Treatment and rehabilitation in vestibular neuritis.

During the acute phase, symptomatic treatment is practically the only option, and a wide variety of drugs are available. For years, much has been focused on the possibility of using corticosteroids in the treatment of vestibular neuritis. Clearly, if we suspect an inflammatory cause, a treatment that reduces that inflammatory process would, if not reduce the severity of the attack, at least help recovery. If the different studies on this matter failed to concord in many aspects, they do however agree that the use of corticosteroids in the acute phase entails long term beneficial effects for the recovery of vestibular function and allows for a better vestibular compensation. The second part of the treatment is the rehabilitation. In my experience most of the patients undergo a spontaneous vestibular compensation in a short time. Nevertheless, some exercises of visual fixation while the patient is still bed-ridden, can accelerate the recovery process. Those patients, in whom certain instability persists, who are too anxious after their experience or those who will demand this type of treatment, are candidates to undergo a rehabilitative vestibular program. In this paper I will comment on the instrumental and non-instrumental techniques that I use in my daily practice.

Characterization of a glucocorticoid receptor and the direct effect of dexamethasone on herpes simplex virus infection of rabbit corneal cells in culture.

Homogenates prepared from a previously established cell line derived from rabbit cornea contain a macromolecule with many properties of a glucocorticoid receptor, namely high affinity (KD = 6 x 10(-9)M) and saturable capacity (135 femtomoles/mg protein) for dexamethasone, extreme heat lability, and a pattern of competition similar to that found in other glucocorticoid target cells. Intact cells specifically bind dexamethasone with an affinity similar to that found in homogenates, and the amount of steroid bound at saturation is approximately 60,000 molecules of dexamethasone per cell. Specific dexamethasone binding was found to be localized to the cell nucleus. The corneal cells were susceptible to infection with herpes simplex virus (HSV). Dexamethasone increased cell susceptibility to the virus and facilitated the spread of the infection throughout the corneal cell culture. This effect was observed at concentrations of dexamethasone as low as 10(-9) M. Tetrahydrocortisol, an inactive glucocorticoid metabolite that does not compete with dexamethasone binding to the receptor, did not enhance HSV infection at a high concentration (10(-5) M). This study demonstrates a direct effect of dexamethasone on corneal cell-HSV interaction in the absence of exogenous immunologic factors. This effect of dexamethasone may be mediated by the glucocorticoid receptor.