International Journal of Pediatric Otorhinolaryngology

46 (1998) 43 – 56

A study of auditory afferent organization in children with

dyslalia

D. Milic' ić a,*, M.N.M.P. Alçada b, L. Pais Clemente a, S. Vec' erina-Volić c,

J. Jurković c, M. Pais Clemente a
a
Department of Otorhinolaryngology, Hospital S. João, Medical School, 4200 Porto, Portugal
b
Department of Biochemistry, Medical School, 4200 Porto, Portugal
c
Department of Otorhinolaryngology, Audiological and Phoniatric Centre, KBC Salata, Medical School, Zagreb, Croatia

Received 15 April 1998; received in revised form 28 August 1998; accepted 30 August 1998

Abstract

The auditory afferent (AA) control is an important feedback mechanism in the speech generation. A different
organization of AA pathways in children with speech alterations is suggested. In order to investigate this possibility
we recorded the auditory brainstem responses (ABR) and middle latency responses (MLR) on monoaural and
binaural click stimulation in a group of 17 normal children with no alteration of the speech (N) and in 16 children
with dyslalia (eight with systematic (S) and eight with non-systematic errors of the speech (NS)). All of children were
normal hearing, with normal ORL and neurological status, right-handed and with the age approximately 7 years old.
A lateralization effect was found in the S group. Normally, it was only found for wave I. The efficiency of both AA
pathways was the same in NS group, indicating a more effective right pathway in more rostral areas. A prolonged
latency (X( =0.25 ms) of wave III was registered on the right side in the NS group compared to normals, as well for
wave V (X( =0.175 ms) with increased sweep rate (21 vs 51 and 71). The effect of sweep rate augmentation was also
studied (21–51–71) on latency values and inter-wave differences in these groups. A successive latency prolongation
(X( =2.97 ms) of MLR wave Na was registered between the N –S –NS groups. In the S group a latency binaural
interaction (BI) of MLR left wave Na was prolonged for 3.52 ms and in the NS group for a further 1.32 ms compared
to normals. Only in the NS group was a prolongation of the BI of the right wave Pa detected (6.76 ms) compared
to normals. Results suggest a different AA organization in children with dyslalia. Possible locations of alterations in
functioning could be pons, and thalamocortical projections. ABR and MLR could evaluate the auditory – speech
capability of children. © 1998 Published by Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Dyslalia; Middle latency response; Auditory brainstem response; Sweep rate; Binaural interaction

* Corresponding author. Present address: Rua da Constituição, 1497-4° Esq, 4200-Porto, Portugal.

0165-5876/98/$ - see front matter © 1998 Published by Elsevier Science Ireland Ltd. All rights reserved.
PII S0165-5876(98)00135-9
44 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56
1. Introduction
The exact location of a speech (articulation and
vocalization) pathway (S.P. Zhang, R. Bandler,
P.J. Davis, Brain stem integration of vocalisation:
role of nucleus retroambigualis, 1995, pers. com-
mun.) is under investigation, indicating the impor-
tance of thalamic [13,33,34] and extrathalamic
structures [32], especially in auditory control
[30,31]. The alteration in development of speech
can be caused by a dysfunction of cortical and
subcortical structures [16].
The auditory brainstem response (ABR) is a
reliable indicator of the auditory function, from
the distal auditory nerve to the inferior collicule
(IC) [35].
The middle latency response (MLR) gives a
representation of higher auditory afferent (AA)
structures, centrally to IC, as well as the reticular
activating system [2] and non-primary divisions of
the auditory thalamocortical pathway [26], pro-
cessing multisensory stimuli. A primary temporal
response of MLR is in children dominated by a
state-dependent labile midline response, generated
by non-primary pathway [21,24]. An MLR could
give information about the auditory function and
discrimination, and also the auditory – speech inte-
gration and feedback control in children [26].
There are some evidences of a different audi-
tory afferent organization in children: those with
a bad phonemic hearing [25], Down’s syndrome
[9,40], neurodegenerative disorders [3], autism and
minimal brain dysfunction [39], reading, writing
and spelling difficulties [31], hyperactive children
[36], developmentally retarded [28] children with
early mild hearing loss associated with otitis me-
dia [12], and in adult males who stutter [5].
Dyslalia is an alteration of articulation, mani-
fested in a slower capability of a realization of
phonemes [38]. It can be distinguished in system-
atic fixed errors (S) and in non-systematic errors
(NS) (with omission, substitution, addition and
metatesis of phonemes), indicating a more pro-
found dysfunction [15].
The aim of this study was to investigate the
possibility of an altered AA organization in chil-
dren with non-developmental dyslalia (older than
6 years).
2. Subjects and methods
All children, with paternal informed consent,
were right-handed, with normal hearing, normal
ORL, neurological and psychological status. In
the control group (N) with no alteration of
speech, we tested four males and 13 females (in
total 17) with mean age 7.47 9 1.07 years (C.V.
14.29%). In a group of children with dyslalia we
tested those with systematic (S) and non-system-
atic (NS) errors of speech. In the S group we had
four males and four females (in total eight) with a
mean age of 6.879 0.64 years (C.V. 9.32%). In
the NS group we had six males and two females
(in total eight) with a mean age of 6.259 0.46
(C.V. 13.99%). In all children median and mode
of age was 7 years.
The recordings were performed with an Am-
plaid MK6 Evoked Potentials Signal Processor,
stimulated by an AS 501 Tone and Click Genera-
tor, an As 500 Mixer and Power amplifier and
standard shielded TDH 49 earphones. Evoked
responses were displayed on Tekstronix 4006-1
display and stored. Standard Ag/AgCl cup elec-
trodes were located on the vertex (+ ), and re-
ferred to the earlobe of the stimulated ear (− ).
The contralateral earlobe electrode served as a
ground. Electrodes were fixed with collodium and
filled with Ultragel (Interprogres, Zagreb). Skin
resistance did not exceed 3 kV.
ABR and MLR recordings were performed in
an acoustically and electrically shielded room on a
lying subject with no sedation. ABR analysis time
was 10 ms; sweep rate (PPS, pulses per second),
21, 51 and 71; sweep count, 2048; LF cut-off, 100
Hz (roll-off 12 dB/octave); HF cut-off, 2000 Hz
(roll-off 6 dB/octave). MLR analysis time was 100
ms; sweep rate, 9; sweep count, 1024; LF cut-off,
20 Hz (roll-off 12 dB/octave); HF cut-off, 100 Hz
(roll-off 6 dB/octave). Stimulation was done with
an alternating click with 100 dB SPL (sound
pressure level) intensity, monaurally and binau-
rally. The recording was performed by an MK 6/6
Audio Automatic Protocol Programme, and an
MK 6/7 Cognitive Evoked Potential Programme.
It was stopped and repeated in any case of obvi-
ous muscular activity, or other artifact interfer-
ence. The testing lasted on average 2 h.
 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56 45

Table 1
Significant ABR and MLR latency right and left difference (Mann–Whitney U-test) in normal children, with systematic and
non-systematic errors of speech

Normals Systematics Non-systematics

Wave Side Diff. (ms) P Wave Side Diff. (ms) P Wave Side Diff. (ms) P

ABR PPS 21
I Left 0.08 0.02
II Left 0.18 0.043
V Left 0.24 0.024
MLR
Na Right 3.35 0.046

ABR, auditory brainstem response; MLR, middle latency response; Diff., prolongation of wave latency; PPS, pulses per second.

