Commission on Dental Competency Assessments (CDCA) ADEX Dental Examination

Correct: The diagnosis of Meniere’s disease is primarily clinical, relying on the identification of a specific cluster of symptoms. According to the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) criteria, documenting the characteristic fluctuating low-frequency sensorineural hearing loss via a standard audiometric evaluation is the essential first step in the diagnostic process. A thorough case history is equally critical to establish the duration and nature of the vertigo episodes, which must last at least 20 minutes to several hours to fit the profile of Meniere’s.

Incorrect: While Electrocochleography (ECochG) can provide supportive evidence of endolymphatic hydrops, it is not the primary or first diagnostic tool due to its variable sensitivity. Recommending medical management like a low-sodium diet or diuretics is a treatment phase action that should only occur after a formal diagnosis is established. Videonystagmography (VNG) is a valuable component of a vestibular workup, but it often shows normal results in the early stages of Meniere’s and does not capture the auditory fluctuations that are the hallmark of the disease.

Takeaway: The initial priority in suspected Meniere’s disease is the clinical documentation of fluctuating low-frequency sensorineural hearing loss and a detailed symptom history.

Correct: The radiographic presentation of a dome-shaped, non-corticated radiopacity on the floor of the maxillary sinus in an asymptomatic patient is the classic description of an antral pseudocyst. These are common incidental findings caused by an accumulation of inflammatory exudate (serum) under the sinus mucosa, lifting the periosteum. Because they are non-destructive and typically do not cause symptoms or sinus ostium obstruction, the standard of care is radiographic monitoring rather than surgical intervention or medication.

Incorrect: A maxillary sinus mucocele is a far more aggressive lesion that is typically symptomatic and characterized by the expansion and thinning of the sinus walls, which is not seen in this non-corticated, stable presentation. Localized mucosal thickening from odontogenic sinusitis would usually be associated with a clear source of infection, such as a non-vital tooth or periodontal disease, and would present as a more generalized thickening of the sinus lining rather than a solitary dome. A surgical ciliated cyst is a specific entity that occurs after trauma or surgery (like a Caldwell-Luc procedure) where sinus epithelium is trapped in the bone; it is usually a well-defined, corticated radiolucency or radiopacity that requires enucleation, which does not fit the clinical history or radiographic appearance of a simple pseudocyst.

Takeaway: An asymptomatic, dome-shaped radiopacity on the maxillary sinus floor without a corticated border is most likely an antral pseudocyst and generally requires only observation.

Correct: A cholesteatoma is a collection of keratinizing squamous epithelium in the middle ear, often resulting from chronic middle ear disease or a retraction pocket. Key clinical signs include foul-smelling discharge (otorrhea), a white keratinous mass, and conductive hearing loss due to potential ossicular erosion.

Correct: Visual Reinforcement Audiometry (VRA) relies on the infant’s ability to perform a conditioned head-turn response toward a sound source. This behavior is physiologically dependent on the maturation of the superior olivary complex (SOC) in the brainstem, which is the first site of binaural integration and is responsible for sound localization. Without the functional development of the SOC and its connections, the infant would not be able to reliably localize the stimulus to receive the visual reinforcement.

Incorrect: Ossification of the external auditory canal primarily affects the physical resonance and acoustics of the ear but does not govern the behavioral motor response of localization. While myelination of the auditory nerve is necessary for general signal conduction, it is the specific processing within the central auditory pathway (the SOC) that enables localization. Changes in the pharyngeal cavity and larynx relate to speech production and Eustachian tube orientation rather than the auditory-motor integration required for VRA.

Takeaway: The clinical application of VRA is fundamentally based on the physiological maturation of the superior olivary complex, which enables the sound localization behavior necessary for the test.

Correct: The audiologist’s role in genetic counseling involves interpreting how genetic results relate to the patient’s hearing loss (phenotype) and providing education on the audiological aspects of the condition. However, the specific calculation of recurrence risks and detailed family planning advice must be handled by a certified genetic counselor or clinical geneticist to whom the audiologist refers the family.

Incorrect: Calculating specific recurrence risk percentages is a specialized task for geneticists and exceeds the audiological scope. Ordering genetic tests for parents is generally a medical function that requires physician oversight or a geneticist’s expertise. Advising on specific reproductive technologies like preimplantation genetic diagnosis involves complex medical and ethical counseling that is outside the standard practice of audiology.

Takeaway: Audiologists provide the link between genetic findings and audiological outcomes but must refer to genetic specialists for recurrence risk and family planning counseling.

