Labyrinthine concussion: Historic otopathologic antecedents of a challenging diagnosis

Bartholomew, Ryan A.; Lubner, Rory J.; Knoll, Renata M.; Ghanad, Iman; Jung, David; Nadol, Joseph B.; Alvarez, Victor E.; Remenschneider, Aaron K.; Kozin, Elliott D.

doi:10.1002/lio2.360

Cited by 15 publications

(11 citation statements)

References 69 publications

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“…The pressure effects from mTBI will extend to the intralabyrinthine compartment and has historically been termed Labyrinthine Concussion (LC). Bartholomew and colleagues ( 4 ) recently published a historical review of the research into LC. In numerous animal studies and clinical reports dating back to the late 1800s, concussions have been reported to result in direct inner ear damage.…”

Section: Pathophysiologymentioning

confidence: 99%

Post-concussive Dizziness: A Review and Clinical Approach to the Patient

Gianoli

2022

Front. Neurol.

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Dizziness is a frequent complaint after head trauma. Among patients who suffer a concussion (mild traumatic brain injury or mTBI), dizziness is second only to headache in symptom frequency. The differential diagnosis of post-concussive dizziness (PCD) can be divided into non-vestibular, central vestibular and peripheral vestibular causes with growing recognition that patients frequently exhibit both central and peripheral findings on vestibular testing. Symptoms that traditionally have been ascribed to central vestibular dysfunction may be due to peripheral dysfunction. Further, our ability to test peripheral vestibular function has improved and has allowed us to identify peripheral disorders that in the past would have remained unnoticed. The importance of the identification of the peripheral component in PCD lies in our ability to remedy the peripheral vestibular component to a much greater extent than the central component. Unfortunately, many patients are not adequately evaluated for vestibular disorders until long after the onset of their symptoms. Among the diagnoses seen as causes for PCD are (1) Central vestibular disorders, (2) Benign Paroxysmal Positional Vertigo (BPPV), (3) Labyrinthine dehiscence/perilymph fistula syndrome, (4) labyrinthine concussion, (5) secondary endolymphatic hydrops, (6) Temporal bone fracture, and (7) Malingering (particularly when litigation is pending). These diagnoses are not mutually exclusive and PCD patients frequently exhibit a combination of these disorders. A review of the literature and a general approach to the patient with post-concussive dizziness will be detailed as well as a review of the above-mentioned diagnostic categories.

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Section: Pathophysiologymentioning

confidence: 99%

Post-concussive Dizziness: A Review and Clinical Approach to the Patient

Gianoli

2022

Front. Neurol.

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“…1). The auditory nerve is particularly vulnerable to external force in the regions of the fundus of the internal auditory canal and the transitional zone (TZ) [36][37][38][39][40][41] . When the medial displacement of the brainstem is greater than that of the cochlea in the temporal bone, the resultant force on the auditory nerve may avulse the auditory neurons from the fundus of the internal auditory canal [36][37][38][39][40][41] .…”

Section: Causes Of Auditory Nerve Degeneration and Related Clinical Issuesmentioning

confidence: 99%

“…damage [36][37][38][39][40][41][42] . Clinically, cases in which the auditory nerve is damaged without damage to HCs are most suitable for cell transplantation because the HCs can provide trophic support, as mentioned above (Fig.…”

Section: Causes Of Auditory Nerve Degeneration and Related Clinical Issuesmentioning

confidence: 99%

“…In patients with a closed head injury even without temporal bone fractures, damage to auditory neurons is observed primarily and/or secondarily following HC damage 36 – 42 . Clinically, cases in which the auditory nerve is damaged without damage to HCs are most suitable for cell transplantation because the HCs can provide trophic support, as mentioned above ( Fig.…”

Section: Introductionmentioning

confidence: 99%

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Cell Transplantation to Restore Lost Auditory Nerve Function is a Realistic Clinical Opportunity

Sekiya

Holley

2021

Cell Transplant

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Hearing is one of our most important means of communication. Disabling hearing loss (DHL) is a long-standing, unmet problem in medicine, and in many elderly people, it leads to social isolation, depression, and even dementia. Traditionally, major efforts to cure DHL have focused on hair cells (HCs). However, the auditory nerve is also important because it transmits electrical signals generated by HCs to the brainstem. Its function is critical for the success of cochlear implants as well as for future therapies for HC regeneration. Over the past two decades, cell transplantation has emerged as a promising therapeutic option for restoring lost auditory nerve function, and two independent studies on animal models show that cell transplantation can lead to functional recovery. In this article, we consider the approaches most likely to achieve success in the clinic. We conclude that the structure and biochemical integrity of the auditory nerve is critical and that it is important to preserve the remaining neural scaffold, and in particular the glial scar, for the functional integration of donor cells. To exploit the natural, autologous cell scaffold and to minimize the deleterious effects of surgery, donor cells can be placed relatively easily on the surface of the nerve endoscopically. In this context, the selection of donor cells is a critical issue. Nevertheless, there is now a very realistic possibility for clinical application of cell transplantation for several different types of hearing loss.