The latency binaural interaction (BI) was calcu-
lated [27]. Data of a stable parameter (latency)
were analyzed by descriptive statistics and Mann –
Whitney U-test.
3. Results
Representative wave forms from each group
tested are presented in Figs. 1 – 3.
3.1. Right–left differences
The only latency prolonged in the N group was
the ABR left wave I (0.08 ms) (Table 1).
In the S group, latencies of waves II and V were
longer (0.18 and 0.24 ms, respectively) on the left
side, with increased significance on higher levels
of wave generation (Table 1).
For the NS group there was no significant
difference between the right – left recording side
for ABR latencies (Table 1).
Wave II was less identifiable in all groups
(Table 2). The identification was reduced from the
N to the S group, with smallest values for the NS
group (Table 2). For the NS group, wave II was
less identifiable on the left than on the right side
(Table 2).
The unique latency prolongation (3.35 ms) reg-
istered in the NS group was from the MLR right
wave Na (Table 1).
3.2. ABR latency differences between the N, S
and NS groups
There was no significant difference in ABR
latency between the N and S groups (Table 3).
Only on highest stimulus presentation rate (PPS
71), was a latency prolongation of right wave III
(0.38 ms) recorded in the NS group compared to
the S group (Table 3).
The difference between the N and NS groups in
ABR recordings was a latency prolongation of the
right wave III at all PPS applied (0.20 ms at PPS
21, 0.19 at PPS 51 and 0.32 ms at PPS 71) (Table
3).
In the NS group the V wave latency was pro-
longed 0.15 ms at PPS 51 and 0.20 ms at PPS 71
compared to normals (Table 3). On higher PPS
(51 vs 71) the difference was bigger and more
significant (Table 3). A prolongation (0.29 ms) of
the right wave III on binaural stimulation at PPS
21 (Table 3) was also recorded. The identification
of waves III and V was similar (Table 2).
3.3. ABR latency differences in the N, S and NS
groups at different sweep rates
In the N group, after increasing PPS from 21 to
51, latencies prolonged for the right waves III
(0.10 ms) and V (0.21 ms) (Table 4). Also, on left
side the latency of wave V was longer (0.38 ms)
(Table 4). Changing PPS from 21 to 71, the
 46
D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56

Fig. 1. Representative wave-forms of auditory brainstem responses (ABR) of sweep rate (PPS) 21, 51 and 71 and middle latency response (MLR) in a group of normal
children. Case: S.B., female, 7 years old.
 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56

Fig. 2. Representative wave-forms of auditory brainstem responses (ABR) of sweep rate (PPS) 21, 51 and 71 and middle latency response (MLR) in a group of children
with systematic errors of speech. Case: M.B., female, 7 years old.
47
 48
D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56

Fig. 3. Representative wave-forms of auditory brainstem responses (ABR) of sweep rate (PPS) 21, 51 and 71 and middle latency response (MLR) in a group children
with non-systematic errors of speech. Case: M.M., male, 7 years old.
 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56 49

Table 2
Identifiable auditory brainstem response (ABR) waves in normal children, with systematic and non-systematic errors of speech

Wave Normal (total n= 17) Systematic (total n = 8) Non-systematic (total n =8)

Right (n) Left (n) Right (n) Left (n) Right (n) Left (n)

ABR Sweep Rate 21

I 15 7
II 12 13 7 7 4
III
V
ABR Sweep Rate 51
I 7 6 7
II 10 9 5 5 4 3
III 16 16 7 7
V 16
ABR Sweep Rate 71
I 16 16 6 6 5 7
II 12 13 4 3 3 1
III 7 7 6
V

Waves with total number were excluded.

