Cortical auditory evoked potentials in children who stutter

International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101

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Cortical auditory evoked potentials in children who stutter Naema Ismail a, Yossra Sallam a, *, Reda Behery a, Ameera Al Boghdady b a b

Faculty of Medicine, AlAzhar University, Egypt Resident of Audiology, New Mansoura General Hospital, Egypt

a r t i c l e i n f o

a b s t r a c t

Article history: Received 2 November 2016 Received in revised form 24 March 2017 Accepted 26 March 2017 Available online 3 April 2017

Introduction: It has been hypothesized that impaired auditory processing influence the occurrence of stuttering. Also, it is suggested that speech perception in children who stutter differed from normal. Auditory processing should be investigated in children who stutter shortly after the onset of stuttering in order to evaluate the extent to which impaired auditory processing contributes to the development of stuttering. CAEPs provide the necessary temporal and spatial resolution to detect differences in auditory processing and the neural activity that is related or time-locked to the auditory stimulus. The primary goal of the present study was to determine the difference in latency and amplitude of P1-N2 complex between children who stutter and non-stuttering children in response to speech stimuli. Material & methods: This case-control study was performed over 60children, 30were non-stuttering children (control group) and 30were children who stutter (study group) ranging in severity from Bloodstien I to Bloodstien IV in the age range of 8e18 years. Results: CAEPs of children who stutter with stuttering severity Bloodstien IV showed significant prolonged latencies and reduced amplitudes when blocks and IPDs were the most predominant core behaviors. P1 and N1 were prolonged in concomitant behaviors. Conclusion: It could be speculated that speech processing was affected in children who stutter with stuttering severity Bloodstien IV at the level of early perceptual auditory cortex. © 2017 Elsevier B.V. All rights reserved.

Keywords: CAEPs Stuttering Auditory processing

1. Introduction Persistent developmental stuttering is a subtype of speech fluency disorders characterized clinically by abnormal frequency or duration of interruption in the flow of speech, namely repetitions, prolongations, and/or blocks [9]. Stuttering presents in the form of overt and covert stuttering. Overt stuttering is characterized by repetitions, prolongations, blocks, and/or intraphonemic disruptions (IPDs). Covert stuttering is characterized by word substitutions and interjections which help to postpone, avoid, and hide the impact of stuttering [5]. The presence of associated concomitant problems like eye blinking, flaring nostrils, head nodding, and feet tapping indicates greater stuttering severity [4]. According to these symptoms [2], rated the severity of stuttering into four degrees; the 1st degree is when stuttering is episodic and consists only of repetitions of which the child is not aware, the 2nd

* Corresponding author. E-mail address: [email protected] (Y. Sallam). http://dx.doi.org/10.1016/j.ijporl.2017.03.030 0165-5876/© 2017 Elsevier B.V. All rights reserved.

degree is when stuttering is chronic or habitual, other forms of interruptions start to appear, and the child is aware of his dysfluency, the 3rd degree is when stuttering occurs in feared situations and word substitution may be used to avoid feared word, and the 4th degree (which is the most advanced form), is when word fear and situation avoidance occur in addition to secondary reactions. Although a variety of theories have been proposed to explain its etiology, the exact cause of stuttering is still unknown [9]. Theories of stuttering incorporate many factors like atypical auditory processing, genetics, personality, linguistic factors and atypical neurophysiology. According to [21], disturbed cerebral dominance in left handed individuals (either with right hemispheric shift or bilateral dominance with low left hemispheric activation) also contributed to the occurrence of stuttering. The main focus in stuttering research has been on speech production, but a growing literature suggests that stuttering may also be characterized by atypical neural mechanisms underlying speech perception. Central speech sound processing is essential for speech acquisition, production and comprehension [14]. Cortical Auditory evoked potentials (CAEPs) are series of positive and negative peaks labeled P1-N1-P2-N2 occurring between

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50and 500ms after stimulus onset. They reflect obligatory neural events for speech representation in the central auditory system independently of the listener attention. The P1eN2 complex has been suggested to be a representation of the sensory encoding of auditory stimulus characteristics [27]. Peaks of CAEPs are generated from the auditory thalamo-cortical pathways involving both primary and association auditory cortices [19]. There were not many studies found in the literature to examine P1- N2 complex in children who stutter. Most of these studies have been done with adults using pure tone stimuli [13]. Speech auditory processing in children who stutter needs to be evaluated cautiously under variability found in neuroimaging. CAEPs proved to be effective measure for speech processing ability. Recent neurological studies have shown abnormal neural activity in the auditory areas in developmental stuttering. Magnetoencephalographic (MEG) studies have demonstrated that subjects with persistent developmental stuttering show functional and structural abnormalities in the central auditory nervous system including unusual activation patterns in the auditory areas [16]. 1.1. Aim of work The aim of the present study is to evaluate cortical auditory evoked potentials' (CAEPs) response in stuttering children, with variable severity of the presenting symptoms, and to compare them with non-stuttering children. 2. Materials and methods This case-control study was performed in the Phoniatric and Audiology Units of AL Mansoura International Hospital, in the period from March 2014 to March 2015, with 60children in the age range of 8e18 years. They were divided into two groups; the study group composed of 30children who stutter, ranging in severity from Bloodstien I to Bloodstien IV, who were tested prior to any therapeutic intervention, and the control group which was composed of 30children, all of them were non stuttering. The control group was selected from volunteers and relatives who visited the Audiology Unit and Otorhinolaryngology Clinics in the hospital. Both groups had bilateral normal peripheral hearing sensitivity (hearing threshold level did not exceed 15 dB at any frequency of the range of 250e8000Hz), normal middle ear function, normal general health condition and fully developed language. Any children having ear problems (as hearing impairment, otological diseases, ototoxic drug intake, ear surgery or head trauma), children complaining from systemic diseases (e.g. any endocrinal, vascular, renal, convulsions or neurological complaints) and children who received previous Phoniatric rehabilitation for stuttering or suffering from any other Phoniatric disorder were excluded. The severity of stuttering among the study group was determined using [2] classification of severity of stuttering. All children underwent complete phoniatric history and evaluation and otological examination. Hearing was tested using basic audiological evaluation such as pure tone audiometry, speech recognition threshold [23], speech discrimination [24], and immittancemetry. Cortical auditory evoked potentials (CAEPs) were done, using speech stimuli, by the Smart Evoked Potentials of Intelligent Hearing System. The collected data were organized, tabulated and statistically analyzed using SPSS (Statistical Package for Social Science) version 16. Qualitative data were described using number and percent. Association between categorical variables was tested using Chisquare test. Chi-square test (X2) was used for comparison between more than two groups. Parametric analysis (student t-test)

