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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 22  |  Issue : 2  |  Page : 135-138

Exploring (central) auditory processing deficits in individuals with Broca's aphasia: Based on case study


1 Department of Audiology, All Institute of Speech and Hearing, Manasagangothri, Mysore, Karnataka, India
2 Department of Speech Language Pathology, All Institute of Speech and Hearing, Manasagangothri, Mysore, Karnataka, India

Date of Web Publication11-May-2016

Correspondence Address:
Prawin Kumar
Department of Audiology, All India Institute of Speech and Hearing, Manasagangothri, Mysore - 570 006, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-7749.182282

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  Abstract 

It is well known fact that persons with lesions involving either the right or left temporal lobe tended to show impaired performances for complex auditory task and showed auditory processing disorder symptoms. Present study was aimed to find out whether auditory processing deficit exists in individuals with Broca's aphasia due to stroke based on case studies outcomes through detailed behavioral and electrophysiological audiological assessment. There were two participants (case 'A' and case 'B') diagnosed as having Boca's aphasia taken for the study. Case 'A' and 'B' were 39 and 29 year old male participated in the study. They were assessed for routine audiological and detailed auditory processing disorders tests like pitch pattern test, gap detection test and dichotic digit test. Further, they were also assessed for electrophysiological tests like click evoked auditory brainstem response and auditory late latency response. The routine audiological tests reveal no peripheral hearing loss in both the cases. However, details behavioral (C)APD tests results revealed overall poorer performance for different tasks in both cases. In addition to that, electrophysiological tests results also revealed abnormal brainstem and cortical responses in both cases. Hence, preliminary report of the present study suggests that cases with lesion (strokes) should be evaluated in detail for auditory processing deficit.

Keywords: Aphasia, Audiometry, Central auditory processing disorders, Stroke


How to cite this article:
Kumar P, Mohan B M, Pavithra K, Naveen C P. Exploring (central) auditory processing deficits in individuals with Broca's aphasia: Based on case study. Indian J Otol 2016;22:135-8

How to cite this URL:
Kumar P, Mohan B M, Pavithra K, Naveen C P. Exploring (central) auditory processing deficits in individuals with Broca's aphasia: Based on case study. Indian J Otol [serial online] 2016 [cited 2019 Nov 21];22:135-8. Available from: http://www.indianjotol.org/text.asp?2016/22/2/135/182282


  Introduction Top


(Central) auditory processing disorder [(C)APD] refers to a deficit observed in one or more of the central auditory processes responsible for the following behaviors such as sound localization and lateralization, auditory discrimination, auditory pattern recognition, temporal aspects of audition (temporal resolution, temporal masking, temporal integration, and temporal ordering), auditory performance with competing acoustic signals, and auditory performance with degraded acoustic signals.[1],[2] Further, APDs may also be defined as a deficit in the auditory pathways of the brain that results in the inability to listen to, or comprehend, auditory information accurately, even though normal intelligence is documented.[3] In addition, (C)APD may coexist with a more global dysfunction that affects performance across modalities such as attention deficit, neural timing deficit, language representation deficit, dyslexia, learning disability, Aphasia, traumatic brain injury, epilepsy, and Alzheimer's disease.[2] Hence, early identification of (C)APD, a disorder of the central auditory nervous system, in patients with head injury is crucial to improve central auditory processing as well as overall auditory function.[4]

Aphasia is the loss or impairment of language caused due to brain damage in which the interpretation and formulation of language symbols are impaired.[5] The posterior inferior frontal gyrus of the left hemisphere is known as Broca's area. This area is reported to be supplied by the upper division of the middle cerebral artery (MCA). This area is in the lower part of the premotor cortex that controls the movements of the face, hand, and arms.[6] Study reported that (C)APD can be seen in more than 50% of adults with traumatic brain injury due to stroke.[7]

Persons with lesions might involve either the right or left temporal lobe which tends to show impaired performances for the complex auditory task and associated with APD symptoms.[8] Cerebral stroke often includes the auditory system, resulting in various types of auditory disorders, but most hemispherical lesions produce subtle hearing dysfunctions. The above lesions can only be detected with sophisticated psychoacoustic and electrophysiological testing. Audiological (C)APD evaluation is essential to ascertain the scope of system deficit and to maximize deficit-based therapeutic effectiveness and improve neural plasticity in individuals with brain lesions.[4]

Aim and objectives

The aim and objective of the study were to find out the presence of (C)APDs in individuals with Broca's aphasia in Case “A” and “B” based on audiological behavioral and electrophysiological assessment.


  Methods Top


Two participants (Case “A” and Case “B”) diagnosed as having Boca's aphasia based on Western aphasia battery considered for the study. A detail structured case history and audiological evaluations which include behavioral and electrophysiological tests were carried out for both the cases. Further, their radiological finding was also included in this study. Case “A” (39-year-old male) and Case “B” (29-year-old male) were reported with the complaint of speech and language difficulties after an attack of stroke. Both cases reported unintelligible speech and right side body weakness. They could express their needs through pointing and vocalization. They had difficulty in following multi-step commands. Medical history of Case “A” reflected high blood pressure which was noticed after stroke. However, Case “B” had a history of cigarette smoking (ten cigarettes per day). The radiological assessment through computerized tomography (Case “A”) and magnetic resonance imaging (Case “B”) report of both the cases revealed acute infarction in left MCA dysfunction due to thrombosis. Based on Western aphasia battery tests, provisional diagnosis made was “Broca's aphasia” in both the cases.

Detailed audiological evaluations were carried out to check the peripheral and central auditory system involvement in both the cases. The routine audiological assessment was done which includes pure tone audiometry, speech audiometry, and immittance meter. In addition to that, transient evoked otoacoustic emissions (TEOAE) and electrophysiological tests such as auditory brainstem response (ABR) and auditory late latency response (ALLR) were done. The above tests help clinician to rule out the involvement of peripheral and central hearing loss. Further, behavioral (C)APD test battery was performed to check whether there is any involvement of central component in these two cases. The test for (C)APD included were pitch pattern test (PPT),[9] gap detection test (GDT),[10] dichotic consonant-vowel (CV)[11] test, and speech in noise (SPIN) test. The above tests were carried out using Madsen orbiter OB-922 (version 2) diagnostic audiometer (United States), GSI Tympstar Immittance meter (United States), ILO (Version 6) otoacoustic emission analyzer (United Kingdom), Biologic navigator pro-AEP systems (United States), and personal computer along with diagnostic audiometer for complete (C)APD assessment. Click-evoked ABR and ALLR were recorded in both ears for both Case “A” and Case “B” using the test protocol mentioned in [Table 1]. Both the cases were made to sit comfortably to ensure a relax posture and minimum rejection rate. Gold cup electrodes were placed after cleaning the electrode placement sites with preparing gel. Conduction paste was used to improve the conductivity of the recording signal from the generator sites. The electrodes were secured to the place using plasters. The electrode placement was kept and followed as per the test protocol [Table 1]. All audiological tests were performed in a sound-treated double-room suite with the ambient noise levels within permissible limits (ANSI S3.1, 1999).[12]
Table 1: Protocol for recording click evoked ABR and ALLR

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  Results Top


Case “A” routine audiological evaluation showed pure tone average and speech reception threshold were within 10 dB HL in both ears. Further, word recognition scores were 100% in both ears. Immittance and TEOAEs finding showed normal middle ear and outer hair cell function in both ears, respectively. The above finding in Case “A” suggests no peripheral hearing loss in both ears.

In addition to that, ABRs revealed the presence of wave I, III, and V peaks with latencies within normal limit for lower repetition rate (11.1/s); however, no peaks were identified at 90.1/s repetition rate in left ear. However, in right ear, no peaks were identified at both lower (11.1/s) and higher (90.1/s) repetition rate. The ALLR showed the presence of P1 and N1 peaks but with abnormal morphology in both ears. Behavioral (C)APD tests were done to assess processing-based deficit in individuals with Broca's aphasia. It was observed that performance was very poorer for PPT, GDT, and dichotic CV test scores in comparison to a typically developing normal age group [Table 2]. However, for SPIN test only left ear showed poorer performance.
Table 2: Details of behavioral (C) APD test scores of case ‘A’ and ‘B’

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Case “B” routine audiological evaluation also showed pure tone average and speech reception threshold <15 dB HL in both ears. Further, word recognition scores were 96% and 100% in right and left ear, respectively. Immittance and TEOAEs finding showed normal middle ear and outer hair cell function in both ears, respectively. The above finding in Case “B” suggests no peripheral hearing loss in both ears. In electrophysiological assessment for Case “B”, ABRs revealed the presence of primary peaks I, III, and V with latencies within normative range for both lower (11.1/s) and higher (90.1/s) repetition rate in both the ears. However, click-evoked ALLR showed abnormal representation in the right ear whereas normal in the left ear for P1 and N1 peaks. Behavioral (C)APD assessment in Case “B” showed poorer performance for PPT and dichotic CV test in both ears. However, the GDT and SPIN were within normal range in comparison to typically developing individuals with intact central auditory processing system [Table 2]. The above (C)APD test results revealed that overall the severity of auditory processing deficit was higher for Case “A” in comparison to Case “B.” It could be because of the depth of lesion more in Case “A” than Case “B” as reflected by behavioral auditory processing task.


