The usual symptoms for CAPD may include:
- Difficulty concentrating and understanding fast or unclear speech
- Difficulty listening and understanding speech in noisy environments
- Difficulty listening in big groups
- Difficulty responding to questions
- Distraction and inattentiveness
- Frequently asking for repetition of information
- Reading, writing and spelling difficulties
- Trouble determining the sound source
- Trouble differentiating sounds
- Trouble remembering information that was heard
- Insensitive to the speaker’s tone of voice
An audiologist will first carry out tests to rule out peripheral hearing loss and middle ear pathologies before conducting an APD assessment. The APD assessment test battery involves 5 to 7 tests to assess different auditory processes which include the binaural integration, binaural separation, temporal patterning, temporal processing and binaural interaction skills. An APD assessment is available for individuals without cognitive impairments and aged 7 year-old and above.
Currently there is no cure for CAPD. However, there are some treatment options that an individual with CAPD may use to cope with their listening difficulties.
- Using hearing aids to amplify speech signals while reducing background noise
- Facing conversational partner, ask conversational partner to talk in a slower pace
- Sitting closer to the speaker in group meetings
- Individual speech therapy sessions that aim to encourage and train auditory processing pathways
Background on Central Auditory Processing Disorder (CAPD) by Clinical Audiologist Ms Vivian Cheung
APD is defined as the incapability of the central nervous system to utilize auditory information, resulting in the impairment of perceiving both non-speech sounds and speech sounds (American Speech-Language-Hearing Association [ASHA], 2005; British Society of Audiology [BSA], 2011). A person with APD experiences hearing difficulties without any deficits in peripheral hearing, language or higher-order cognition (ASHA, 2005; Sharma et al., 2009; Rosen et al., 2010; Witton, 2010; BSA, 2011). ASHA (1996) states that people with APD have poor performances in one or more of the auditory processes or mechanisms. These auditory processes include but not limited to sound localization, sound lateralization, auditory discrimination, auditory pattern recognition, temporal processing, and auditory performance decrements with competing, or degraded acoustic signals (ASHA, 1996). APD limits a person’s ability in continuously transmitting, analyzing, organizing, transforming, elaborating, storing, retrieving and using the information in audible signals (ASHA, 2014). To give a real-life example, a school-aged child with APD may experience difficulties in spelling, reading, and understanding information that are verbally-instructed in the classroom, which may lead to poor academic performances. As for a working adult, the individual may frequently miss some important messages during a conversation. Or when talking to a co-worker in busy places, the individual has trouble understanding.
According to BSA (2018), there are three different categories of APD. The first category is developmental APD which involves childhood-developed APD with normal audiometric hearing thresholds and unknown cause (BSA, 2018). The second category is acquired APD, which is associated with ageing, brain lesions or neurological traumas (BSA, 2018). The third category is secondary APD which is caused by, or occurs simultaneously with peripheral hearing impairment (BSA, 2018).
Auditory processing is complicated as it involves the interaction of multiple regions in the brain (Sharma et al., 2009; Bellis & Bellis, 2015). Even though the etiology of APD is still not well recognized, neurodevelopmental delay or abnormal neural function is sometimes recognized as the underlying problem (Wilson et al., 2004; ASHA, 2005; Moore, 2006; BSA, 2011; Bellis & Bellis, 2015; Tomlin & Rance, 2016). Wilson et al. (2004) suggest that there are three types of ‘underlying neurophysiological and/or neuromaturational deficits’ which associates with the commonly observed behaviours in APD (p.89).
The first and the most common deficit is the neuromorphological disorder which involves the mislocation of neurons around ‘the auditory region of the corpus callosum’ in the left hemisphere, and the abnormal condition of gyri which are abnormally small and overmuch (Wilson et al., 2004, p.89; Bellis & Bellis, 2015). The second deficit is the neuromaturational delay of the CANS (Wilson et al., 2004; Bellis & Bellis, 2015). A study conducted by Tomlin and Rance (2016) supports the notion that there is a maturational difference at cortical level between children who have APD and children without APD. There is a maturational delay observed in the CANS of children with APD (Tomlin & Rance, 2016). The maturational delay affects the myelination of neural pathways, which impedes rapid intra-hemispheric and inter-hemispheric transmission of information (Tomlin & Rance, 2016). The third and least common deficit is related to neurologic disorders, diseases or insults, including the degeneration or death of nerve cells or traumatic brain injury (Wilson et al., 2004; Bellis & Bellis, 2015). The examples of diseases that can possibly cause APD are bacterial meningitis or Lyme disease (Bamiou et al., 2001). As for traumatic brain injury, an individual is likely to have APD when the injury specifically lesions the posterior corpus callosum, due to the disconnection between two auditory hemispheres (Bamiou et al., 2001)