Authors

  1. Galgon, Anne K. PT, MPT, PhD
  2. Holmberg, Janene M. PT, DPT

Article Content

Clinicians are in debt to this well-controlled foundational research that is a critical step in advancing evidence-based vestibular rehabilitation (VR). We are also pleased that it is being published in Journal of Neurologic Physical Therapy, where VR physical therapists can access this type of research. This article not only contributes new information about individual recovery from end-organ vestibular lesions but also alludes to potential enhancements in the effectiveness and specificity of one of VR's most unique treatment paradigms, gaze stabilization. Loss of gaze stabilization is a hallmark feature of vestibular hypofunction and the vestibular ocular reflex (VOR) is the primary mechanism that allows optimal visual acuity when we are in motion.1 Although we know achieving optimal VOR gaze stabilization is not the only means by which patients heal after vestibular insults,2 research is supporting that recovery of VOR gain has been associated with high probability of improved dynamic balance and decreased fall risk and should be a desirable outcome to facilitate in rehabilitation.3

 

Research has identified several VOR modulating factors in healthy adults that possess the potential to enhance VOR exercise prescriptions; however, more guidance and further clarifying clinical research have been needed to translate this knowledge to clinical practice.4,5 This study provides some foundational evidence that one modifying factor, vergence, does create significant angular VOR gain modulation and could potentially drive greater VOR improvement in certain patient populations.6,7 Although a small sample size, this is the first article to take a varied clinical population, much like what clinicians encounter, with a wide spectrum of chronicity and pathophysiology and specifically look at healthy versus lesioned side VOR gain. Other studies have looked at single pathologies and only the lesioned side and failed to show any preservation of vergence-mediated VOR gain.6 It is interesting to note that the results presented here support that there are some patients who will recover a significant amount of VOR gain to the lesioned side where it has been assumed from previous research that recovery comes only from adaptation of healthy side and central compensation.6 In other words, some patients may retain a greater potential and could be challenged more effectively to achieve fuller potential.

 

Chang and Schubert present an articulate explanation of how "near viewing" creates the demand and need for higher VOR gain to stabilize vision. The "near viewing," describe here, is much different at 15 cm than the traditional "near viewing" at arm's length. Our current Vestibular Hypofunction Clinical Practice Guideline8 was unable to give us very many parameters other than to strongly recommend gaze stabilization exercises be performed at optimal speeds for specific length of time. This was based on a literature review at that time that supported that patients can drive healing by forcing a critical error signal, more specifically a retinal slip. This is important because, despite current research showing that inducing retinal slip can modify VOR gain,5,9 traditional VR gaze stabilization exercises have failed to show improvements in VOR gain, although dynamic visual acuity (DVA) improves.2 Research is also supporting a critical threshold of retinal slip that is required to drive vestibular adaptation.10 If the gaze stabilization exercises do not meet this threshold, then improvements in symptoms and DVA may be limited to only central substitution or habituation processes.2 This article attempts to address these issues and alludes to a potential new gaze stabilization exercise parameter that incorporates very near convergence demands. Although they found that the gain does not increase to the lesion side in most patients, it could still offer a greater error signal and impact the gain on the healthy side. Modulation of gain enhancement primarily to the healthy side could initially sound unremarkable; however, it needs to be understood that the exercises VR clinicians prescribe are different from those prescribed for head impulse testing. Where head impulse testing intentionally removes healthy side contribution, sinusoidal-functional speed exercises that VR clinicians prescribe and patients perform would still be tapping into healthy side VOR modulation.

 

The finding of increased compensatory saccade amplitude with near targets could also suggest a possible enhancement to clinical VOR testing, again if supported by further research. The cardinal sign of vestibular hypofunction is a corrective saccade and if it is amplified with near targets, clinicians could perhaps increase the sensitivity of their "bedside head impulse test." By performing head impulse with near target in individuals with confirmed convergence, clinicians might better identify vestibular hypofunction when traditional testing is negative. Clinical relevance also is found in the fact that the results in this study were obtained utilizing clinically available monocular vestibular head impulse test (vHIT) technology, as opposed to scleral coil technology,5-7,9 and they assured convergence capacity by bedside screening that could be clinically replicated.

 

This article represents a critical step to furthering the specificity of gaze stabilization exercises and as VR clinicians we should be inspired to have further evidence of the robust adaptability of the VOR. This article offers support that we may be able to tap into this vergence-mediated response to foster greater, faster, more efficient and perhaps more effective recovery. It is exciting to consider that even partial preservation of this powerful vergence-mediated VOR enhancement may change the way we prescribe our usual gaze stabilization exercises after further clinical studies confirm the clinical relevance and corroborate the functional impact of these findings.

 

REFERENCES

 

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