Why “Normal Hearing” Shouldn’t Be a Gatekeeper for Auditory Processing Disorder (APD) Testing

Why this conversation matters to me, both personally and professionally.

Audiology is a deeply rule-bound, traditional profession. We are trained to rely on clear metrics: thresholds, decibels, tymps, reflexes, waveforms. In many ways, that precision is a strength. But auditory processing disorder (APD) doesn’t fit cleanly into that model.

It doesn’t give us the same yes/no answers that tone-based audiometry does. It lives in a gray zone where symptoms vary, patterns overlap, and no single test can definitively confirm or rule it out. That discomfort is part of why APD remains one of the most misunderstood and gatekept diagnoses in audiology today.

In some countries, the criteria for APD are tightly defined, requiring individuals to have hearing thresholds no worse than 20 dB HL across frequencies. That threshold exists because the research used it to control the study population. But it’s a mistake to treat it as a clinical truth. There are real problems with assuming “normal” is defined solely by the audiogram.

First, hearing loss is not always stable. Many children have fluctuating conductive hearing loss due to fluid or Eustachian tube dysfunction. If a child is tested during a “good hearing day,” they may appear to qualify. A week later, they wouldn’t.

Second, tones have nothing to do with understanding speech. They are useful for measuring detection, but they don’t tell us how a brain organizes language in real-world conditions, in noise, when tired, or when stressed.

And third, focusing only on pure-tone audiometry ignores the entire context of developmental auditory access, which plays a major role in how APD shows up in children.

This is especially true for individuals with Ehlers-Danlos Syndrome (EDS). In EDS, connective tissue fragility can affect the middle ear (through lax ligaments and poor Eustachian tube function), leading to fluctuating conductive hearing loss.

But EDS can also impact inner ear and neural structures, contributing to sensorineural hearing loss, auditory neuropathy spectrum disorder (ANSD), or hypermobility-related vascular instability that compromises auditory signal transmission. These disruptions may not be visible on a pure-tone audiogram—especially when hearing “returns to normal”—but they leave a mark.

Just like a flood that recedes, the water level might drop, but the debris and damage left along the riverbank still impair the flow. The same applies to the auditory system: the thresholds may normalize, but the effects of deprivation and disorganized input persist.

Audiology as a profession often leans heavily on things we can see or measure, ideally with objective tests that suggest lesions or damage. That need for physiological certainty has shaped how we’ve approached APD. But in the case of APD, that argument doesn’t hold water.

Many of our current tests were created not to diagnose developmental auditory differences in children, but to localize damage in adults—veterans with blast injuries, stroke patients, individuals with known central lesions. That was the origin of much of our test battery. And the assumptions baked into that history still shape our thinking today.

But APD is not just about damage. It’s about access, timing, integration, fatigue, and language clarity. These challenges can exist with or without measurable lesions. And if we keep narrowing our criteria to fit a rigid definition, we will continue excluding the very people who most need support.

That’s why I asked the question, and that’s why I’m posting about this topic now.

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Here’s the question I originally asked in another APD group:

“Do you believe that any amount of hearing loss automatically rules out a diagnosis of auditory processing disorder? If so, what evidence are you using to support that view?”

Another audiologist responded respectfully, first emphasizing her country’s adherence to the tradition of patients needing to measure as having normal hearing in order to test for APD, and then raising the point that many children who once had hearing loss, but now test in the “normal” range, often lose their services or accommodations, even though their auditory and academic challenges may persist. She pointed out how unfortunate and frustrating that can be for families.

I completely agree with her concern, and I want to add another layer to the conversation.

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Auditory processing is not a single pathway. It’s a river system.

The main flow represents how the brain organizes and makes meaning from sound. But upstream, there are dozens of tributaries: mild or fluctuating hearing loss, auditory neuropathy, sensory processing differences, developmental language delay, chronic otitis media, cognitive fatigue, and more.

If any of those upstream factors are disrupted…

That is, if the sound is distorted, delayed, or inconsistently available, the river downstream doesn’t flow properly. Children may struggle with speech-in-noise, following directions, or keeping up with spoken language.

But instead of investigating those interactions, many providers have been taught: “If there’s any hearing loss, you can’t test for APD.”

Let’s clarify: That belief comes directly from research protocol, not clinical need.

Yes, most APD test batteries were normed on people with normal audiograms. That helps ensure clean data. But real life isn’t a research lab. People don’t come in clean categories. And hearing loss doesn’t erase APD, it can make it worse.