increase of wave III latency was higher on the
right than on the left side (0.17 vs 0.15 ms), as
well for wave V (0.31 vs 0.23 ms) (Table 4). The
latency of the wave I was prolonged (0.1 ms) only
on the right side (Table 4). The identification of
the wave was similar (Table 2).
In the S group, changing PPS from 21 to 51,
prolonged latencies of right waves II (0.17 ms)
and V (0.32 ms) (Table 4). On the contrary to
wave V, wave II was less identified at higher PPS
(Table 2).
In the NS group a latency prolongation of right
wave V was progressively higher and more signifi-
cant with increase in PPS (0.31 ms at PPS 21 vs 51
and 0.46 ms at PPS 21 vs 71) (Table 4). This
relation could be similar for left wave V, if a
prolongation of 0.33 ms at PPS 21 vs 51 was not
on the limit of significance (p = 0.05). Wave III
(0.17 ms) was registered only on the left side in
the NS group, and only on alteration of PPS from
21 to 51 (Table 4). There was no prolongation
of the wave III latency on either side at PPS 71
compared to PPS 21 (Table 4). The identifica-
tion of wave III was similar in the NS group
(Table 2).
3.4. ABR inter-wa6e differences in the N, S and
NS groups
The left III–V inter-wave latency difference
(IW) was significantly higher (0.15 ms) in the S
group compared to the N group at PPS 71 (Table
5). In the NS group, the left III–V IW was
significantly higher (0.16 ms) at PPS 21 than in
the S group (Table 5). Compared to the N group,
at the same PPS 21, the right I–III IW was
significantly higher (0.16 ms) on binaural stimula-
tion in the NS group (Table 5). On ipsilateral
stimulation the same I–III right IW difference
(0.14 ms) was on the limit of significance (P=
0.05).
3.5. MLR latency differences between the N, S
and NS groups
For MLR a difference between the N and S
groups was a 3.02 ms latency prolongation of the
right wave Na (Table 6). The latency of the right
wave Na was 2.91 ms longer in the NS group than
in the S group (Table 6). The registered prolonga-
tion of the wave Na latency, between the N and
50 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56

Table 3
Significant ABR latency differences (Mann–Whitney U-test) at sweep rates 21, 51, 71 in normal children, with systematic and
non-systematic errors of speech

Normals/systematics Systematics/non-systematics Normals/non-systematics

Wave Side Diff. (ms) P Wave Side Diff. (ms) P Wave Side Diff. (ms) P

ABR PPS 21
III Right 0.20 0.004
III B. Right 0.29 0.001
ABR PPS 51
III Right 0.19 0.005
V Right 0.15 0.032
ABR PPS 71
III Right 0.38 0.015 III Right 0.32 0.001
V Right 0.20 0.010

ABR, auditory brainstem response; PPS, pulses per second; Diff., prolongation of wave latency.

NS groups, was the the sum (5.93 ms) of the N There were no significant gender differences in
versus S, and S versus NS difference on the right either group.
side (Table 6). In the NS group, on binaural
stimulation, the latency of left wave Na was pro-
longed (2.21 ms) compared to normals (Table 6). 4. Discussion

3.6. Binaural interaction (BI) latency
There were no significant BI values for ABR.
BI values were significant only for the MLR Na
and Pa wave latency (Table 6). The BI of wave
Na was prolonged in the S group on the left side
(3.52 ms) (Table 6). In the same group, the pro-
longation of BI of the right Na wave (4.07 ms)
was on the limit of significance (P = 0.05) (Fig. 1).
There was no difference in BI between the S and
NS groups (Table 6). In the NS group, a prolon-
gation of the BI of the left Na wave latency (4.84
ms) was registered when compared to the N group
(Table 6). In the same group, for the right side, a
prolongation of the BI of the Na wave (6.36 ms)
was on the limit of significance (P =0.05) (Fig. 1).
The BI for Pa wave latency was prolonged in
the NS group compared to the N group, for the
right side (6.76 ms) (Table 6). The prolongation of
the BI of the left wave Pa (4.18 ms) was on the
limit of significance (P =0.05) in the same group
comparison (Fig. 1).
In the S group compared to normals, the BI for
the wave Pa was similarly prolonged for the both
sides, but not statistically significant (Fig. 1).
A lateralization effect on ABR was found in the
S group, as suggested in normal children [31,37]
(Table 1). In our normal group, it was only
confirmed for wave I, but with a very small
difference (Table 1). The efficiency of both AA
pathways was the same in our NS group up to IC,
as described in reading, writing and spelling
difficulties [31] (Table 4). Our results indicate also
a more effective right pathway in more rostral
thalamocortical divisions (Table 1).
All of our latency values were within the limits
of normative values for ABR [14,43] and MLR
[22,41] for the 7-year-old age group. Differences
between our groups could not be related only to
immaturity, even as a complex process [7]. Our
results cannot be limited exclusively to myeliniza-
tion as one of maturational process [25]. It could
be also a difference in functioning [9,39,40], possi-
bly genetically determined [11].
These differences could be prolonged ABR la-
tencies (X( = 0.25 ms) of the waves representing
the middle pons on the right side in the NS group,
when compared to normal children (Table 3).
With an augmented neural overload (PPS 51 and
71) in the NS group compared to normal, we
 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56 51

