Scuba Diving-Induced Inner-Ear Pathology: Imaging Findings of Superior Semicircular Canal and Tegmen Tympani Dehiscence

Background

Superior semicircular canal dehiscence (SSCD) is characterized by loss of the bone overlying the superior semicircular canal of the inner ear and was first described by Minor and colleagues in 1998 [1]. Patients presenting with SSCD often experience hearing loss, disequilibrium, autophony, oscillopsia, and noise-induced vertigo [1,2]. Cadaveric studies have shown that SSCD has an approximate incidence of 0.7% [3], while radiological studies have reported an incidence rate of 3–9%, making SSCD a relatively rare disorder [4,5]. Interestingly, it has been shown that approximately 2% of patients have asymptomatic dehiscence of the superior semicircular canal [6]. It has been postulated that the hallmark symptoms of SSCD are secondary to a ‘third window’ effect [1–8]. Briefly, dehiscence of the segment of temporal bone, located above the superior semicircular canal, creates a ‘third window,’ which increases inner-ear immittance and perturbs normal endolymph dynamics, particularly when exposed to high-level sounds or pressure changes [8–11]. Hence, patients with suspected SSCD will typically show an air-bone gap (conductive hearing loss) and rotational nystagmus induced by pressure changes (Henebert’s sign) or sound (Tullio phenomenon) upon examination [2,10–12].

Although the exact etiology of SSCD is unknown, it is thought that the presence of a thin bony laminar overlying the inner ear predisposes a patient to SSCD following a second event [13]. Second events such as a head trauma, erosion due to weight of the temporal lobe, or a rapid increase in middle-ear pressure are thought to disrupt the thin overlying temporal bone [3,9,13–15]. However, only a few reports have highlighted the diagnosis of SSCD following trauma to the head [16–18]. Furthermore, to our knowledge, only 2 cases of SSCD due to increased middle ear pressure have been reported, one associated with scuba diving, and a second associated with childbirth [19,20]. Of note, SSCD can occur in association with dehiscence of the tegmen tympani (TTD), which overlies the middle ear [21–26], making it likely that the same predisposition for SSCD exists for TTD [27]. Cortés et al reported a case of temporal lobe injury due to temporal bone rupture during scuba diving, highlighting the susceptibility of the temporal bone to the pressures that can occur during scuba diving [28]. Here, we present a case report suggesting that SSCD with associated TTD can occur secondary to the increased pressure associated with scuba diving.

Case Report

A 52-year-old Puerto Rican man with a past medical history of hypercholesterolemia, gastritis, and chronic low back pain secondary to a lumbar herniated disc, presented to the emergency department with vertigo, dizziness, vomiting, and mild hearing loss in the right ear. He stated that he was a professional scuba diving instructor and that he spent several hours a week diving. His symptoms began 4 days ago after a scuba diving session. During this session, he performed 4 dives to 100 feet of salt water (FSW) with a surface interval of 15 minutes and a bottom time of 35 minutes each. The total time in the water was approximately 4 hours. Importantly, he reported that he did not take the appropriate safety precautions and did not perform decompressions stops while ascending from the dives. He was able to complete all dives without incident. However, when returning to his boat, he blew his nose, which led to a sensation of fullness and pressure in the right ear, as well as dizziness. During the following 4 days, he reported that his symptoms persisted and were aggravated by 4 episodes of vomiting.

Upon evaluation, the patient denied chest pain, respiratory difficulty, or cutis marmorata. On physical examination, the patient was found to have severe vertigo that limited his ambulation, and hearing loss in the right ear. Moreover, he was found to have bilateral tympanosclerosis, erythema, and tym-panic membrane retraction; therefore, he was diagnosed with inner-ear barotrauma. Given the history of diving without decompression stops, he was treated with recompression therapy on USN-TT6 to prevent further deterioration and avoid residual neurological deficit. After recompression therapy, he reported improvement in symptoms but continued to have debilitating vertigo, for which a brain and a temporal bone MRI, including a high-resolution fast-field echo (FFE) sequence, were ordered to rule out potential neurovascular pathologies and tympanic membrane rupture, respectively. The brain MRI showed no neurological or neurovascular pathologies, but the bilateral temporal bone MRI in the sagittal plain showed questionable thinning of the osseous coverage of the right superior semicircular canal, which was suggestive of segmental dehiscence of the right superior semicircular canal (Figure 1). Of note, the meninges overlying the suspected right superior semicircular canal defect had a normal MRI appearance. To confirm the findings, a high-resolution computed tomography (HRCT) of the temporal bone without contrast was performed. The HRCT in the Pöschl projection confirmed right superior semicircular canal dehiscence and associated tegmen tympani dehiscence (Figure 2A), which was observed in 4 contiguous slices, with an intact left superior semicircular canal and tegmen tympani (Figure 2B). The patient was scheduled for outpatient evaluation with the Otolaryngology service for evaluation with a vestibular evoked myogenic potential (VEMP) test, but was unfortunately lost to follow-up.

