Diving-related inner ear barotrauma (IEB) and inner ear decompression sickness (IEDS) most often result in permanent severe cochleovestibular deficits, unless immediate diagnosis is reached and the correct treatment is commenced early. Nine cases of sport-diving-induced inner ear injuries that were referred to the Israeli Naval Hyperbaric Institute between October 1987 and September 1989 are presented with regard to evaluation, treatment, and follow-up. The diagnosis was IEB in five divers and IEDS in four. Explorative tympanotomy was carried out with remarkable results in two patients with IEB, while the remaining three were relieved by bed rest alone. Three of the four IEDS patients were recompressed according to the extended US Navy Table 6 with good short-term results. The role of complete otoneurological evaluation in the decision-making process leading to the correct diagnosis and treatment is emphasized.
Comment This study shows that mal de debarquement is a benign, transient picture of a tumbling or swinging sensation but not true vertigo. The phenomenon seems to be quite common among crew members of fairly small seagoing vessels (73%). None of our subjects suffered persistent mal de debarquement3 or requested medical attention.The occurrence of mal de debarquement was positively correlated with all the parameters ofsusceptibility to seasickness but was not correlated with experience at sea-that is, both inexperienced and experienced crew members had the sensation to a similar degree.The nature of mal de debarquement, its short latency and limited duration, and its relation to prolonged sea voyages and rough sea conditions can be explained within the framework of sensory adaptation to ship motion. Passengers and crew on board ship are exposed to a series of unnatural and conflicting vestibular, visual, and proprioceptive stimuli which, according to the neural mismatch and sensory rearrangement theory, may cause seasickness and, at the same time, adaptation to specific ship motion.2 This adaptation is often expressed in the familiar sensation of "getting one's sea legs," using the leg muscles to oppose the motion of the waves. After return to land these newly acquired sensorimotor patterns are no longer appropriate, giving rise to mal de debarquement, which lasts until readaptation is achieved.Further studies measuring vestibulo-oculoproprioceptive interactions during mal de debarquement are warranted in order to clarify the neurophysiological basis of this phenomenon.
Histological and functional derangements of the vestibular system have been reported in laboratory animals exposed to high levels of noise. However, clinical series describe contradictory results with regard to vestibular disturbances in industrial workers and military personnel suffering from noise induced hearing loss (NIHL). The purpose of the present study was to evaluate vestibular function in a group of subjects with documented NIHL, employing electronystagmography (ENG) and the smooth harmonic acceleration (SHA) test. Subjects were 22 men suffering from NIHL and 21 matched controls. Significantly lower vestibulo-ocular reflex gain (p = 0.05), and a tendency towards decreased caloric responses were found in the study group. No differences in the incidence of vertigo symptoms, spontaneous, positional and positioning nystagmus, directional preponderance and canal paresis in the ENG, or the SHA test phase and asymmetry parameters were observed between the groups. These results demonstrated a symmetrical centrally compensated decrease in the vestibular end organ response which is associated with the symmetrical hearing loss measured in the study group. Statistically significant correlations were found between the average hearing loss, the decrement in the average vestibulo-ocular reflex gain (p = 0.01), and ENG caloric lateralization (p = 0.02). These correlations might indicate a single mechanism for both cochlear and vestibular noise-induced injury. The results imply subclinical, well compensated malfunction of the vestibular system associated with NIHL.
IEDCS related to compressed-air recreational diving is more common than previously thought, and might occur even when no decompression schedule violation took place. Prompt diagnosis leading to the early commencement of hyperbaric oxygen recompression therapy is the key to complete recovery of cochlear and vestibular function.
We assessed the influence of dimenhydrinate, cinnarizine and transdermal scopolamine on the ability to perform simulated naval crew tasks. The effect of single doses of dimenhydrinate, 100 mg, cinnarizine, 50 mg, and one transdermal scopolamine patch on psychomotor performance was evaluated using a double-blind, placebo-controlled, randomized, crossover design in three separate studies. A total of 60 young naval crew (20 for dimenhydrinate, 15 for cinnarizine and 25 for transdermal scopolamine) underwent a battery of computerized and paper and pencil performance tests, and filled out a questionnaire on side-effects and well-being self-assessment. Dimenhydrinate significantly impaired decision reaction time and auditory digit span. Most of the subjects who took dimenhydrinate also reported a subjective decrease in well-being and general performance abilities. Cinnarizine and transdermal scopolamine did not affect performance abilities. Cinnarizine was free of significant side-effects. Dry mouth was the only significant side-effect of transdermal scopolamine. These findings could be explained by the well-known sedative properties of dimenhydrinate and not by a specific effect on any particular cognitive or motor function. Our results suggest that dimenhydrinate, 100 mg, adversely affects psychomotor function, whereas single doses of cinnarizine, 50 mg, and transdermal scopolamine appear to be free of side-effects on performance and seem to be a preferable anti-seasickness drug for use by a naval crew.
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