Minimal access spinal technologies aim primarily at minimizing the trauma associated with surgical exposure of the spine.
Lumbar plexus injuries which occur during anterior or transpsoas lumbar spine exposure and placement of instruments have been reported.
We report here that a history of prolonged corticosterone exposure increases dendritic spine density in deep-layer prelimbic cortex.
This situation continues, even though there is a possible health risk for repeated X-ray exposure to healthy spines and organs [ 40].
However, surgeons require more intraoperative fluoroscopy and ionizing radiation exposure during minimally invasive spine surgery for localization, especially for guidance in instrumentation placement.
In addition, we present more direct evidence from basic research studies that exposure to stress alters spine morphology, function and plasticity and that antidepressants, particularly new rapid acting agents, reverse these effects.
After 48 h exposure to Aβ peptides, spine densities and types were measured in primary neurons.
On the other hand, we found a significant negative correlation between longer duration of ART, especially PI exposure, and both lumbar spine and femoral neck BMD on univariate analysis.
Although this difference was statistically non-significant, this general pattern is in agreement with evidence that acute injection stress, unlike chronic stressor exposure, results in dendritic spine proliferation in the medial prefrontal cortex.
These findings together suggest that prolonged corticosterone exposure initially eliminates dendritic spines in deep-layer prelimbic cortex, but that spine density "rebounds" with a recovery period, and spines then ultimately over-proliferate.