Table 4
Significant ABR latency difference (Mann–Whitney U-test) between sweep rates 21, 51 and 71 in normal children, with systematic
and non-systematic errors of speech

Normals Systematics Non-systematics

Wave Side Diff. (ms) P Wave Side Diff. (ms) P Wave Side Diff. (ms) P

Sweep rate 21 vs 51
II Right 0.17 0.034
III Right 0.10 0.007
V Right 0.21 0.006 V Right 0.32 0.031 V Right 0.31 0.007
III Left 0.17 0.049
V Left 0.38 0.011
Sweep rate 51 vs 71
V Right 0.15 0.049
Sweep rate 21 vs 71
I Right 0.10 0.007
III Right 0.17 0.001
V Right 0.31 0.0001 V Right 0.46 0.001
III Left 0.15 0.030
V Left 0.23 0.014 V Left 0.41 0.011

ABR, auditory brainstem response; Diff., prolongation of wave latency.

observed a progressive prolongation (X( = 0.175
ms) of latency, even though lately contested [10],
at more rostral parts (wave V) on the same side
(Table 3). Also, the right wave III and its latency
prolongation could be involved in a subtle differ-
entiation between systematic and non-systematic
errors of the speech (identified only on highest
PPS) (Table 3).
These differences could be a result of gender
disproportion in our NS group. The prolongation
of latencies of ABR in adult males is known [16].
But, our calibration results, as well as results in
this study did not show any significant latency
change between males and females. A gender dis-
proportion in the NS group is a characteristic of
this type of speech pathology with a predomina-
tion in the male population, usually accompanied
with lateralization difficulties [15,38]. Our result
could also present a difference in functioning in
this specific NS speech alteration.
In the group of normal children the expected
prolongation of wave latencies at higher sweep
rate (PPS 51) was confirmed, representing the
middle and upper pons [42,47], on the right side
(Table 4). The only latency prolongation regis-
tered on left side in this group, at PPS change
from 21 to 51, was of wave V latency (Table 4). In
the N group on higher informational overload
(PPS 21 vs 71) the prolongation was bilateral, even
though it was greater and more significant on the
right side, corresponding to adult values [4].
No significant prolongation of the latency was
registered on the left side in children with system-
atic errors of the speech with alteration of PPS
(Table 4). In the S group, as in the N group, a
prolongation of wave V was registered on the right
side, but only on alteration of PPS 21 to 51 (Table
4). A latency prolongation of right wave II (Table
4) was also registered. This could be attributed to
low identification of this wave (Table 2).
In the NS group the equity of two AA pathways
was suggested, especially on higher neural over-
load with a more significant prolongation of the
latency at more cranial levels. The left wave III
latency prolongation (on PPS 51 vs 21) could
mean a detection of more subtle differences on the
contralateral side (Table 4).
The expected prolongation of latency with aug-
mentation of sweep rate was found in the normal
group (Table 4). The change of PPS from 51 to 71
was not significant in the N and S groups. This
could indicate that an increase of PPS does not
necessarily evoke a linear prolongation of latency.
This indicated more an existence of the threshold
52 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56
Table 5
Significant ABR inter-wave latency differences (Mann–Whitney U-test) in normal children, with systematic and non-systematic
errors of speech at sweep rates 21 and 71
Normals/systematics Systematics/non-systematics
IW Side Diff. (ms) P IW Side
ABR PPS 21
III–V Left
ABR PPS 71
III–V Left 0.15 0.024
ABR, auditory brainstem response; IW, inter-wave latency differences; Diff., prolongation of wave latency; PPS, pulses per second.
for a neural reaction, which is not only progres-
sive adaptation [16]. It depends on types of electri-
