Steroid dosage for bell's palsy

As a glucocorticoid , the lipophilic structure of prednisolone allows for easy passage through the cell membrane where it then binds to its respective glucocorticoid receptor (GCR) located in the cytoplasm. Upon binding, formation of the GC/GCR complex causes dissociation of chaperone proteins from the glucocorticoid receptor enabling the GC/GCR complex to translocate inside the nucleus. This process occurs within 20 minutes of binding. Once inside the nucleus, the homodimer GC/GCR complex binds to specific DNA binding-sites known as glucocorticoid response elements (GREs) resulting in gene expression or inhibition. Complex binding to positive GREs leads to synthesis of anti-inflammatory proteins while binding to negative GREs block the transcription of inflammatory genes. [28]

The etiology of Bell's palsy has not been as yet completely elucidated and the treatment is empirical and controversial. The two most common forms of treatment are steroid therapy and surgery. On the basis of the pathophysiology of Bell's palsy that edema as well as primary or secondary ischemia lead to both compression and hypoxia, Stennert employed high doses of cortisone for a strong antiphlogistic and anti-edematous effect, and dextran in combination with pentoxifylline to increase peripheral nerve perfusion and reported high recovery rate. Since the past 3 years, we have been treating patients with Bell's palsy with a high dose of steroid plus low-molecular dextran (SD therapy). Hydrocortisone was added directly to 500 ml of dextran solution with ATP and vitamins, starting with 500 mg and finally down with 100mg during 7 days. Before we had adopted this regimen, the patients with Bell's palsy were treated with orally-administrated steroid. A half dose of steroid was administrated in the latter regimen. SD therapy was employed in 120 cases of Bell's palsy, and its results were compared with those of 82 cases with orally-administrated steroid. In a total of 67 cases with incomplete palsy, all cases obtained complete recovery within one month after the onset regardless of the mode of treatment. Each patients with complete palsy was examined with a nerve excitability test (NET) at the first visit and one week later. According to the response of NET, the patients with complete palsy were divided into the following three groups; "good", "poor" and "absent". In "good" group, all cases with SD therapy had complete recovery, while the recovery rate of 31 cases with orally-administrated steroid therapy was 90%. This difference was statistically significant (p less than ).(ABSTRACT TRUNCATED AT 250 WORDS)

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Steroid dosage for bell's palsy

steroid dosage for bell's palsy

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