I n t e r n a t i o n a l J o u r n a l o f N e u r o r e h a b i l i t a t i o n ISSN: 2376-0281 International Journal of Neurorehabilitation Georgescu, Int J Neurorehabilitation Eng 2017, 4:4 DOI: 10.4172/2376-0281.1000282 Open Access Commentary Volume 4 • Issue 4 • 1000282 Int J Neurorehabilitation, an open access journal ISSN: 2376-0281 *Corresponding author: Mădălina Georgescu, MD, PhD, Associate Professor, Univer- sity of Medicine and Pharmacy ‘Carol Davila’ Bucharest, Romania, Tel: +40722544115; E-mail: madalina.georgescu@gecad.com; madalina.georgescu@otomed-center.ro Received July 11, 2017; Accepted August 03, 2017; Published August 10, 2017 Citation: Georgescu M (2017) Vestibular Rehabilitation – Recommended Treatment for Permanent Unilateral Vestibular Loss. Int J Neurorehabilitation 4: 282. doi: 10.4172/2376-0281.1000282 Copyright: © 2017 Georgescu M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Vestibular Rehabilitation – Recommended Treatment for Permanent Unilateral Vestibular Loss Mădălina Georgescu 1,2 * 1 University of Medicine and Pharmacy ‘Carol Davila’ Bucharest, Romania 2 Audiology and Vestibulogy Department, Institute of Phono-Audiology and Functional ENT Surgery Bucharest, Romania Equilibrium is a complex network, based on several sensorial information – somatosensorial, visual and vestibular. Normal input from all three sensorial systems as well as matched sensorial information are required for normal human balance. Vestibular sensorial structures are in the inner ear, in the posterior labyrinth and they are responsible for detecting any angular and linear acceleration of head and body. In response to movement, efects of gravity and the position in space of the head and body, relatively to ground, vestibular sensorial hair cells are stimulated and action potentials originated here are send to the nervous central system. Any disruption in normal functioning of one of the vestibular sensorial structures leads to an asymmetry between the two vestibular pathways, which are interpreted as rotation. As consequence of this vestibular nuclei activity asymmetry, spinning sensation and nystagmus appears. Acute unilateral vestibular loss (UVL) induces severe static and dynamic defcits, with long lasting efects on balance, thus reducing patients’ quality of life. Lesions in the inner ear (viral or bacterial labyrinthitis) or vestibular ganglia or nerve (vestibular neuritis, zoster oticus) induce permanent vestibular defcit. Neural lesions are much more difcult to recover and this occurs due to vestibular compensation, not due to reversible lesions. Viral infection of the vestibular sensorial system, known as vestibular neuritis is the most common cause of UVL and the second most common cause of peripheral vestibular syndrome. It is a pathological condition that usually afects active, healthy, middle- aged people. Worsening the health-related quality of life (HRQoL) in this category of people has a negative impact on their social life and work performance, leading not only to psychological damage (low self- confdence, depression, frustration), but also economical losses (long medical leave, poor concentration and performance). Vestibular neuritis it is also known as vestibular neuronitis, acute labyrinthitis, unilateral acute vestibular palsy, epidemic vertigo. It is caused by reactivation of a retrovirus (herpes simplex type I) which determines degenerative lesions in the vestibular nerve, vestibular ganglia or/and vestibular hair cells. It usually appears in viral infection context, usually in spring and autumn, with “epidemic” character. Hearing is never afected in vestibular neuritis [1,2]. Vestibular neuritis is clinically expressed as long-lasting vertigo (more than 24 h), nausea, vomiting and severe gait impairment, caused by static defcits (lesions of the vestibular structures). Tese symptoms have a sudden onset and high severity from the very beginning of the disease, but resolves by themselves in three to fve days from the onset. History, together with bed-side vestibular examination, head impulse test (clinical or video head impulse test - vHIT) [3] and pure tone audiometry allow positive diagnostic of vestibular neuritis (Figure 1). More important for patient’s well-being are the dynamic defcits which occur in the frst week. Reduced gain of vestibulo-ocular and vestibulo-spinal refexes impedes on patient’s capacity to perform daily activities. Afer the acute stage, vestibular objective tests are required, in order to quantify vestibular defcit (posturography, rotatory and caloric test in videonystagmography and vestibular evoked myogenic potentials – VEMP) (Figure 2). Viral infection can afect one or both branches of the vestibular nerve, superior and inferior, causing a partial or complete vestibular neuritis. Usually, the superior vestibular branch is afected and this leads to caloric hypo- or arefexia on the damaged side. Cervical VEMP (cVEMP) is recommended for inferior vestibular nerve branch evaluation. It is important to know the extension of the vestibular impairment in order to quantify the defcit and appropriate customise the vestibular rehabilitation program. Another reason for evaluating both superior and inferior vestibular nerve branches is to council the patient regarding long-term evolution of the disease. When a partial neuritis occurs, any lesion on the posterior semi-circular canal or saccule will become symptomatic, since information from these sensorial structures will be send through the normal functioning inferior vestibular nerve. BPPV is the most common complication of a partial vestibular neuritis and patients should be aware of this. Natural recovery mechanism is based on central vestibular compensation, which reduces vestibular activity on the healthy part and increase vestibular activity on the lesion side, by opening closed synapses and stimulating new formation of neural sprouts (Figure 3). Central compensation is a neuroplasticity model of recovery afer a UVL. Tis mechanism has its highest intensity one week afer vestibular injury and continues slowly on a long period of time (one year). For this reason, vestibular suppressant treatment recommended during acute onset of the vestibular neuritis should not exceed three days of administration [4]. In order to obtain a maximum gain recovery in a short period of time, central compensation should be facilitated through long- term administration of betahistine and vestibular rehabilitation (VR) programs. VR is a physical treatment which allows recovery of the balance defcits by creating new patterns of reaction to diferent daily balance situation. Tis combined treatment protocol of UVL patients is widely accepted [5-7] for a faster and more complete recovery of the unilateral vestibular loss. VR is based on specifc programs of physical exercises that can diminish the negative efects of the vestibular impairment. VR sessions are recommended weekly. VR exercises target a reset of the brain through habituation