What is APD?

APD is a complex designation referring to any auditory element believed to require atypical cerebral processing of sounds. A primary conclusion from this analysis is the significant ambiguity and persistent (courteous) dissent concerning the symptoms, tests, stimuli, mechanisms, and therapies suitable for defining, diagnosing, and treating APD. The objective of this work is to elucidate these concerns and assess them based on the latest empirical findings, thus promoting a more profound understanding and the establishment of a consensus. This research focuses solely on behaviorally characterized Antisocial Personality Disorder (APD) and has a pronounced personal bias towards APD in pediatric groups.

A primary problem in addressing APD is the lack of agreement on the precise definition of the term “disorder.” The U.S. National Institute on Deafness and Other Communication Disorders (NIDCD) states, “Although your child appears to ‘hear normally,’ he or she may struggle to utilize those sounds for speech and language.” Audiological societies across the Atlantic have similarly characterized Auditory Processing Disorder (APD) as a deficiency in multiple facets of auditory perception, encompassing temporal, spectral, and binaural hearing, along with the sequencing and categorization of sounds. These descriptions collectively underscore the fundamental significance of the impairment(s). Consequently, APD has been and, in certain instances, continues to be referred to as Central Auditory Processing Disorder (CAPD or C/APD). A consensus is emerging regarding the utilization of non-speech test materials. It is well acknowledged that Auditory Processing Disorder (APD) frequently manifests as a speech-perception issue and may be a contributing factor to language difficulties, including dyslexia and specific language impairment (SLI). It is fascinating that whereas many, maybe the majority, of individuals with language difficulties excel in auditory processing (psychoacoustic) tests utilizing non-speech stimuli (e.g., tones and broadband noises), some do not. Thus, auditory processing disorder (APD) can be differentiated from language impairments mainly using non-verbal assessments.

These ostensibly consensus assertions conceal a complex array of difficulties and entrenched theoretical stances. It is wise to recognize that APD is a relatively recent concept that has arisen from several sources. Anecdotal clinical studies indicate that a significant proportion of individuals referred to audiology and speech-language pathology (SLP) clinics exhibit hearing issues while possessing normal pure-tone thresholds. Educators and guardians frequently recognize a cohort of youngsters exhibiting a perceived “listening” deficiency despite normal auditory capabilities, a notion supported by the aforementioned NIDCD statement. Furthermore, researchers and individuals engaged in age-related hearing loss have acknowledged that, besides challenges in sound detection, older adults often exhibit subpar performance on several psychoacoustic assessments.

Auditory Processing Disorder (APD) is presently diagnosed via multiple referral paths, leading to various diagnostic and interpretative challenges. Primary concerns encompass (i) the conflation of auditory processing disorders with language impairments, (ii) the risk of misdiagnosis involving peripheral hearing losses (conductive or sensorineural) or auditory neuropathy/dysynchrony, (iii) the likelihood of concurrent peripheral hearing loss influencing or exacerbating auditory processing disorder, and (iv) ambiguity regarding the precise levels of auditory perception impacted by the condition. Audiological organizations worldwide have classified Auditory Processing Disorder (APD) based on temporal, spectral, and binaural processing, among other criteria, a system originating from a task force report by the American Speech-Language-Hearing Association (ASHA). The approach considers auditory processing disorder (APD) as a deficiency in central auditory systems while recognizing that cognitive aspects, including attention and neuronal timing, may also play a role in certain instances. APD is not confined to children; it also manifests in adults, with indications of increased frequency among the elderly. The concept of Auditory Processing Disorder (APD) has been influenced by different referral pathways, resulting in varied diagnoses among professionals: audiologists may classify cases as APD, speech-language therapists (SLTs) may diagnose Specific Language Impairment (SLI), educational psychologists may recognize dyslexia, and psychiatrists may contemplate autistic-spectrum disorders.

According to ASHA (2005) and BSA (2005), Auditory Processing problem (APD) is characterized as a problem affecting the recognition, discrimination, ordering, grouping, and localization of sounds, particularly focusing on non-speech sound processing. The etiology of APD is intricate and diverse. The extent to which central and peripheral causes contribute to the wide array of symptoms classified as APD remains ambiguous. Outer hair cell pathology is now recognized to cause both spectral and temporal processing impairments; nonetheless, these deficits are frequently cited as core indicators of auditory processing disorder (APD), despite APD being commonly referred to as central auditory processing disorder (C)APD. If peripheral dysfunction is not the primary cause, several central candidates arise, including the extensive descending pathways from the core auditory cortex that project to all levels of the central auditory system and significantly affect neuronal activity throughout the ascending auditory pathway. APD has been associated with defined language processing impairments, such as dyslexia (SRD) and specific language impairment (SLI). In various studies, an unexpectedly high percentage of individuals diagnosed with Specific Language Impairment (SLI) or Specific Reading Disability (SRD) based on language and reading evaluations also exhibit subpar performance on psychoacoustic assessments of non-speech detection and discrimination, such as auditory backward masking and pure-tone frequency discrimination.

