[Built-in emergency brake in the balance system. Animal experiment research shows that a hierarchy of mechanisms compensate after acute peripheral vestibular decline].
A sudden unilateral loss of peripheral vestibular input results in the onset of acute dizziness and imbalance associated with spontaneous nystagmus, postural instability and nausea. Fortunately, these symptoms ameliorate rapidly, even without treatment, due to central nervous plastic changes which are collectively termed "vestibular compensation". This concept has become a widely accepted research model for studying lesion-induced plasticity. Recent research has dealt in particular with the plasticity of the medial vestibular nuclei that mediate the horizontal vestibulo-ocular reflex. Studies range from a cellular level in vitro to a functional level in vivo. Taken together, results from such studies have contributed greatly to what is known of vestibular compensation today. This article summarises evidence for several plasticity mechanisms that drive the recovery of spontaneous nystagmus, one of which is dependent on an endocrine stress-response. In the long run, such knowledge might influence the management and treatment of patients with balance disorders.
Abteilung Neurobiologie, Ludwig-Maximilians Universität, München.
Anna K
AK
Magnusson
Richard
R
Tham
D000818:Animals; D004244:Dizziness / Q000503:physiopathology; D006801:Humans; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D017120:Nystagmus, Optokinetic / Q000187:drug effects / Q000502:physiology; D011187:Posture; D051381:Rats; D015837:Vestibular Diseases / Q000503:physiopathology*; D014724:Vestibular Function Tests; D014722:Vestibule, Labyrinth / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology