A Prospective and Retrospective Observational Study of Symptoms and Mechanisms of Recovery in People With Inner Ear Decompression Sickness (IEDS)

Decompression sickness after diving can occur following a rapid ascent. Here, nitrogen, absorbed by the body when breathing compressed air at depth, comes out of solution and forms microbubbles in the blood. Inner ear decompression sickness (IEDS) accounts for approximately 20% of all cases of decompression sickness. The vestibular system is involved in ~85% cases of IEDS resulting in symptoms of vertigo, nausea, vomiting and unsteadiness with hearing loss and tinnitus.

The strong association of IEDS with a patent foramen ovale (50-73% of cases) suggests that a shunted venous gas embolism causes damage to the vestibular apparatus, which is particularly vulnerable due to its low perfusion and thus slow inert gas washout, compared to the cochlea and other brain structures. It is hypothesised that the nitrogen bubbles within the blood vessels trigger an inflammatory reaction in the endothelium with a coagulation cascade that leads to hypoxic injury and/or that there is direct damage to the membranous labyrinth. Animal models of rapid decompression suggest that it can cause a haemorrhage within the labyrinth with ectopic bone growth and fibrosis occurring over the next month. Advances in the imaging of the inner ear using a gadolinium-based contrast agent (GBCA) allow us to explore structural changes in human divers. Imaging can also help to differentially diagnose another potential cause of diving induced dizziness, superior structural dehiscence syndrome

Decompression sickness and the subsequent inflammatory response requires emergency treatment using with hyperbaric oxygen. The effects of hyperbaric therapy and rehabilitation are not uniform across participants, factors affecting recovery include a high clinical score on admission and a delay in hyperbaric recompression of over 6 hours. Complete recovery is seen in only about 30% of cases. Previous studies have highlighted that people who do not fully recover can have a variety of symptoms that can affect work, hobbies and well-being. These include feelings of instability in some situations (working at a height and with movement) and imbalance in the dark or when changing position.

In people with permanent vestibular pathology, symptoms can still improve due to central adaptive processes within the brain termed vestibular compensation. Clinical studies in other types of peripheral vestibular dysfunction show that it is possible to facilitate the compensation process and symptom recovery through vestibular rehabilitation. Early access to vestibular rehabilitation is now routine practice at the Diving Diseases Research Centre (DDRC) where patients are treated in the South-West UK. This is coupled to diagnosis and monitoring of vestibular function using objective laboratory tests (rotary testing) and clinical tests.

Animal studies highlight the mechanisms underlying vestibular compensation following a peripheral nerve lesion. These focus on changes in the interconnections between brainstem nuclei (e.g. vestibular nuclei) and the cerebellum and re-weighting of the relative importance of multi-sensory sensory inputs. Human studies in chronic peripheral dysfunction also suggest there are recovery-related changes in cortical areas that normally process vestibular information over time. Functional changes in the acute stages include an increase in contralesional activity in the parietoinsular vestibular cortex as well as interlinked subcortical areas (posterolateral thalamus, anterior cingulate gyrus, pontomesencephalic brainstem, hippocampus) with a decrease in activity was seen in the visual, somatosensory and auditory cortices. Structural changes over the first 3 months post lesion include increases in grey matter volume in the vestibular cortex, bilateral hippocampus, visual cortices and the cerebellum.