Glucocorticoid
In neurosurgery practice glucocorticoids are commonly used.
Glucocorticoids (GCs) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), which is present in almost every vertebrate animal cell. The name glucocorticoid (glucose + cortex + steroid) derives from its role in the regulation of the metabolism of glucose, its synthesis in the adrenal cortex, and its steroidal structure.
A less common synonym is glucocorticosteroid.
The administration of glucocorticoids (GCs) after traumatic brain injury (TBI) is controversial. Clinical evidence reveals the deleterious effects of GCs, but the mechanism remains unclear. Previous studies indicate that GCs impair wound healing by affecting endothelial progenitor cell (EPC) function and inhibiting angiogenesis after skin injury. Thus, we hypothesize that the central deleterious effect of GCs is associated with reduced EPCs and angiogenesis after TBI. Using a controlled cortical impact model, we examined the dynamic changes in circulating EPCs and in the regional microcirculation within 14 days of TBI by flow cytometry analysis and contrast-enhanced ultrasound, respectively. The modified neurological severity score (mNSS) and Morris water maze assay were used to assess neurological recovery. Angiogenesis and hippocampal neuron counts were assessed using immunohistochemistry analysis and hematoxylin and eosin staining 14 days after TBI. Compared with the TBI control group, dexamethasone treatment significantly reduced the number of circulating EPCs on days 1, 3, 7 and 14 (P<0.05);decreased the number of CD31+ cells, the peak intensity and the number of hippocampal neurons on day 14 (P<0.05);increased the latency on days 12 and 13 (P<0.05);and reduced the percentage of time spent in the goal quadrant (P<0.05) on day 14. Similarly, dexamethasone increased the mNSS on days 7 and 14 (P<0.05). A strong correlation was observed between these results at 14 days after TBI (r=0.815-0.892, P<0.05). These data indicate that DEX inhibits the mobilization of EPC levels and angiogenesis around the lesion after TBI, which may contribute to neuronal cell loss and impaired neurofunction 1).
A study demonstrates a significant decrease in the rate of scoliosis surgery for Duchenne muscular dystrophy (DMD) from 2001 to 2012. It appears that the decline in surgical treatment could be related to the publication and landmark study demonstrating decreased progression of scoliosis with glucocorticoid treatment 2).