was used for comparison between means of two groups only. Significance was adopted at p < 0.05 for interpretation of results of tests of significance [28]. Post-hoc test was calculated for significant values after ANOVA to determine which comparisons contributed strongly to the significant values [12]. 3. Results Thirty children exhibited developmental stuttering were included in this study. They were classified according to the severity of stuttering into Bloodstien I (three children), Bloodstien II (four children), Bloodstien III (sixteen children) and Bloodstien IV (seven children). They were compared to thirty fluent children as a control group. Both groups are matched as regard age, gender and handedness. Table 2 shows the frequency of occurrence of different symptoms among the study group. The predominant symptom among stutterers Bloodstien I was repetition, whereas stutterers Bloodstien II exhibited repetitions and prolongations in addition to secondary reactions. Stutterers Bloodstien III and IV displayed repetitions, prolongations, blocks, and intraphonemic disruptions in addition to secondary reactions and associated concomitant behaviors. Children who stutter had prolonged latencies and smaller amplitudes in both ears than controls and in the right ear than the left according to absolute latencies and amplitudes of P1, N1, P2 and N2. But, none of these differences had reached a statistically significant level (p > 0.05) as shown in Table 3 and Figs. 1e3. Because the differences between Bloodstien IV and the control group were close to reach a statistically significant level, further analysis using t-test was required because t-test is mainly designed to investigate the significance between 2 groups. Bloodstien IV children who stutter had statistically significant prolonged latencies and smaller amplitudes of P1, N1, P2 and N2 than the control group as shown in Table 4 and Fig. 3. Children who stutter with positive family history had prolonged latencies and smaller amplitudes in both ears than stutterers with negative family history according to absolute latencies and amplitudes of P1, N1, P2 and N2. None of these differences had reached a statistically significant level (p > 0.05) as shown in Table 5. Regarding absolute latencies and amplitudes of P1- N2 complex, Table 6 showed that both groups had prolonged latencies in the right ear (left hemisphere) than in the left ear (right hemisphere). Left handed stutterers had prolonged latencies and smaller amplitudes in both ears than right handed children who stutter. None of these differences had reached a statistically significant level (p > 0.05). Children who stutter had prolonged latencies in both ears than controls and in the right ear than in the left according to absolute latency of P1, N1, P2 and N2 when repetition and prolongation were the predominant core behaviors. Bloodstien IV had the most prolonged latency than other types. None of these differences had reached a statistically significant level (p > 0.05). Stutterers had statistically significant prolonged latencies (p < 0.05) in both ears than controls and in the right ear than in the left according to absolute latency of P1, N1, P2 and N2 when blocks were the predominant core behaviors. Bloodstien IV had the most prolonged latency than other types. Stutterers had statistically significant prolonged latencies (p < 0.05) in both ears than controls and in the right ear than in the left according to absolute latency of P1, N1 and P2 when IPDs were the predominant core behaviors as shown in Table 7. Bloodstien IV had the most prolonged latency than other types. Post-hoc test was done after ANOVA to determine if there was a statistically significant difference between Bloodstien IV children

N. Ismail et al. / International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101

95

Table 1 Characters of the study group. Items

ControlNo ¼ 30

Study No ¼ 30(23 M þ 7 F) Bl st. I No ¼ 3 No

Gender

M F Mean ± SD range R L positive negative

Age/y Handedness Family history

Bl st. II No ¼ 4 %

3 10% e e 12.56 ± 1.4 8e18 3 10% e e 3 100%

Bl st. III No ¼ 16

No

%

No

10% 3.33%

12 40% 4 13.33% 12.83 ± 1.96 8e18 13 43.33% 3 10% 5 31.25% 11 68.75%

25% 75%

P

X2¼.053

0.543

t ¼ 0.876

0.452

X2¼0.766

0.453

Bl st. IV No ¼ 7

3 1 11.32 ± 1.46 8e18 4 e 1 3

13.33%

Test of sig.

%

No

%

No

5 16.66% 2 6.66% 12.95 ± 1.46 8e18 3 10% 4 13.33% 1 14.28% 6 85.71%

%

23 76.66% 7 23.33% 12.8 ± 1.58 8e18 23 76.66% 7 23.33% e e

2

X ¼ 0.566

0.657

BL st. ¼ Bloodstien, No ¼ numbers of children, % ¼ percent of detectability,sig. ¼ significance, y ¼ year, R ¼ right ear, L ¼ left ear, SD ¼ standard deviation, Min ¼ minimum, Max ¼ maximum, M ¼ male, F ¼ female, X2 ¼ Chi square test, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

Table 2 Symptomatology of stuttering in study group. Symptoms

Bl st. I No ¼ 3

(a) Core behaviors

Repetition Prolongation Blocks IPDs Secondary reactions concomitant problems

(b) Other symptoms

Bl st. II No ¼ 4

Bl st. III No ¼ 16

Bl st. IV No ¼ 7

No

%

No

%

No

%

No

%

3 e e e e e

10

2 2 e e 3 e

6.66 6.66

3 3 5 5 10 8

10 10 16.66 16.66 33.33 26.66

1 1 2 3 6 6

3.33 3.33 6.66 10 20 20

10

BL st. ¼ Bloodstien, No ¼ numbers of children, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

Table 3 CAEPs absolute latencies (in ms) and amplitudes (in mV) in Study versus control. CAEP peaks

Ear

Bl.st I

Bl. st. II

Bl. st. III

Bl. st. IV

Control

ANOVA

P value

P1 Lat.

R L

0.608 1.496

0.612 0.226

N2 Lat.

R L

1.854 1.295

0.148 0.285

P1 Amp.

R L

1.259 0.567

0.297 0.639

N1 Amp.

R L

7.621 1.730

0.321 0.171

P2 Amp.

R L

1.201 1.251

0.318 0.324

N2 Amp.

R L

78. 7 ± 12.4 79.6 ± 13.4 t ¼ 0.214 P ¼ 131.7 ± 13.7 132.3 ± 13.5 t ¼ 0.214 P ¼ 177.9 ± 10.6 180.5 ± 10.7 t ¼ 0.234 P ¼ 223.3 ± 9.3 224.7 ± 11.6 t ¼ 0.084 P ¼ 3.9 ± 1.12 3.87 ± 1.77 t ¼ 0.983 P ¼ 3.57 ± 0.92 3.51 ± 0.78 P ¼ 0.643 1.9 ± 0.4 1.8 ± 0.51 P ¼ 0.196 3. 9 ± 0.92 4.1 ± 1.74 P ¼ 0.432

0.724 0.751

R L

93.2 ± 12.8 90.5 ± 12.27 t ¼ 0.154 P ¼ 142.3 ± 12.2 141 ± 13.44 t ¼ 0.654 P ¼ 190.8 ± 12.3 185.3 ± 16.5 t ¼ 0.214 P ¼ 235.67 ± 6.8 231.2 ± 11.4 t ¼ 0.324 P ¼ 3.02 ± 1.25 3.13 ± 1.95 t ¼ 0.983 P ¼ 2.01 ± 0.47 2.5 ± 0.86 P ¼ 0.756 0.81 ± 0.5 0.83 ± 0.39 P ¼ 0.326 3.13 ± 1.2 3.19 ± 0.54 P ¼ 0.543

0.442 0.404

P2 Lat.

84.6 ± 10.3 83.91 ± 15.7 t ¼ 0.434 P ¼ 0.431 140.74 ± 11.4 138.04 ± 13.5 t ¼ 0.235 P ¼ 0.315 185.57 ± 12.7 184.7 ± 19.97 t ¼ 0.235 P ¼ 0.063 229.4 ± 8.47 227.91 ± 9.4 t ¼ 0.454 P ¼ 0.654 3.32 ± 0.98 3.35 ± 1.8 t ¼ 0.983 P ¼ 0.0652 2.6 ± 0.52 2.7 ± 0.69 P ¼ 0.129 1.1 ± 0.5 1.12 ± 0.48 P ¼ 0.453 3.3 ± 1.7 3.37 ± 0.73 P ¼ 0.765

0.375 0.629

R L

82.3 ± 11.2 81.5 ± 12.3 t ¼ 0.234 P ¼ 135 ± 10.13 133 ± 12.1 t ¼ 0.634 P ¼ 180± 11.2 179.6 ± 12.3 t ¼ 0.564 P ¼ 226.2 ± 12.3 225 ± 10.89 t ¼ 0.764 P ¼ 3.5 ± 1.3 3.57 ± 0.71 t ¼ 0.983 P ¼ 2.9 ± 0.72 3.01 ± 1.7 P ¼ 0.145 1.3 ± 0.3 1.35 ± 0.28 P ¼ 0.612 3.5 ± 1.5 3.56 ± 1.4 P ¼ 0.387

1.56 0.583

N1 Lat.

80.45 ± 10.4 80.34 ± 11. 4 t ¼ 0.234 P ¼ 132.6 ± 12.7 131.2 ± 10.5 t ¼ 0.164 P ¼ 181.3 ± 11.7 176.5 ± 9.6 t ¼ 0.234 P ¼ 223.4 ± 10.6 222.6 ± 8.3 t ¼ 0.454 P ¼ 3.74 ± 1.54 3.79 ± 1.31 t ¼ 0.983 P ¼ 3.2 ± 0.76 3.3 ± 0.93 P ¼ 0.136 1.6 ± 0.42 1.64 ± 0.53 P ¼ 0.654 3. 8 ± 0.94 3.82 ± 1.67 P ¼ 0.178

0.834 1.357

0.481 0.265

0.125

0.231

0.053

0.236

0.321

0.213

0.432

0.062

0.564

0.324

0.214

0.149

0.129

0.093

0.431

0.412

0.231

0.084

0.965

0.561

CAEPs ¼ Cortical Auditory Evoked Potentials, Bl st. ¼ Bloodstien, Lat. ¼ latency, ms ¼ milliseconds, R ¼ right ear, L ¼ left ear, ANOVA ¼ Analysis Of Variance, 6546 P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

who stutter and controls when blocks and IPDs were the predominant core behavior. Children who stutter had smaller amplitudes in both ears than controls and in the right ear than in the left according to absolute amplitude of P1, N1, P2 and N2 when repetition and prolongation were the predominant core behaviors. Bloodstien IV had the

smallest amplitude than other types. None of these differences had reached a statistically significant level (p > 0.05). Stutterers had statistically significant smaller amplitudes (p < 0.05) in both ears than controls and in the right ear than in the left according to absolute amplitude of P1, N1, P2 and N2 when blocks were the predominant core behaviors. Bloodstien IV had the

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Fig. 1. P1- N2 complex of CAEPs recorded from 12 years old right handed normal fluent child (control) response to/ba/syllables at 70dB nHL.

Fig. 2. P1- N2 complex of CAEPs recorded from 13 years old right handed Bloodstien II stuttering child in response to/ba/syllables at 70dB nHL.

Fig. 3. P1- N2 complex of CAEPs recorded from 16 years old right handed Bloodstien IV stuttering child in response to/ba/syllables at 70dB nHL.

smallest amplitude than other types. Stutterers had statistically significant smaller amplitudes (p < 0.05) in both ears than controls and in the right ear than in the left according to absolute amplitude of P1 and N1 when IPDs were the predominant core behaviors. Bloodstien IV had the smallest amplitude than other types. as shown in Table 8. Post-hoc test was done after ANOVA to determine if there was statistically significant differences between stutterers Bloodstien IV and controls when blocks and IPDs were the predominant core behavior. Children who stutter had prolonged latencies and smaller amplitudes in both ears than controls and in the right ear than in the left according to secondary reactions of stuttering. But, none of these differences had reached a statistically significant level (p > 0.05) as shown in Table 9. Children who stutter had statistically significant prolonged latencies (p < 0.05) in both ears than controls and in the right ear than in the left according to absolute latency of P1 and N1 with concomitant behaviors of stuttering. Post hoc test revealed the difference between Bloodstien IV stutterers versus control as

shown in Table 10. Children who stutter had smaller amplitudes in both ears than controls and in the right ear than in the left according to absolute amplitude of P1, N1, P2 and N2 with concomitant behaviors of stuttering. But, none of these differences had reached a statistically significant level (p > 0.05) as shown in Table 10. Post hoc test determined the presence of statistically significant prolonged latencies in Bloodstien IV children who stutter than controls according to associated concomitant behaviors.

4. Discussion Auditory processing should be investigated in children who stutter shortly after the onset of stuttering in order to evaluate the extent to which impaired auditory processing contributes to the development of stuttering prior to therapeutic intervention. CAEPs provide the necessary temporal and spatial resolution to detect differences in auditory processing and the neural activity that is related or time-locked to the auditory stimulus [18]. The characters of the study group were displayed in Table 1. The

N. Ismail et al. / International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101 Table 4 CAEPs absolute latencies (in ms) and amplitudes (in mV) in Bloodstien IV versus control. CAEP peaks

ear

Bl. st. IV

Control

t-test

P value

P1 Lat.

R L R L R L R L R L R L R L R L

93.2 ± 12.8 90.5 ± 12.27 142.3 ± 12.2 141 ± 13.44 190.8 ± 12.3 185.3 ± 16.5 235.67 ± 6.8 231.2 ± 11.4 3.02 ± 1.25 3.13 ± 1.95 2.01 ± 0.47 2.5 ± 0.86 0.81 ± 0.5 0.83 ± 0.39 3.13 ± 1.2 3.19 ± 0.54

78. 7 ± 12.4 79.6 ± 13. 4 131.7 ± 13.7 132.3 ± 13.5 177.9 ± 10.6 180.5 ± 10.7 223.3 ± 9.3 224.7 ± 11.6 3.9 ± 1.12 3.87 ± 1.77 3.57 ± 0.92 3.51 ± 0.78 1.9 ± 0.4 1.8 ± 0.51 3. 9 ± 0.92 4.1 ± 1.74

2.34 2.683 2.742 2.704 2.878 2.66 2.831 2.735 2.959 2.567 2.621 2.730 2.201 2.251 2.834 2.357

0.0432* 0.031* 0.041* 0.031* 0.024* 0.043* 0.045* 0.035* 0.032* 0.029* 0.031* 0.041* 0.028* 0.032* 0.021* 0.035*

N1 Lat. P2 Lat. N2 Lat. P1 Amp. N1 Amp. P2 Amp. N2 Amp.

CAEPs ¼ Cortical Auditory Evoked Potentials, Bl st. ¼ Bloodstien, Lat. ¼ latency, ms ¼ milliseconds, R ¼ right ear, L ¼ left ear, ANOVA ¼ Analysis Of Variance, 6546 P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

97

development that was related to male sex hormone testosterone. In stuttering, part of the left side of the brain might grow more slowly than the right leading to a change in the usual dominance patterns of the brain [7] (3). family history for stuttering: seven boys of the study group (23%) had positive family history. In families, the male to female ratio of stuttering is approximately 2:1 [22]. The use of speech stimuli in the current study for recording CAEPs was preferred because children who stutter usually have impaired speech processing [14]. In the present study, children who stutter had prolonged latencies and smaller amplitudes of P1, N1, P2 and N2 in both ears than controls and in the right ear (left hemisphere) than the left ear (right hemisphere). These differences reached a statistically significant level in stuttering severity Bloodstien IV. The prolonged latencies of P1eN2 complex indicated delayed neural conduction and auditory processing disorders especially with severe phases of stuttering [10]. The reduced amplitude of CAEPs indicated that smaller number of synchronously active neurons responded to the stimulus and lesser cortical auditory activation with impaired processing [4]. These results could be explained on the basis of alpha excitability cycle theory. In stuttering, small number of the

Table 5 CAEPs absolute latencies (in ms) and amplitudes (in mV) in children who stutter with þve family history and children who stutter with -ve family history. CAEP peaks

Ear

Positive family history No ¼ 7

Negative family history N0¼ 23

Control No ¼ 30

ANOVA

P value

P1 Lat.

R L

0.442 0.404

0.724 0.751

P2 Lat.

R L

0.608 1.496

0.612 0.226

N2 Lat.

R L

1.854 1.295

0.148 0.285

P1 Amp.

R L

1.259 0.567

0.297 0.639

N1 Amp.

R L

7.621 1.730

0.321 0.171

P2 Amp.

R L

1.201 1.251

0.318 0.324

N2 Amp.

R L

78. 7 ± 12.4 79.6 ± 13. 4 t ¼ 0.532 P ¼ 0.412 131.7 ± 13.7 132.3 ± 13.5 t ¼ 0.524 P ¼ 0.231 177.9 ± 10.6 180.5 ± 10.7 t ¼ 0.514 P ¼ 0.084 223.3 ± 9.3 224.7 ± 11.6 t ¼ 0.562 P ¼ 0.965 3.9 ± 1.12 3.13 ± 1.77 T ¼ 652 P ¼ 0.561 3.5 ± 0.92 2.97 ± 0.78 T ¼ 0.331 P ¼ 0.643 1.9 ± 0.4 1.3 ± 0.51 T ¼ 0.376 P ¼ 0.196 3. 9 ± 0.92 3.5 ± 1.74 T ¼ 0.397 P ¼ 0.432

0.375 0.629

R L

80.45 ± 10.4 80.34 ± 11. 4 t ¼ 0.324 P ¼ 0.125 132.6 ± 12.7 131.2 ± 10.5 t ¼ 0.234 P ¼ 0.231 185.3 ± 11.7 182.5 ± 9.6 t ¼ 0.565 P ¼ 0.153 227.4 ± 10.6 225.6 ± 8.3 t ¼ 0.534 P ¼ 0.236 2.6 ± 1.3 2.7 ± 0.71 T ¼ 0.352 P ¼ 0.324 2.6 ± 0.72 2.7 ± 1.7 T ¼ 0.842 P ¼ 0.145 0.94 ± 0.3 1.15 ± 0.28 T ¼ 0.982 P ¼ 0.612 3.1 ± 1.5 3.31 ± 1.4 T ¼ 0.832 P ¼ 0.387

1.56 0.583

N1 Lat.

83.8 ± 9.3 82.1 ± 11.1 t ¼ 0.564 P ¼ 0.323 136.1 ± 11.43 134.2 ± 10.11 t ¼ 0.544 P ¼ 0.515 189.2 ± 10.4 185.3 ± 11.6 t ¼ 0.538 P ¼ 0.218 230.3 ± 10.1 228 ± 11.19 t ¼ 0.764 P ¼ 0.302 2.44 ± 1.54 2.5 ± 1.31 T ¼ 0.332 P ¼ 0.321 2.33 ± 0.76 2.5 ± 0.93 T ¼ 0.376 P ¼ 0.136 0.79 ± 0.42 0.87 ± 0.53 T ¼ 0.672 P ¼ 0.654 2.82 ± 0.94 2.9 ± 1.67 T ¼ 0.852 P ¼ 0.178

0.834 1.357

0.481 0.265

Bl st. ¼ Bloodstien, No ¼ numbers of children, Amp. ¼ amplitude, mV ¼ microvolt, R ¼ right ear, L ¼ left ear, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

age range between eight and eighteen was chosen for two reasons (1): definitive diagnosis of stuttering was not established before that age. Before that age, children were more likely to suffer from physiological dysfluency than developmental stuttering [20] (2). N1 and P2 components of CAEPs begin to appear after 7 years of age [8]. P1 and N1 peak latencies reach adult-like waveform at approximately 18 years of age [25]. Other criteria of the study group included (1): male predominance: the study group included 23 boys and 7 girls. The male to female ratio was about 3:1 which approximates the universal male to female ratio of 3e4: 1 in stuttering [4] (2). handedness: seven boys of the study group (23%) were left handed stutterers. Atypical hand preference was considered a marker of atypical cerebral dominance which might come from a variation in fetal brain

brain cells of similar frequencies (narrow tuning) responded to the auditory stimulus resulting in less potential neural processing of incoming and outgoing neural events. Disturbed excitability of alpha cells led to disturbed synchronization of input and output of sensory stimuli which were needed for the natural performance of speech [6]. Children who stutter with positive family history had more prolonged latencies and smaller amplitudes of P1, N1, P2 and N2 in both ears than controls and stutterers with negative family history. Although these differences did not reach a statistically significant level, positive family history may lead to exacerbation and persistence of the symptoms. [4] found anatomical abnormalities in positive family history stutterers as decreased gray matter and increased white matter volume in auditory cortical areas (planum

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Table 6 CAEPs absolute latencies (in ms) and amplitudes (in mV) in right handed versus left handed children who stutter. CAEP peaks

Ear

Right handed stutterers No ¼ 23

Left handed stutterers No ¼ 7

T test

P value

P1 Lat.

R L R L R L R L R L R L R L R L

80.45 ± 10.4 80.34 ± 11. 4 132.6 ± 12.7 131.2 ± 10.5 181.3 ± 11.7 176.5 ± 9.6 223.4 ± 10.6 222.6 ± 8.3 2.74 ± 1.54 2.9 ± 1.31 2.63 ± 0.76 2.8 ± 0.93 0.97 ± 0.42 1.1 ± 0.53 3. 1 ± 0.94 3.3 ± 1.67

82.3 ± 11.2 81.5 ± 12.3 135 ± 10.13 133 ± 12.1 180± 11.2 179.6 ± 12.3 226.2 ± 12.3 225 ± 10.89 2.3 ± 1.3 2.5 ± 0.71 2.25 ± 0.72 2.4 ± 1.7 0.74 ± 0.3 0.85 ± 0.28 2.7 ± 1.5 2.9 ± 1.4

1.56 0.583 0.442 0.404 0.608 1.496 1.854 1.295 1.259 0.567 7.621 1.730 1.201 1.251 0.834 1.357

0.375 0.629 0.724 0.751 0.612 0.226 0.148 0.285 0.297 0.639 0.321 0.171 0.318 0.324 0.481 0.265

N1 Lat. P2 Lat. N2 Lat. P1 Amp. N1 Amp. P2 Amp. N2 Amp.

Bl st. ¼ Bloodstien, No ¼ numbers of children, Amp. ¼ amplitude, mV ¼ microvolt, R ¼ right ear, L ¼ left ear, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

Table 7 CAEPs absolute latencies (in ms) in study versus control according to core behaviors of stuttering. Core behaviors

CAEP peaks

Ear

Bl. st. I

Bl. st. II

Bl. st. III

Bl. st. IV

Control

ANOVA

P value

Repetition

P1 Lat.

R L

1.83 2.71

0.158 0.212

N2 Lat.

R L

2.17 1.21

0.231 0.314

P1 Lat.

R L

2.23 2.49

0.347 0.242

N1 Lat.

R L

e e

1.12 1.19

0.256 0.760

P2 Lat.

R L

e e

1.83 2.77

0.678 0.242

N2 Lat.

R L

e e

2.17 1.21

0.253 0.674

P1 Lat.

R L

2.232 2.491

0.037* 0.021*

0.034* 0.023*

N1 Lat.

R L

1.129 1.194

0.030* 0.031*

0.021* 0.031*

P2 Lat.

R L

1.839 4.774

0.038* 0.022*

0.015* 0.026*

N2 Lat.

R L

2.173 1.216

0.023* 0.041*

0.025* 0.032*

P1 Lat.

R L

2.232 2.491

0.031* 0.023*

0.023* 0.021*

N1 Lat.

R L

1.129 1.194

0.031* 0.042*

0.031* 0.032*

P2 Lat.

R L

1.839 4.774

0.021* 0.022*

0.014* 0.021*

N2 Lat.

R L

78.7 ± 12.4 79.6 ± 13.4 P ¼ 0.432 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.196 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.643 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.196 78.7 ± 12.4 79.6 ± 13.4 P ¼ 0.312 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.166 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.232 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.186 78.7 ± 12.4 79.6 ± 13.4 P ¼ 0.431 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.646 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.649 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.542 78.7 ± 12.4 79.6 ± 13.4 P ¼ 0.243 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.443 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.483 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.683

0.230 0.110

R L

89.85 88.59 P ¼ 0.543 142.68 141 P ¼ 0.326 198.11 193.79 P ¼ 0.756 235.67 230.73 P ¼ 0.326 84.34 83.5 P ¼ 0.593 146.7 146.2 P ¼ 0.316 185.5 177.33 P ¼ 0.143 235.6 227.23 P ¼ 0.226 110± 12.82 108.5 ± 11.96 P ¼ 0.543 166 ± 12.28 155 ± 8.4174 P ¼ 0.357 211.5 ± 9.05 209.33 ± 7.7 P ¼ 0.716 249.67 ± 6.92 247 ± 7.47 P ¼ 0.397 105.2 ± 11.8 100.5 ± 12.2 P ¼ 0.307 165.34 ± 12.2 158 ± 10.417 P ¼ 0.367 200.5 ± 11.5 198.33 ± 11.7 P ¼ 0.337 240.67 ± 6.92 239.2 ± 7.42 P ¼ 0.347

1.12 1.19

P2 Lat.

82 ± 12.6 80.5 ± 13.1 P ¼ 0.765 144 ± 10.6 140.5 ± 10.6 P ¼ 0.453 185.5 ± 12.9 177.3 ± 12.2 P ¼ 0.129 230.6 ± 11.3 229.4 ± 10.1 P ¼ 0.453 82.2 ± 10.6 80.5 ± 10.4 P ¼ 0.715 143.6 ± 11.3 140.5 ± 18.6 P ¼ 0.443 188.1 ± 12.9 186.7 ± 11.2 P ¼ 0.865 233.6 ± 9.3 229.4 ± 9.2 P ¼ 0.413 89.81 ± 10.69 83.59 ± 13.14 P ¼ 0.715 150.68 ± 11.6 148.05 ± 8.4 P ¼ 0.118 195.11 ± 14.9 193.79 ± 8.25 P ¼ 0.129 241.68 ± 9.36 239.42 ± 9.5 P ¼ 0.178 88.84 ± 10.6 85.579 ± 12.1 P ¼ 0.358 145.68 ± 11.6 143.05 ± 11.4 P ¼ 0.438 192.11 ± 12.9 184.79 ± 11.2 P ¼ 0.098 233.68 ± 9.36 230.4 ± 11.9 P ¼ 0.218

0.127 0.392

R L

79.7 ± 11.4 77.45 ± 11.9 P ¼ 0.387 132.8 ± 10.4 130.9 ± 12.2 P ¼ 0.612 180.6 ± 13.8 175 ± 12.3 P ¼ 0.145 229.9 ± 10.2 227.5 ± 9.3 P ¼ 0.612 79.7 ± 10.45 77.4 ± 11.95 P ¼ 0.327 132.82 ± 9.4 130.9 ± 11.7 P ¼ 0.622 180.6 ± 10.8 175 ± 13.41 P ¼ 0.287 228.91 ± 7.2 226.73 ± 8.3 P ¼ 0.612

2.23 2.49

N1 Lat.

79.7 ± 12.1 79.8 ± 11.3 P ¼ 0.178 132.4 ± 12.4 131.8 ± 12.8 P ¼ 0.654 180.6 ± 12.8 178.8 ± 11.7 P ¼ 0.136 224.8 ± 10.5 223.7 ± 8.9 P ¼ 0.654

2.173 1.216

0.123 0.365

0.034* 0.032*

Prolongation

IPDs

Blocks

Post hoc test

N. Ismail et al. / International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101

99

Table 8 CAEPs absolute amplitudes (in mV) in study versus control according to core behaviors of stuttering. Core behaviors

CAEP peaks

Ear

Bl. st. I

Bl. st. II

Bl. st. III

Bl. st. IV

Control

ANOVA

p-value

Repetition

P1 Amp.

R L

1.83 1.77

0.168 0.232

N2 Amp.

R L

2.17 1.21

0.123 0.304

P1 Amp.

R L

2.23 2.49

0.127 0.292

N1 Amp.

R L

1.14 1.19

0.130 0.510

P2 Amp.

R L

1.83 2.77

0.368 0.512

N2 Amp.

R L

2.17 1.21

0.123 0.521

P1 Amp.

R L

2.232 2.491

0.032* 0.026*

0.019* 0.043*

N1 Amp.

R L

1.129 1.194

0.033* 0.031*

0.027* 0.035*

P2 Amp.

R L

1.839 3.074

0.021* 0.011*

0.315 0.527

N2 Amp.

R L

2.173 1.216

0.032* 0.043*

0.435 0.638

P1 Amp.

R L

2.232 2.491

0.042* 0.032*

0.033* 0.044*

N1 Amp.

R L

1.129 1.194

0.043* 0.044*

0.023* 0.042*

P2 Amp.

R L

1.839 4.774

0.118 0.122

0.036* 0.023*

N2 Amp.

R L

3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.412 3.5 ± 0.92 2.97 ± 0.78 P ¼ 0.332 1.9 ± 0.4 1.3 ± 0.51 P ¼ 0.832 3. 9 ± 0.92 3.5 ± 1.74 P ¼ 0.532 3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.163 3.5 ± 0.92 2.97 ± 0.78 P ¼ 0.173 1.9 ± 0.42 1.3 ± 0.51 P ¼ 0.553 3.9 ± 0.92 3.5 ± 1.74 P ¼ 0.453 3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.133 3.5 ± 0.92 2.97 ± 0.78 P ¼ 0.453 1.9 ± 0.4 1.3 ± 0.51 P ¼ 0.283 3.9 ± 0.92 3.5 ± 1.74 P ¼ 0.483 3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.383 3.5 ± 0.92 2.97 ± 0.78 P ¼ 0.613 1.9 ± 0.4 1.3 ± 0.51 P ¼ 0.643 3.9 ± 0.92 3.5 ± 1.74 P ¼ 0.183

0.330 0.310

R L

2.43 2.93 P ¼ 0.443 2.1 2.55 P ¼ 0.563 1.33 0.93 P ¼ 0.547 3.2 3.3 P ¼ 0.243 2.13 2.33 P ¼ 0.165 1.7 1.85 P ¼ 0.745 0.533 0.593 P ¼ 0.715 2.2 2.45 P ¼ 0.317 0.6833 ± 1.25 0.93 ± 1.3095 P ¼ 0.447 - 0.7 ± 0.47 - 0.95 ± 0.86 P ¼ 0.547 0.633 ± 0.545 0.833 ± 0.39 P ¼ 0.747 -0.9 ± 1.229 1.05 ± 0.554 P ¼ 0.167 1.233 ± 1.25 1.453 ± 1.39 P ¼ 0.247 1.67 ± 0.497 1.25 ± 0.866 P ¼ 0.073 0.5433 ± 0.345 0.6433 ± 0.239 P ¼ 0.647 3.72 ± 1.49 3.85 ± 0.554 P ¼ 0.567

1.12 1.19

P2 Amp.

