Axons that have been disconnected form the injury site must grow all the way back to their original cells to reconnect with them. Axons that have been damaged will sprout short distances but they often stop at the injury site. There is much debate concerning why the axons do not continue growing. Several theories have been popular. For many years, scientists thought that glial cell proliferation (glial scar) around the injury site mechanically prevented axonal growth.
The axons that have been disconnected from their cell bodies will die. This takes place over a period of days or even weeks.
However, the cells that the axons contact usually are not killed, unless they have been directly injured by the mechanical trauma. Likewise, the cells that the axons come from also usually survive the axonal injury unless they are close to the injury site.
fine the “acute” phase of spinal cord injury as the period during which damage may be continuing.
“Subacute” is when the spinal cord is beginning to resolve the damage and starting repair. There is then a period of recovery that may take years. At the end of that period, when recovery has stabilized and the condition is stable, I would use the descriptor “chronic” spinal cord injury.
The spinal cord is seldom cut by injury unless the injury is due to a bullet or knife. In most cases, the spinal cord is compressed either slowly or rapidly by bone or disc displaced against the spinal cord. The extent and cause of damage depend on the speed of compression. Slow and prolonged pressure damages the spinal cord by blocking blood flow to the cord.
Spinal cord white matter is generally more resistant to ischemia (loss of blood flow) than brain.
NIL-A is a neuroimmunophilin that was developed by Guilford and Amgen for Parkinson’s disease . A second generation product, NIL-A succeeds an earlier immunophilin product called GPI-1046. Preclinical development of GPI-1046 itself appears to have been suspended . Data from efficacy and pharmacokinetic studies with NIL-A were presented at the Acute Neuronal Injury: New Therapeutic Opportunities meeting in August of 1998, Las Vegas, USA. The compound apparently possesses 50% oral bioavailability, and approximately 25 fold greater efficacy compared with GPI 1046, as well as a superior half life and absorption profile.
Neurons (nerve cells) in the brain, spinal cord, and peripheral nerve send axons (nerve fibers) up and down the spinal cord in spinal tracts. These spinal tracts are called white matter because axons are coated with a membrane called myelin and myelin appears white. In the spinal cord, white matter is usually situated close to the surface of the cord, arranged into several columns called the anterior, posterior, and lateral columns. The spinal cord contains neurons located in the middle part of the spinal cord. The areas of the spinal cord that contain neurons is called gray matter. The gray matter is most abundant in the parts of the spinal cord that connect to the arms and legs, called the cervical and lumbosacral enlargements.
The term rT3 refers to a form of tri-iodo-thyronine, one of the active iodinated thyroid hormone. Thyroid hormones are made by the thyroid gland. Thyroid hormones have long been recognized to regulate metabolism (energy activity) of cells. Thyroid hormones are iodinated (the reason why iodine is important for our diet), usually coming from sea salt. There are two forms of iodinated thyroid hormones: T3 and T4. These respectively contain two iodines and three iodines. T3 has several forms, depending on where the iodine attaches to the hormone. One of these is rT3. Cells contain a variety of iodeinases (enzymes that remove iodines).
Average Yearly Expenses
|Severity of Injury||First Year||Each Subsequent Year|
|Incomplete any Level||$168,627||$11,817|