  Discussion Top


In this study, both the participants showed normal peripheral hearing sensitivity up to cochlea. However, the detailed audiological (behavioral and electrophysiological) evaluation results revealed abnormal representation at brainstem and cortical level in both the participants. In Case “A,” the absence of wave V at higher repetition rate (90.1/s) in left ear and absence of all peaks for both lower (11.1/s) and higher repetition rate in the ABRs for right ear is an indication of retrocochlear pathology in both ears. This probably represents abnormal processing of acoustic stimuli at brainstem or cortical region. Further, presence of abnormal ALLR responses in both ears which represent cortical areas could be affected because of lesion or deficit beyond brainstem levels. In addition, behavioral (C)APD assessment test results revealed poor temporal processing ability as well as poor temporal resolution ability secondary to lesion. In Case “B,” the presence of responses for click-evoked ABR in both ears with good morphology at lower and higher repetition rate suggested no indication of retrocochlear pathology in both ears. In addition, it could also mean that the processing of acoustic signals intact up to brainstem area. However, the presence of abnormal ALLR waveform probably indicating there is a cortical lesion in both ears. Further, the detailed behavioral (C)APD assessment test results revealed abnormal temporal processing and binaural integration deficit in both ears. This could be because of diffused lesion in the frontal area secondary to lesion.

This study finding in Case “A” and “B” is in consonance with other studies [13],[14],[15] in spite of those individuals had traumatic head injury. However, in this study, clients had abnormal representation of acoustic stimuli at brainstem and cortical levels due to stroke. Literature suggested that pathological changes at the level of brainstem and auditory cortex, vascular insults involving medial carotid artery can cause considerable tissue damage to gray and white matter in temporoparietal regions of the brain. This lesion among the most common anomalies affecting the functioning of the auditory cortex and associated areas leads to (C)APD symptoms.[16]


  Conclusion Top


The present case study highlights the importance of detailed audiological evaluation including behavioral (C)APDs test and electrophysiological evaluations in individuals with Broca's aphasia. It is concluded that individuals with Broca's aphasia may be associated with (C)APDs. Hence, detailed audiological evaluation is suggested for these individuals so that area of deficit can be known and appropriate rehabilitation training can be provided for better life.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Bellis TJ. Assessment and Management of Central Auditory Processing Disorders in the Educational Setting: From Science to Practice. 2nd ed. Clifton Park, New York: Delmar Learning; 2003.  Back to cited text no. 1
    
2.
American Speech-Language-Hearing Association. Central auditory processing: Current status of research and implications for clinical practice. Am J Audiol 1996;5:41-54.  Back to cited text no. 2
    
3.
Richard GJ. Intervention for cognitive-communicative and language factors associated with (C)APD. In: Chermak GD, Musiek FE, editors. Handbook of (Central) Auditory Processing Disorder: Comprehensive Intervention. Vol. II. San Diego, CA: Plural Publishing; 2007. p. 291-4.  Back to cited text no. 3
    
4.
Musiek FE, Chermak G. Testing and treating (C)APD in head injury patients. Hear J 2008;61:36-8.  Back to cited text no. 4
    
5.
Darley FL. Aphasia. Philadelphia: W. B. Saunders Co.; 1982.  Back to cited text no. 5
    
6.
Bhatnagar SC. Neuroscience for the Study Communicative Disorders. 2nd ed. Baltimore, Maryland: Lippincott Williams and Wilkins; 2002.  Back to cited text no. 6
    
7.
Bergemalm PO, Lyxell B. Appearances are deceptive? Long-term cognitive and central auditory sequelae from closed head injury. Int J Audiol 2005;44:39-49.  Back to cited text no. 7
    
8.
Kimura D. Cerebral dominance and the perception of verbal stimuli. Can J Psychol 1961;15:166-71.  Back to cited text no. 8
    
9.
Shivani T. Maturational Effect of Pitch Pattern Sequence Test. An Unpublished Independent Project. Mysore: University of Mysore; 2003.  Back to cited text no. 9
    
10.
Shivaprakash S. Gap Detection Test-Development of Norms. An Unpublished Independent Project. Mysore: University of Mysore; 2003.  Back to cited text no. 10
    
11.
Yathiraj A. Dichotic CV Test- Revised. Mysore: Developed at Department of Audiology, All India Institute of Speech and Hearing; 1999.  Back to cited text no. 11
    
12.
ANSI. American National Standard: Maximum Permissible Ambient Noise Levels for Audiometric Test Rooms, ANSI S3.1. New York: American National Standards Institute, Inc.; 1999.  Back to cited text no. 12
    
13.
Hall JW. Handbook of Auditory Evoked Responses. Boston: Allyn and Bacon; 1992.  Back to cited text no. 13
    
14.
Fligor BJ, Cox LC, Nesathurai S. Subjective hearing loss and traumatic brain injury exhibits abnormal brainstem auditory evoked responses: A case report. Arch Phys Med Rehabil 2002;83:141-3.  Back to cited text no. 14
    
15.
Musiek FE, Baran JA. Pinheiro ML. Neuroaudiology: Case Studies. San Diego: Singular Publishing Group; 1994.  Back to cited text no. 15
    
16.
Musiek FE, Chermak GD. Diagnosis of (central) auditory processing disorder in traumatic brain injury: Psychophysical and electrophysiological approaches. ASHA Lead 2009;14:16-19.  Back to cited text no. 16
    



 
 
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