cal activity at certain neural levels, and
inhibitory–excitatory interactions [16]. In the NS
group this change, PPS 51 vs 71, was significant,
which could be also a difference in functioning
(Table 4).
A certain immaturity of higher AA pathways
could be indicated for all groups. This could
correspond to a still not established lateralization
effect in AA pathways, which is adequate to the
age of the children studied and to the level of the
developmental process (Table 4) [6,7] and its ros-
tro-caudal orientation [47].
On a habitual information presentation (PPS
21) there was no IW difference between the N and
S groups. The III–V IW difference between the N
and S groups was detected only on PPS 71, on the
left side (Table 5). This suggests that the location
of a probable alteration in systematic errors of the
speech is at the upper contralateral pons. This
could be evidence that systematic errors of the
speech are more subtle alterations.
A prolonged left III – V IW difference (0.16 ms)
was detected at PPS 21 (Table 5) between the S
and NS groups.
The difference between normal and NS groups
is a prolongation of I – III IW on PPS 21, detected
on the right side (0.16 ms) (Table 5). So, non-sys-
tematic errors of speech could have an alteration
at the level of the more ipsilateral lower pons, as
well as at the upper more contralateral pons.
Our inter-wave relations of ABR waves could
indicate an altered functioning of the pons in
Normals/non-systematics
Diff. (ms) P IW Side Diff. (ms) P
I–III B. Right 0.16 0.027
0.16 0.027
children with an alteration of the speech [18].
From our results, in right-handed persons, it is
dependent on caudal more ipsilateral levels in
more profound alterations, as well on more ros-
tral contralateral levels (Table 5). The results in
children with bad phonemic hearing show only a
significant prolongation of I–III IW on the right
side [25]. So, the location of the alteration in
non-systematic errors of speech and bad phone-
mic hearing is the same. Bad phonemic hearing
could be a constitutional part of a dysfunction
causing a non-systematic alteration of the speech.
On higher levels of AA pathways, the latency of
the subcortical Na wave [19] on the right side, was
progressively augmented (X( = 3.96 ms) with a
progression in the alteration of the speech (Table
5).
It is known that a Pa wave [8] and higher ABR
waves [45] show a binaural occlusion effect with a
convergent projection [27,29]. We did not find any
significant ABR BI difference in our groups, with
our values shorter than in adults [27].
Compared to normal children we detected a
prolongation of MLR BI of the left wave Na, in
the S group for 3.52 ms and in the NS group for
a further 1.32 ms (Table 6). The successive latency
prolongation (6.36 ms, not referred in Table 6) of
the right wave Na for these two groups is only
suggested.
The expected BI prolongation of the wave Pa
(6.76 ms) was registered only in NS group, on the
right side in relation to normal (Table 6). The
same was only suggested for the left wave Pa in
this group (not referred in Table 6).
 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56
Table 6
Significant MLR and latency binaural interaction differences (Mann–Whitney U-test) in normal children, with systematic and
non-systematic errors of speech
Normals/systematics Systematics/non-systematics
Wave Side Diff. (ms) P Wave Side
MLR
Na Right 3.02 0.020 Na Right
Binaural Interaction MLR
Na Left 3.52 0.037
MLR, middle latency response; Diff., prolongation of wave latency; B. Right, binaural right; B. Left, binaural left.
For a S group the same prolongation of BI Pa
wave latency was registered, but not statistically
significant, excluding its clinical utility (Fig. 4).
This could be an indication of a continuing
process of maturation [23] of MLR with its final-