3.326 ± 0.96 3.45 ± 1.1 P ¼ 0.965 2.5 ± 0.51 2.63 ± 0.65 P ¼ 0.765 0.566 ± 0.5 0.96 ± 0.48 P ¼ 0.565 3.59 ± 1.7 3.7 ± 0.73 P ¼ 0.335 2.72 ± 0.966 2.94 ± 1.87 P ¼ 0.487 1.96 ± 0.52 2.12 ± 0.69 P ¼ 0.377 0.766 ± 0.5 0.988 ± 0.483 P ¼ 0.367 2.93 ± 1.7 3.12 ± 0.73 P ¼ 0.548 1.326 ± 0.968 1.945 ± 1.87 P ¼ 0.218 1.569 ± 0.53 1.69 ± 0.659 P ¼ 0.118 0.96 ± 0.53 1.11 ± 0.49 P ¼ 0.558 2.1 ± 1.7 2.3 ± 0.73 P ¼ 0.254 2.96 ± 0.9168 3.15 ± 1.2 P ¼ 0.098 2.59 ± 0.542 2.98 ± 0.629 P ¼ 0.295 1.146 ± 0.523 1.27 ± 0.484 P ¼ 0.218 3.79 ± 1.73 3.843 ± 0.78 P ¼ 0.208

0.117 0.092

R L

3.2 ± 1.325 3.4 ± 0.7231 P ¼ 0.547 1.99 ± 0.967 3.5 ± 1.87 P ¼ 0.367 0.54 ± 0.321 0.945 ± 0.285 P ¼ 0.357 4.5 ± 1.5 5.2 ± 1.4 P ¼ 0.377 3.2 ± 1.325 3.4 ± 0.723 P ¼ 0.148 2.32 ± 0.967 2.5 ± 1.87 P ¼ 0.358 1.24 ± 0.331 1.745 ± 0.28 P ¼ 0.568 3.35 ± 1.5 3.4 ± 1.4 P ¼ 0.218

2.23 2.49

N1 Amp.

3.1 ± 1.42 3.73 ± 1.7 P ¼ 0.278 2.6 ± 0.89 2.59 ± 0.97 P ¼ 0.378 1.2 ± 0.51 1.1 ± 0.64 P ¼ 0.352 3.31 ± 0.95 3.9 ± 1.74 P ¼ 0.568

2.173 1.216

0.343 0.234

0.041* 0.042*

Prolongation

IPDs

Blocks

temporale and Wernickes area). Those anatomical abnormalities in the auditory cortex resulted in more auditory inhibition, in case of positive family history, which appears as prolonged latencies and smaller amplitudes of the CAEPs components. Left handed children who stutter had prolonged latencies and smaller amplitudes of P1, N1, P2 and N2 in both ears than right handed children who stutter. Handedness is correlated with anatomy of the sylvian fissure (surround the auditory cortex and P1 generators). Left handedness is an index of asymmetrical perceptual functions surrounding the sylvian fissure. Atypical anatomical features present in left handed individuals who stutter may lead to increasing stuttering severity [7]. This hemispheric difference in stuttering could be explained by some organic theories of stuttering such as the cerebral dominance theory [26] and the auditory processing under active theory [15]. The cerebral dominance theory suggested that abnormal inter hemispheric relationships were found in stuttering with increased right hemispheric activations and decreased left-hemispheric activations in stuttering [26]. The auditory processing under active theory indicated that inhibition in the auditory areas (superior temporal gyrus and Heschl's

Post hoc test

gyrus) occurred in stuttering may lead to delayed conduction time (prolonged CAEP latencies) and low cortical presentation (reduced CAEP amplitudes) [15]. Regarding core behaviors of stuttering repetitions and prolongation had no effect on the absolute latencies or amplitudes of P1, N1, P2 and N2 in children who stutter when compared to controls. However, there were statistically significant differences as prolonged latencies and smaller amplitudes of P1, N1, P2 and N2 on the right ear (left hemisphere) of Bloodstien IV stutterers when blocks and IPDs were the predominant core behaviors when compared to controls. In the current study, statistically significant prolonged latencies and reduced amplitudes of P1, N1, P2 and N2 over the left hemisphere indicate left auditory cortex inhibition, which occurs in severe phases of stuttering as Bloodstien III and Bloodstien IV; however it did not reach a statistically significant level in Bloodstien III. There were no differences between Bloodstien I, Bloodstien II phases and control as regards CAEPs indicating those two phases were better in cortical auditory activation and less in stuttering severity [3]. [17] results correlated with the results of the present study

100

N. Ismail et al. / International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101

Table 9 CAEPs absolute latencies (in ms) and amplitudes (in mV) in study versus control according to secondary reactions of stuttering. CAEP Peaks

ear

Bl. st. II

Bl. st. III

Bl. st. IV

Control

ANOVA

p-value

P1 Lat.

R L

0.342 0.331

R L

1.839 4.774

0.332 0.442

N2 Lat.

R L

2.173 1.216

0.235 0.141

P1 Amp.

R L

2.232 2.491

0.117 0.092

N1 Amp.

R L

1.129 1.194

0.330 0.330

P2 Amp.

R L

1.839 1.774

0.168 0.322

N2 Amp.

R L

78.7 ± 11.4 79.6 ± 13.4 P ¼ 0.267 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.163 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.145 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.157 3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.157 3.5 ± 0.92 2.97 ± 0.78 P ¼ 0.259 1.9 ± 0.4 1.3 ± 0.51 P ¼ 0.057 3.9 ± 0.92 3.5 ± 1.74 P ¼ 0.977

1.129 1.194

P2 Lat.