At least 5% of children referred to audiology services are determined to have no hearing loss. Numerous individuals describe challenges in auditory perception, particularly with speech, and are diagnosed with auditory processing disorder (APD), despite the absence of global consensus on the definition of APD. Professional organizations on both sides of the Atlantic have presented classifications indicating that Auditory Processing Disorder (APD) encompasses hearing issues resulting from compromised bottom-up processing of auditory stimuli by the brain within the central auditory system. To evaluate this idea, we conducted a survey on auditory processing (AP) in children with normal hearing from the general community. We evaluated speech perception, cognition, and communication and listening abilities to examine an alternative hypothesis that subpar performance on these measures (APD) arises from compromised top-down processing, which is recognized to influence the bottom tiers of the auditory system. The designation APD was initially introduced at the 1974 assembly of the American Speech, Language, and Hearing Association (R. W. Keith, PhD, personal written communication, 2009), followed by a symposium on “central auditory dysfunction” convened in Cincinnati, Ohio, in 1977. A dispute regarding the role of auditory perception in language difficulties was already underway. Prior research on central lesions and auditory processing capacity has demonstrated the flaws and limitations of hearing dictated by cerebral function. Currently, the notions of Auditory Processing Disorder (APD) encompass abnormalities due to brain lesions as well as auditory factors contributing to learning difficulties in otherwise healthy children. Despite the belief among numerous experts that Auditory Processing Disorder (APD) lacks sufficient specificity for scientific investigation, there exists a significant demand for enhanced diagnosis and management among caregivers and professionals working with children exhibiting deficient listening skills. A fundamental inquiry is whether auditory processing disorder (APD) results from a diminished capacity to encode sounds essential for speech perception. While evaluating speech perception appears to be the most apparent method to tackle this issue, speech encompasses language-specific characteristics that necessitate processing beyond the auditory system, including coarticulation, semantic elements, and grammar. Consequently, it is unfeasible to ascertain whether compromised speech perception in the absence of hearing loss is due to Auditory Processing Disorder (APD) or language deficits. Perception assessments also encompass significant non-sensory processing. A listener generally needs to focus on and retain the sequence of delivered sounds, thereafter identifying which sound possessed a distinctive characteristic (e.g., pitch). This study differentiates sensory and non-sensory contributions to two fundamental aspects of auditory perception, specifically time and frequency, by comparing performance on nearly identical tasks to develop measures of auditory processing (AP).

Auditory Deprivation

Auditory Processing Disorder (APD) exists at the convergence of hearing impairment and language difficulties, both of which have significant genetic determinants. Recent findings in the genetics of Specific Language Impairment (SLI) indicate distinct genes associated with different language-related characteristics, and similar genetic analytic techniques may be relevant to Auditory Processing Disorder (APD). Nonetheless, certain data indicate contextual factors may contribute to specific characteristics of APD, such as tone sequencing, suggesting that APD may be more acquired than hereditary. The most compelling direct evidence for Auditory Processing Disorder (APD) arises from instances of natural auditory deprivation, especially prolonged otitis media with effusion (OME).

Two independent studies published in 1991—conducted by Pillsbury, Grose, and Hall, and by Moore, Hutchings, and Meyer—revealed that children undergoing treatment for chronic otitis media with effusion displayed deficient binaural hearing, as evidenced by diminished binaural unmasking. This impairment occurred in the absence of effusion and normal audiometric results, suggesting a central cause rather than peripheral dysfunction. Subsequent research, including a prospectively monitored cohort with a recorded lifetime history of OME (Hogan & Moore, 2003), validated and expanded upon these findings. These investigations indicated that binaural unmasking develops later in infants with a low frequency of otitis media with effusion (OME). In usually developing children aged 7–8 years with a history of OME, auditory processing through binaural hearing may be relatively inferior to that of adults. As individuals age, the impact of OME on binaural hearing and associated auditory processes that facilitate speech perception decreases. This attenuation seems to result from at least two factors:

• The peak prevalence of OME occurs in the second year of life and declines thereafter, with a sharper drop after age five.
• The sequelae of OME are at least partly reversible, leading to improvements over time.

Longitudinal research conducted by Hall, Grose, and Pillsbury provides empirical evidence of reversibility, demonstrating that children treated for chronic OME exhibited progressive improvement in binaural unmasking over a period exceeding four years. Approximately 2 to 3 years after therapy, their performance was statistically indistinguishable from that of matched controls. An interpretable hypothesis is that reliance on inadequate cues due to deprivation during the OME period can be mitigated by the re-acquisition of normal cues once the deprivation is lifted, demonstrating brain plasticity that originally hindered and later enhanced auditory processing. Recent research has concentrated on evaluating the hypothesis that central auditory processing deficiencies arise from modified auditory input. The main subjects have been adult listeners with equipment positioned in one ear to intentionally eliminate localization cues, thus imitating unilateral input alterations. Concurrent with the naturalistic deprivation observed in otitis media with effusion (OME), these listeners exhibit early inaccuracies in sound localization soon following device introduction. In the ensuing days to weeks, their localization performance enhances despite the auditory input remaining modified. Current evidence indicates that active auditory training expedites the recovery trajectory. Engaging listeners in sound localization activities during the recovery phase seems to leverage brain plasticity to restore or compensate for impaired binaural cues.