ization in 12–14 years old [7]. It could also be just
another indication of altered function of AA path-
ways in children with the speech problems, already
suggested by inter-wave relations.
Our results indicate more an alteration of a
functioning of higher AA pathways as suggested
by Wada and Starr [45]. McPherson et al. [27]
registered significant differences in BI MLR be-
tween adults and term infants (conceptional age
between 38–41 weeks). The Na and Pa wave
latency values were significantly shorter in term
children than in adults [27]. The prolongation of
BI Na and Pa, progressively augmenting with the
alteration of the speech in our results, cannot
indicate only immaturity.
A difference in the functioning, without a sub-
stantial structural alteration, was found in insulin-
dependent diabetics [44], hypoxia [17] and
lidocaine injections in the cerebrospinal fluid [46],
suggesting a neural dysfunction. The speculations
could be elicited about a difference in excitatory –
inhibitory orientation in binaurally influenced
neurons [29].
This latency prolongation was not found in
communicative disorders [22], cerebral lesion with
aphasia [20] or in receptive developmental lan-
guage disorder (RDLD) [1]. The conditions ap-
plied in all of these studies were different. Any-
way, a Pa wave latency prolongation was ob-
53
Normals/non-systematics
Diff. (ms) P Wave Side Diff. (ms) P
2.91 0.031 Na Right 5.93 0.0003
Na B. Left 2.21 0.027
Na Left 4.84 0.011
Pa Right 6.76 0.016
served in cerebral lesion with aphasia [20]. In the
work with RDLD all the subjects were older than
in our work, and the matching control group in
the same work was significantly older than the
examined group [1]. Still, shorter latencies for
wave III and V were registered in the RDLD
group.
Smith and co-workers did not find any differ-
ences in detection of Na and Pa waves between
normal children, those with communicative disor-
ders, mentally retarded and children with miscella-
neous disorders [22]. The age groups were well
matched. But, we suppose that the results in our
study cannot be compared to those of children
with communicative disorders. The group determi-
nation as ‘communicative disorder’ is, in our opin-
ion, too wide, and the attribute analyzed is
different (latency versus detection).
Possible errors in our study could result from a
small number of subjects and differences in sex
and age distribution. A more exact and limited
classification of speech disorders should be applied
as well as the use of a more physiological stimulus.
5. Conclusions
(1) There was some evidence of a different
auditory afferent organization in children with
dyslalia. (2) In right-handed children with system-
atic errors of speech, the efficiency of the con-
tralateral upper pons and primarily contralaeral
thalamocortical projections could be altered. (3) In
right-handed children with non-systematic er-
54 D. Milic' ić et al. / Int. J. Pediatr. Otorhinolaryngol. 46 (1998) 43–56

Fig. 4. Middle latency response (MLR) latency binaural interaction (BI) differences (Mann – Whitney U-test) in normal children,
with systematic and non-systematic errors of speech.

rors of the speech, there was no lateralization Acknowledgements

effect on the auditory afferent pathway up to IC.
In this group, we registered alterations in auditory
afferent pathways at the level of lower ipsilateral
and upper contralateral pons and primarily con-
vergent thalamocortical projections with an al-
tered efficacy. (4) The ABR and MLR could serve
as diagnostic methods in the auditory – speech
evaluation in children. (5) It was suggested that
non-systematic errors of speech are more pro-
found alteration of the speech.
The first author thanks Professor Dr Ksenija
Ribaric for her orientation and help provided on
the initial phase of this work.
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