92 ± 9.8 91.5 ± 11.29 P ¼ 0.323 146 ± 12.28 145 ± 10.4174 P ¼ 0.183 192.5 ± 19.05 190.33 ± 16.7 P ¼ 0.442 240.67 ± 6.9 238 ± 7.4 P ¼ 0.413 2.53 ± 1.25 2.63 ± 1.3095 P ¼ 0.914 1.7 ± 0.47 1.95 ± 0.86 P ¼ 0.073 0.73 ± 0.545 0.833 ± 0.39 P ¼ 0.513 2.03 ± 1.229 2.15 ± 0.554 P ¼ 0.412

0.141 0.222

R L

90.8 ± 10.69 87.57 ± 11.11 P ¼ 0.107 144.68 ± 11.6 142.5 ± 10. 1 P ¼ 0.187 188.91 ± 11.9 187.79 ± 18.2 P ¼ 0.162 236.68 ± 9.36 234.42 ± 9.09 P ¼ 0.347 2.76 ± 0.96 2.94 ± 1.87 P ¼ 0.247 2.166 ± 0.532 2.493 ± 0.659 P ¼ 0.345 0.916 ± 0.5 0.96 ± 0.48399 P ¼ 0.367 2.613 ± 1.72 2.743 ± 0.736 P ¼ 0.307

2.232 2.491

N1 Lat.

82 ± 10.93 80.7 ± 10.45 P ¼ 0.214 138.82 ± 9.4 134.9 ± 19.2 P ¼ 0.564 186.6 ± 11.2 183 ± 12.3 P ¼ 0.253 232.7 ± 8.3 229.9 ± 7.2 P ¼ 0.654 3.22 ± 1.35 3.5 ± 0.71 P ¼ 0.344 2.63 ± 0.967 2.8 ± 1.87 P ¼ 0.564 0.99 ± 0.321 1.25 ± 0.285 P ¼ 0.454 2.9 ± 1.5 - 3.2 ± 1.484 P ¼ 0.454

2.173 1.216

0.133 0.314

CAEP ¼ Cortical Auditory Evoked Potential, mV ¼ microvolt, Bl st. ¼ Bloodstien, Amp. ¼ amplitude, ms ¼ milliseconds, R ¼ right ear, L ¼ left ear, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

Table 10 CAEPs absolute latencies (in ms) and amplitudes (in mV) in study versus control according to concomitant behaviors of stuttering. CAEPs peaks

Ear

Bl. st. III

Bl. st. IV

Control

ANOVA

p-value

Post hoc test

P1 Lat.

R L

0.013* 0.031*

3.129 3.194

0.032* 0.031*

0.041* 0.034*

P2 Lat.

R L

1.839 4.774

0.334 0.422

0.317 0.458

N2 Lat.

R L

2.173 1.216

0.412 0.643

0.335 0.437

P1 Amp.

R L

2.232 2.491

0.117 0.092

N1 Amp.

R L

1.129 1.194

0.330 0.310

P2 Amp.

R L

1.839 4.774

0.168 0.312

N2 Amp.

R L

78.7 ± 12.4 79.6 ± 13.4 P ¼ 0.183 131.7 ± 13.7 132.3 ± 13.5 P ¼ 0.107 177.9 ± 10.6 180.5 ± 10.7 P ¼ 0.983 223.3 ± 9.3 224.7 ± 11.6 P ¼ 0.387 3.9 ± 1.12 3.13 ± 1.77 P ¼ 0.223 P ¼ 0.081 2.97 ± 0.78 P ¼ 0.088 1.9 ± 0.4 1.3 ± 0.51 P ¼ 0.245 3.9 ± 0.92 3.5 ± 1.74 P ¼ 0.297

0.037* 0.021*

R L

102 ± 12.62 99.3 ± 10.26 P ¼ 0.187 159 ± 12.28 157 ± 11.174 P ¼ 0.764 192.5 ± 13.05 190.33 ± 12.7 P ¼ 0.133 240.67 ± 9.92 237.±9.42 P ¼ 0.664 2.76 ± 0.9668 2.935 ± 1.087 P ¼ 0.247 1.166 ± 0.532 1.591 ± 0.659 P ¼ 0.103 0.866 ± 0.5 0.867 ± 0.48399 P ¼ 0.058 1.913 ± 1.7 2.04 ± 0.7376 P ¼ 0.298

4.282 4.491

N1 Lat.

88.81 ± 10.699 86.89 ± 9.104 P ¼ 0.564 149.68 ± 11.61 143.05 ± 11.46 P ¼ 0.283 188.11 ± 12.9 183.79 ± 18.2 P ¼ 0.587 232.68 ± 9.36 230.42 ± 9.09 P ¼ 0.083 3.2 ± 1.325 3.4 ± 0.7231 P ¼ 0.158 2.31 ± 0.967 2.5 ± 1.087 P ¼ 0.227 0.94 ± 0.321 1.245 ± 0.245 P ¼ 0.313 2.5 ± 1.5 3.2 ± 1.484 P ¼ 0.703

2.173 1.216

0.123 0.304

CAEP ¼ Cortical Auditory Evoked Potential, Bl st. ¼ Bloodstien, No ¼ numbers of children, Amp. ¼ amplitude, mV ¼ microvolt, R ¼ right ear, L ¼ left ear, P > 0.05 statistically insignificant,*P < 0.05 statistically significant, **P < 0.01 highly statistically significant.

indicating that the greater the severity of stuttering, the more reduced CAEPs amplitudes in individuals who stutter. Secondary reactions of stuttering were presented in Bloodstien II, III and IV, but they did not significantly affect CAEPs in children who stutter when compared to controls. However [11], claimed that stuttering severity and auditory inhibition increase with secondary reactions. Concomitant behaviors of stuttering were presented in Bloodstien III and IV. They significantly affected latencies, not amplitudes, of P1 and N1 components of CAEPs. The results of the current study

indicated that the presence of the concomitant behaviors increased the stuttering severity in children who stutter. The statistically significant prolonged latencies of P1 and N1 in the right ear in Bloodstien IV than controls indicated left auditory cortex inhibition and increasing stuttering severity [1] [4]. proposed that concomitant behaviors are the emotional activity associated with stuttering. They indicate greater stuttering severity and abnormal right hemispheric activity as the right hemisphere is generally associated with emotions as a compensatory mechanism to left hemispheric insufficiency.

N. Ismail et al. / International Journal of Pediatric Otorhinolaryngology 97 (2017) 93e101

5. Conclusion From the current study, the following can be concluded: a CAEPs of children who stutter with stuttering severity Bloodstien IV showed significant prolonged latencies and reduced amplitudes when blocks and IPDs were the most predominant core behaviors. P1 and N1 were prolonged in concomitant behaviors. b It could be speculated that speech processing was affected in children who stutter with stuttering severity Bloodstien IV at the level of the early perceptual auditory cortex. c Impaired CAEPs of children who stutter supports the central auditory processing underactivity theory of stuttering.

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