Reversible and controlled peripheral vestibular loss by continuous infusion of ropivacaine (Narop) into the round window niche of rats.

This paper describes a method for achieving a peripheral vestibular blockade in rats by instillation of local anaesthetics over the round window membrane through a permanently implanted cannula. Being rapidly reversible, the effect of the anaesthetic drug is easily controlled by a single continuous infusion, which can be repeated at any time. The method offers a unique opportunity to study the consequence of single or repeated transient vestibular loss without any use of general anaesthetics, which may be a severe confounding factor. Such studies might shed light on balance disorders related to permanent vestibular loss or episodic vestibular dysfunction. To evaluate the method, spontaneous horizontal eye movements were recorded during the first 4 h of continuous infusion. Unilateral infusion of ropivacaine gave rise to a high-frequency spontaneous nystagmus, reaching levels that have not been documented after a surgical labyrinthectomy under general anaesthesia. This vestibulo-oculomotor behaviour is consistent with a previous report using a single intratympanic instillation of lidocaine to achieve a short-lasting vestibular blockade. In the present study, it was demonstrated that the initial high-frequency nystagmus decreased during the first 100 min of infusion before stabilizing at the same level as recorded when the effect of general anaesthesia has worn off after a surgical ablation. When the transient vestibular blockade was repeated by a second infusion during the following day, the nystagmus frequency saturated on a significantly lower level than during the first blockade. Also, serial single infusions, with recovery between each functional vestibular loss, gave rise to a less severe nystagmus. It is suggested that this phenomenon is an expression of the behavioural concept of 'vestibular habituation', the neural substrate of which is rather unknown.

[Built-in emergency brake in the balance system. Animal experiment research shows that a hierarchy of mechanisms compensate after acute peripheral vestibular decline]. / Inbyggd nödbroms i balanssystemet. Hierarki av mekanismer kompenserar efter akut perifert vestibulärt bortfall visar djurexperimentell forskning.

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.