Correct: In cases of true unilateral profound hearing loss, a ‘shadow curve’ must appear during unmasked testing. This occurs because sound presented to the impaired ear at high intensities (typically 40-60 dB HL for supra-aural headphones) travels through the bones of the skull to the cochlea of the non-test (normal) ear. If a claimant reports a 95 dB HL loss but shows no shadow curve in the normal ear, they are likely suppressing their response, which is a hallmark indicator of non-organic hearing loss or malingering.

Incorrect: A Speech Reception Threshold within 5 dB of the pure-tone average indicates excellent internal consistency and suggests organic hearing rather than pseudohypacusis. Recruitment is a physiological phenomenon associated with cochlear hair cell damage and is not an indicator of non-organic loss. A low false-alarm rate during catch trials suggests the patient is a reliable observer and is following instructions correctly, which contradicts a finding of pseudohypacusis.

Takeaway: The absence of a shadow curve in unilateral hearing loss testing is a primary indicator of non-organic behavior because it contradicts the physical principles of interaural attenuation and cross-hearing.

Correct: The hallmark of Auditory Neuropathy Spectrum Disorder (ANSD) is the preservation of outer hair cell function (evidenced by OAEs or the Cochlear Microphonic) alongside abnormal or absent neural synchrony (evidenced by the ABR). To confirm the diagnosis, clinicians must identify the Cochlear Microphonic (CM). By reversing the stimulus polarity (rarefaction vs. condensation), the CM will invert in phase, whereas neural components like the ABR waves do not. This distinction is critical to ensure the response seen is pre-neural and not a synchronous neural wave.

Incorrect: Acoustic reflexes are typically absent or significantly elevated in ANSD, but they are not the primary diagnostic criterion for the disorder itself. Behavioral observation audiometry is highly subjective and unreliable for determining thresholds in infants, especially in ANSD where behavioral thresholds can vary significantly from ABR findings. Wave V latency-intensity functions are invalid in ANSD because the ABR is characteristically absent or severely dyssynchronous, making it impossible to use ABR waves to estimate behavioral thresholds or fit hearing aids.

Takeaway: The definitive diagnostic indicator for ANSD is the presence of a cochlear microphonic in the absence of a synchronous ABR, which must be verified using polarity reversal techniques.

Correct: In geriatric patients, the phenomenon of phonemic regression describes a situation where speech understanding is poorer than would be predicted by the pure-tone audiogram. This is largely attributed to neural changes, including the loss of spiral ganglion cells and degeneration within the central auditory pathways (such as the cochlear nuclei and auditory cortex). These changes impair the temporal resolution and neural synchrony necessary to distinguish speech signals from competing background noise, even when the quiet-room word recognition remains relatively high.

Incorrect: Cerumen accumulation typically results in a conductive hearing loss that affects overall sensitivity but does not specifically explain the neural processing deficit seen in speech-in-noise tasks. Ossicular stiffening or otosclerosis is a middle ear pathology that is not the primary driver of age-related sensorineural or neural speech processing declines. Stapedius muscle hypertrophy is not a characteristic of the aging auditory system; in fact, the acoustic reflex often weakens or becomes absent in cases of age-related sensorineural hearing loss.

Takeaway: Age-related speech-in-noise deficits are often driven by neural and central auditory pathway degeneration rather than peripheral sensitivity loss alone.

Correct: In cases of Auditory Neuropathy Spectrum Disorder (ANSD), the primary clinical challenge is the dyssynchrony of the auditory nerve rather than a simple loss of sensitivity. Because pure-tone thresholds (the audiogram) often fail to predict speech perception abilities in these patients, management decisions must be driven by functional outcomes. If a patient is not meeting age-appropriate speech and language milestones or shows poor speech perception despite hearing aids providing adequate audibility, they are considered candidates for cochlear implantation, which can provide the necessary temporal cues that the dyssynchronous nerve cannot.

Incorrect: The disappearance of the cochlear microphonic is a diagnostic marker but does not necessarily dictate a change in management strategy. An increase in DPOAE amplitude is not a typical clinical finding in ANSD and would not indicate a need for a cochlear implant, as DPOAEs reflect outer hair cell function, not neural synchrony. Stabilization of pure-tone thresholds at 40 dB HL is misleading because a patient with ANSD may have relatively good thresholds but still have zero percent speech discrimination, making the audiogram an unreliable metric for determining the success of amplification.

Takeaway: Management of ANSD prioritizes functional speech-language development and auditory skill acquisition over traditional audiometric thresholds due to the unpredictable nature of neural dyssynchrony.