intact. A recent cerebral blood flow
study noted hypoperfusion over poste¬
rior sylvian regions bilaterally in a
child with severe receptive problems
and a normal computed tomographic
scan, suggesting that dysfunction can
 be quite subtle.37 However, given the
nature and paucity of the evidence, it is
not possible to discount a possible sub-
cortical contribution that may serve to
degrade bilaterally the elaboration of
responses at the cortical level: neurons
responsive insome fashion to fre¬
quency modulation are found through
much of the upper central auditory
nervous system.24
We conclude that (1) children with
receptive developmental dysphasia
differ significantly from those with
expressive developmental dysphasia
and normal children in cortical re¬
sponses evoked by rapid frequency-
modulated tones; (2) a fundamental
auditory problem rooted in pathophys-
1. Benton AL. Developmental aphasia and
brain damage. Cortex. 1964;1:40-52.
2. Tallal P, Piercy M. Developmental aphasia:
rate of auditory proecessing and selective impair-
ment of consonant perception. Neuropsychologia.
1974;12:83-93.
3. Tallal P, Piercy M. Developmental aphasia:
the perception of brief vowels and extended stop
consonants. Neuropsychologia. 1975;13:69-74.
4. Tallal P, Stark R, Curtiss B. The relation be-
tween speech perception impairment and speech
production impairment in children with develop-
mental dysphasia. Brain Lang. 1976;3:305-317.
5. Frumkin B, Rapin I. Perception of vowels
and consonant-vowels of varying duration in lan-
guage impaired children. Neuropsychologia. 1980;
18:443-454.
6. Cromer RF. The basis of childhood dyspha-
sia: a linguistic approach. In: Wyke M, ed. Devel-
opmental Dysphasia. Orlando, Fla: Academic
Press Inc; 1978:85-134.
7. Leonard LB. Phonological deficits in children
with development language impairment. Brain
Lang. 1982;16:73-86.
8. Lowe A, Campbell RA. Temporal discrimi-
nation in aphasoid and normal children. J Speech
Hear Res. 1965;8:313-314.
9. Tallal P, Piercy M. Defects of auditory per-
ception in children with developmental dyspha-
sia. In: Wyke M, ed. Developmental Dysphasia.
Orlando, Fla: Academic Press Inc;1978:63-84.
10. Eisenson J. Aphasia and Related Disorders
in Children. New York, NY: Harper & Row Pub-
lishers Inc; 1984.
11. Ludlow CL. Children's language disorders:
recent research advances. Ann Neurol. 1980;7:497\x=req-\
507.
12. Ludlow CL, Cudahy EH, Bassich GL, Brown
GL. Auditory processing skills of hyperactive,
language impaired and reading disabled boys. In:
Lasky EZ, Katz J, eds. Central Auditory Process-
ing Disorders: Problems ofSpeech, Language and
Learning. Baltimore, Md: University Park Press;
1983:163-184.
13. Beagley HA. The role of ERA in the diag-
nosis of receptive aphasia in children. Arch Ohren
Nasen Kehlkopfheilkd. 1971;198:152-153.
14. Cohen M. Rapin I. Evoked potential audi-
Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/14/2015
iology of central mechanisms con¬
cerned with frequency-modulation
analysis exists in receptive language-
impaired children, and this represents
a major impediment to language de¬
velopment; (3) poor steady-state audi¬
tory evoked responses appear to be ex¬
cellent neurophysiological markers of
receptive developmental dysphasia in
children. Furthermore, the results
provide clinical evidence to support the
suggestion that frequency-modulation
analysis is critically involved in the
auditory analysis of speech since ab¬
normal cortical evoked responses to
frequency modulations are so strongly
associated with severe speech recep¬
tion problems. They also underline the
References
ometry in neurologically impaired children. In:
Naunton R, Fernandez C, ed. Evoked Electrical
Activity in the Auditory Nervous System. Orlan-
do, Fla: Academic Press Inc; 1978:551-572.
15. Mason SM, Mellor DH. Brain stem, middle
latency and late cortical evoked potentials in
children with speech and language disorders.
Electroencephalogr Clin Neurophysiol. 1984;
59:297-309.
16. Whitfield I, Evans EF. Responses of audi-
tory cortical neurons to stimuli of changing fre-
quency. J Neurophysiol. 1965;28:655-672.
17. Evans E. Neural processes for the detection
of acoustic patterns and for sound localization. In:
Schmitt F, Worden F, eds. Neurosciences: Third
Study Program. Cambridge, Mass: MIT Press;
1984:131-145.