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Even the American Academy of Audiology (2010) says:

“Mild, stable, or managed hearing loss does not necessarily preclude assessment [for APD] if the stimuli are appropriately audible.”

And ASHA’s Practice Portal (2023) states:

“CAPD may coexist with peripheral hearing loss and may continue to be present when the hearing loss has been resolved.”

Musiek & Chermak (2013) emphasize:

“Hearing loss does not preclude a diagnosis of APD. It is important to assess central auditory function even in the presence of peripheral deficits.”

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It is certainly unfair to remove support from children whose hearing “returns to normal” after chronic fluid or otitis media. But it’s equally unfair to deny APD evaluation to those who have stable, mild, or high-frequency hearing loss just because their thresholds don’t fit a traditional research profile.

The idea that we shouldn’t test someone for APD because they don’t meet research norms, like staying strictly within a 20 dB hearing range, has no clinical justification. None of the test manuals explicitly say that hearing must be perfectly normal to be tested. That cutoff exists to keep research samples homogeneous, not to reflect the real diversity of individuals who struggle with auditory processing.

Precluding people with hearing loss from being evaluated for APD on that basis alone doesn’t protect science, it restricts access to care.

And while it’s absolutely true that kids with hearing loss who later test normal often lose services unfairly, that’s not a reason to turn around and exclude others from evaluation just because they fall outside research-defined norms.

The truth is, the population isn’t homogeneous, and that’s exactly what makes auditory processing disorder so challenging, and so important, to identify.

APD has heterogeneous causes, and trying to fit all patients into a single category for the sake of data clarity risks leaving many behind.

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Why are we still using these tests?

Here’s something we don’t talk about enough: Most APD tests were developed to assess adults with acquired brain injuries, like stroke, trauma, or blast exposure.

Much of our early understanding of central auditory dysfunction came from WWII veterans who could no longer process speech clearly despite having intact cochleas. These were fully developed brains with localized damage.

“The original concept of central auditory disorders was largely derived from studies of adults with known lesions of the central auditory nervous system.”

— Musiek & Chermak, 2007

We now apply those same tools to children with developmental auditory deprivation, neurodivergent processing patterns, or asynchronous language acquisition, and then wonder why their scores don’t match expectations.

The tests weren’t made for them. But their struggles are just as real.

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So what’s the solution?

Andy Vermiglio (2016) has argued that APD testing lacks diagnostic accuracy because there is no true gold standard, and we’re applying tools meant to detect lesions in adults to a much messier clinical population.

David Moore (2018) further notes that our tendency to draw a firm line between “peripheral” and “central” auditory problems is more theoretical than practical.

Real people rarely divide so neatly. And when we insist they must, we risk making APD so narrow that it “doesn’t exist”—not because it isn’t real, but because we’ve defined it into obscurity.

It’s important for research to use homogeneous groups. But APD is not homogeneous. It presents differently across children with different histories, hearing levels, developmental profiles, and neurological wiring.

If we limit the definition to only those who pass pure-tone testing, we are not protecting the diagnosis, we’re hollowing it out.

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So instead of asking, “Is the hearing normal?”… let’s instead ask:

“Is the child functionally able to access sound and language in a consistent, reliable, meaningful way?”

We should be investigating how much of an impact each variable: peripheral hearing, central processing, fatigue, developmental history is having on communication.

And we should do our best to separate them out, not rule them out.

Because when the river isn’t flowing clearly, we don’t just test the surface.

We follow the tributaries upstream, until we understand why the downstream current is turbulent and breaking down.

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References:

American Speech-Language-Hearing Association. (2023). Central Auditory Processing Disorder (Practice Portal). https://www.asha.org/.../central-auditory-processing.../

American Academy of Audiology. (2010). Guidelines for the Diagnosis, Treatment and Management of Children and Adults with Central Auditory Processing Disorder. https://audiology-web.s3.amazonaws.com/.../CAPD...

Musiek, F. E., & Chermak, G. D. (2007). Handbook of Central Auditory Processing Disorder, Volume I: Auditory Neuroscience and Diagnosis. Plural Publishing.

Musiek, F. E., & Chermak, G. D. (2013). Handbook of Central Auditory Processing Disorder, Volume II: Comprehensive Intervention. Plural Publishing.

Vermiglio, A. J. (2016). On the clinical entity in audiology: (Central) auditory processing disorder. Journal of the American Academy of Audiology, 27(7), 610–627.

Moore, D. R. (2018). Editorial: Auditory processing disorder (APD). Ear and Hearing, 39(4), 617–620.