Letter to the Editor
I agree with the editorial by Fan-Gang Zeng, PhD, (Hearing Journal. 2018; 71(12):6) about the sonic attack issue that “the audiological community has remained surprisingly quiet even though both the source of the attack and its main symptoms are right up our alley.” On the other hand, perhaps this is a wise course of action since so little information has been provided about the symptoms of the afflicted individuals. In addition to the University of Pennsylvania study cited by Dr. Zeng, a recent study conducted at the University of Miami and the University of Pittsburgh described some results from vestibular and cognitive tests of individuals who reported suffering from the attack and control subjects (https://doi.org/10.1002/lio2.231). These are the only two articles as far as I (and Dr. Zeng) can tell that describe what happened to those afflicted, and even these studies do not provide a comprehensive set of measurements of auditory, vestibular, and cognitive functions. Such a lack of information means that commenting on the sonic attack would be mostly speculative. And speculation may be harmful.
There seems to be two main mysteries: What exactly are the symptoms and what caused them? The two journal articles and some of the media reports provide some information about the symptoms. There are a range of hearing, vestibular, and cognitive dysfunctions among those afflicted. Perhaps the most puzzling aspect of what has been reported is the wide range of symptoms, from inner ear disorders to cognitive challenges. The causation question has two parts: What occurred in the inner ear and the brainstem that might explain such wide-ranging symptoms, and what external agent caused whatever occurred?
Given the caveats provided above and the fact that details on blood supply are not right up my alley, I hesitantly suggest that perhaps some aspect of compromised blood supply to the inner ear and brainstem might be involved. A single arterial system, the vertebral artery, supplies the inner ear and brainstem with blood and therefore metabolism. A compromised blood supply would affect hearing, vestibular, and brainstem functions, all cited as possible sites of the disorders in these patients. The inner ear is the most sensitive metabolic organ in the body, and it is well known that damage to stria vascularis (the metabolic engine of the inner ear where blood from the vertebral artery is deposited) can cause noticeable disruption in hearing and vestibular functions. In addition, brainstem function, such as memory, requires good metabolic controls. Decades of work on tinnitus show that it is not necessary for there to be an actual sound for one to perceive a sound, even a loud sound in some cases. It seems reasonable to assume that sudden metabolic damage throughout the brainstem might trigger a tinnitus-like perception of sound. Such metabolic aggression might not last for a long time, meaning that the severity of patients’ symptoms might change over time, as they apparently have in a few cases.
Thus, a compromised blood supply connects some of the dots, but the dots are fuzzy and many are missing. So this brings us full circle: More information is required and this “hypothesis” says nothing about what might have caused such a compromised blood system. If the symptoms are related in some way to the blood supply and metabolic function, this only opens up the possibilities as to what external factor(s) caused the symptoms. In addition to the sonic and concussive causes that have already been suggested, a compromised blood supply could be dependent on a pathogen (e.g., bacterial or viral) or on some form of radiation.
Until more is known, I doubt that even the most erudite speculations will turn out to fully explain the mysteries surrounding these sonic attacks.
William A. Yost, PhD
Research Professor, Spatial Hearing Laboratory
College of Health Solutions
Arizona State University
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