18. Funkenstein HH, Winter P. Response to
acoustic stimuli of units in auditory cortex of
awake squirrel monkeys. Exp Brain Res. 1973;
18:469-488.
19. Kay RH, Matthews D. On the existence in
human auditory pathways of channels selectively
tuned to the modulation present in frequency
modulated tones. J Physiol. 1972;225:657-677.
20. Regan D, Tansley B. Selective adaptation to
frequency-modulated tones: evidence for an in-
formation-processing channel sensitive to fre-
quency changes. J Acoust Soc Am. 1979;65:1249\x=req-\
1257.
21. Gardner R, Wilson J. Evidence for direction
specific channels in the processing of frequency
modulation. J Acoust Soc Am. 1979;66:704-709.
22. Whitfield IC. 'Edges' in auditory informa-
tion processing. In: Proceedings of the 23rd Inter-
national Congress of Physiological Sciences; Sep-
tember 5-9, 1965; Tokyo, Japan. Abstract No.
29:19.
23. Abbs J, Sussman H. Neurophysiological
feature detectors and speech perception: a discus-
sion of theoretical implications. J Speech Hear
Res. 1971;14:23-26.
24. Kay RH. Hearing of modulation in sounds.
Physiol Rev. 1982;62:894-975.
25. Green GGR, Rees A, Stefanatos GA. A
method of recording evoked responses to fre-
quency modulated sounds in man. J Physiol.
1980;307:10p.
separate processing channels involved
in frequency- and amplitude-modula¬
tion analysis and demonstrate that
these channels can be selectively im¬
paired.
We thank Freda Newcombe, DPhil, the Neu¬
ropsychology Unit, Department of Clinical Neu¬
rology, Radcliffe Infirmary, Oxford, England, and
Roy H. Kay, DPhil, the University Laboratory of
Physiology, Oxford (England), for supporting this
project and allowing the use of facilities in their
laboratories. We thank W. John Bannister, for his
excellent technical assistance. We are also grate¬
ful to John Lea, MSc, Moor House School, Oxted,
England, Sandya Naidoo, MA, Dawn House
School, Mansfield, England, and Martin Roberts,
MA, Cherwell School, Oxford, England, for orga¬
nizing our testing of their pupils.
26. Rapin I, Allen DA. Progress towards a no-
sology of developmental dysphasia. In: Fukuyama
Y, Arima M, Maekawa K, Yamaguchi K, eds. Child
Neurology. Princeton, NJ: Excerpta Medica;
1982:25-35.
27. Bannister WJ. A versatile wave form gen-
erator for auditory research. J Physiol. 1980;
307:9p.
28. Jasper HH. The ten twenty system of the
International Federation. Electroencephalogr
Clin Neurophysiol. 1958;10:371-375.
29. Green GGR, Kay RH, Rees A. Responses
evoked by frequency-modulated sounds recorded
from the human scalp. J Physiol. 1979;296:21-22.
30. Stefanatos GA. Non Verbal Abilities in
Communication Disorders. Oxford, England: Ox-
ford University; 1984, Thesis.
31. Bailey PJ. Aspects of categorical processing
of speech sounds in man: on the determinants of
phonetic category boundaries. In: Creutzfeld O,
ed. Hearing Mechanisms and Speech. New York,
NY: Springer-Verlag NY Inc; 1979:301-317.
32. Liberman AM, Cooper FS, Shankweiler M,
Studdert-Kennedy M. Perception of the speech
code. Psychol Rev. 1967;74:431-461.
33. Liberman AM, Studdert-Kennedy M. Pho-
netic perception. In: Held R, Leibowitz HW, Teu-
ber HL, eds. Handbook of Sensory Physiology.
New York, NY:Springer-Verlag NY Inc; 1978;
8:143-178.
34. Bishop DMV. Comprehension of spoken,
written and signed sentences in childhood lan-
guage disorder. J Child Psychol Psychiatry.1982;
23:1-20.
35. Arlinger S, Elberling C, Bak C, Kofoed B,
Lebech J, Saermark K. Cortical magnetic fields
evoked by frequency glides of a continuous tone.
Electrocencephalogr Clin Neurophysiol. 1982;54:
642-653.
36. Landau WM, Goldstein R, Kleffner ER.
Congenital aphasia: a clinicopathologic study.
Neurology. 1960;10:915-921.
37. Lou HC, Henrikson L, Bruhn P. Focal cere-
bral hypoperfusion in children with dysphasia
and/or attention deficit disorder. Arch Neurol.
1984;41:825-829.