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“…The following data were collected from patients' medical records: sex, age, current medical history (course of disease, symptoms during attack, duration of attack, factors induced the attacks, triggering factors, and accompanying symptoms), underlying diagnosis (including labyrinthine infarction, dizziness/vertigo of unclear origin, vestibular neuritis, autoimmune inner ear disease, Ménière's disease, vestibular migraine, otitis media, vestibular paroxysmia, labyrinthine concussion, intralabyrinthine hemorrhage) (Figure 1), results of physical examination upon admission, and auxiliary examinations (such as immune-related laboratory tests, MRI and CT of the brain). Regarding the diagnosis of the above-mentioned underlying diagnosis, labyrinthine infarction, vestibular neuritis, labyrinthine concussion and intralabyrinthine hemorrhage are diagnosed according to patients' medical history, cochleovestibular evaluation and neurovascular imaging (8)(9)(10)(11), vestibular migraine, Ménière's disease and vestibular paroxysmia are diagnosed based on the diagnostic criteria suggested by Barany society (12)(13)(14), autoimmune inner ear disease is diagnosed according the medical history, vestibulocochlear evaluation and immune-related laboratory tests (15,16), otitis media is diagnosed according to the criteria reported by Gates et al (17).…”

Section: Clinical Data Collectionmentioning

confidence: 99%

Clinical Characteristics of Patients With Dizziness/Vertigo Accompanied by Posterior Semicircular Canal Hypofunction

Liu

et al. 2021

Front. Med.

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Objective: To investigate the clinical characteristics of patients with dizziness/vertigo accompanied by loss of the posterior canal(s) (LPC).Methods: Clinical data of 23 patients with LPC were collected. We determined video-head-impulse test (vHIT) gains of all six semicircular canals and correlated vHIT findings with other vestibulo-cochlear tests, including caloric test, ocular and cervical vestibular-evoked myogenic potentials (oVEMP, cVEMP), pure tone audiometry (PTA), and analyzed the differences in clinical manifestations of patients with LPC with different etiologies.Results: LPC was identified in 23 patients. At the time of disease onset, most patients presented with dizziness (47.8%) and vertigo (30.4%) only, and some patients (21.7%) complained of unsteadiness. Among these 23 patients with LPC, there were 14 (60.9%) patients of isolated LPC (ILPC), 21 (91.3%) patients of unilateral LPC (ULPC), and 2 (8.7%) patients of bilateral LPC (BLPC). (1) Among 14 patients with ILPC, 13 (92.9%) patients had unilateral ILPC, the rate of ipsilesional impairment on caloric test, or oVEMP/cVEMP test or PTA ipsilesionally was 53.8% (7/13) in patients with unilateral ILPC. The causes of unilateral ILPC were vertigo/dizziness of unclear origin (38.5%), labyrinthine infarction (15.4%), vestibular migraine (15.4%), and other diseases (30.8%); (2) among 21 patients with ULPC, 7 patients (33.3%) were accompanied with horizontal semicircular canal hypofunction ipsilesionally, the abnormal rate of caloric test, or oVEMP/cVEMP tests or PTA ipsilesionally was 57.1%. The causes of ULPC were vertigo/dizziness of unclear origin (33.3%), autoimmune inner ear disease (14.3%), labyrinthine infarction (14.3%), vestibular neuritis (9.5%), vestibular migraine (9.5%), and other diseases (19.0%); (3) among two patients with BLPC, one patient presented with unsteadiness, the causes of BLPC were vestibular paroxysmia and autoimmune inner ear disease.Conclusion: vHIT is a fast and effective method for assessing LPC, which can be used to detect isolated PC dysfunction. The causes of ILPC were peripheral origin or central origin. Patients with ILPC and ULPC mostly presented with dizziness/vertigo, and ULPC was often accompanied by ipsilateral vestibulo-cochlear impairment.

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Labyrinthine concussion: Historic otopathologic antecedents of a challenging diagnosis

Cited by 15 publications

References 69 publications

Post-concussive Dizziness: A Review and Clinical Approach to the Patient

Post-concussive Dizziness: A Review and Clinical Approach to the Patient

Cell Transplantation to Restore Lost Auditory Nerve Function is a Realistic Clinical Opportunity

Clinical Characteristics of Patients With Dizziness/Vertigo Accompanied by Posterior Semicircular Canal Hypofunction

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