Discussion

Although the exact etiology of SSCD is unclear, it is thought that both primary and secondary factors are involved. The presence of a thin segment of bone overlying the superior semicircular canal is a strong predisposing factor for SSCD following a trauma to the head or increased inner-ear pressure [2,10–12,15,16].

A few studies have reported a diagnosis of SSCD following trauma to the head, but to our knowledge only a single case of SSCD associated with scuba diving has been reported [19]. Kitajima et al presented the case of young woman who had episodes of vertigo that occurred during scuba diving. In contrast, our patient did not present symptoms while scuba diving, rather, we discuss the presentation of SSCD immediately following an event of inappropriate scuba diving. Moreover, we also report the concomitant finding of TTD, which has frequently been reported in association with SSCD.

Our patient reported performing several repetitions of diving at a significant depth, without consideration for proper decompression on ascent. For this reason, our patient was treated with recompression therapy, with inadequate response of symptoms. Interestingly, diving without proper techniques for pressure equalization can lead to increased pressure in the middle and inner ear, with subsequent barotrauma, which may present with pain or pressure in the ear, as well as decreased hearing or vertigo [29–32]. Although significantly less frequent, barotrauma has been reported to cause rupture of the temporal bone, indicating a susceptibility of the temporal bone to changes in middle- and inner-ear pressure [28]. This highlights the importance of performing high-resolution imaging of the temporal region in patients presenting with symptoms that could be related to injury of the middle and inner ear due to increased pressure such as that which occurs following scuba diving with inadequate decompression techniques.

Currently, MRI is the most accurate technique for detecting neurological damage secondary to decompression sickness [33]. As seen in our case, an MRI of the inner ear can suggest the presence of SSCD but has low sensitivity and specificity for this disorder. Therefore, patients with a recent history of diving and suspected SSCD should undergo HRCT imaging of the temporal region. Importantly, HRCT with imaging reconstruction of the superior circular canal along the transverse (Stenvers view) and longitudinal (Pöschl view) axes is required for proper identification of SSCD and remains the most common diagnostic modality with the highest sensitivity. Unfortunately, given the poor compliance of our patient with outpatient Otolaryngology service, and lack of a positive VEMP test, we are unable to fully discard the possibility that the identified SSCD and TTD are not in and of their own the cause for this patient’s symptoms.

We suggest the inclusion of SSCD within the differential diagnosis of vertigo after inadequate diving that does not respond to recompression therapy. Moreover, we highlight the importance of a HRCT of the temporal region with evaluation in the Stenvers and Pöschl views, to correctly identify the etiology of these patients’ symptoms. This can further accelerate proper treatment of the underlying cause and referral for otolaryngology evaluation and surgical management if necessary.

Conclusions

We encountered the case of a 52-year-old scuba diver who reported vertigo after an event of improper diving techniques. To our knowledge, SSCD directly associated with scuba diving has been reportedly only once previously. Moreover, concomitant SSCD and TTD after scuba diving has never been reported.

Nevertheless, the increased inner-ear pressure that occurs during scuba diving may cause dehiscence of the bone overlying the superior semicircular canal and tegmen tympani. Given the prevalence of asymptomatic SSCD and TTD, it is possible that the increased pressure experienced during scuba diving does not directly cause dehiscence, but rather converts asymptomatic temporal dehiscence to symptomatic temporal dehiscence. Therefore, we recommend that SSCD and TTD be included in the diagnostic algorithm of patients presenting with vertigo after scuba diving, and evaluation of the temporal bone using HRCT. This will accelerate proper evaluation and surgical management if required. Moreover, this study highlights the danger of inadequate decompression techniques during scuba diving, and emphasizes the importance of proper education regarding safe practices.