What happens when the spinal cord is injured? (I find this really interesting ... please like if you do too and Ill post more like this ...) Traumatic spinal cord injury usually begins with a sudden, mechanical blow or rupture to the spine that fractures or dislocates vertebrae. The damage begins at the moment of primary injury, when the cord is stretched or displaced by bone fragments or disc material. Nerve signaling stops immediately but may not return rapidly even if there is no structural damage to the cord. In severe injury, axons are cut or damaged beyond repair, and neural cell membranes are broken. Blood vessels may rupture and cause bleeding into the spinal cord’s central tissue, or bleeding can occur outside the cord, causing pressure by the blood clot on the cord. Within minutes, the spinal cord near the site of severe injury swells within the spinal canal. This may increase pressure on the cord and cut blood flow to spinal cord tissue. Blood pressure can drop, sometimes dramatically, as the body loses its ability to self-regulate. All these changes can cause a condition known as spinal shock that can last from several hours to several days. There is some controversy among neurologists about the extent and impact of spinal shock, and even its definition in terms of physiological characteristics. It appears to occur in approximately half of the cases of spinal cord injury and is usually directly related to the size and severity of the injury. During spinal shock, the entire spinal cord below the lesion becomes temporarily disabled, causing complete paralysis, loss of all reflexes, and loss of sensation below the affected cord level. The primary injury initiates processes that continue for days or weeks. It sets off a cascade of biochemical and cellular events that kills neurons, strips axons of their protective myelin covering, and triggers an inflammatory immune system response. This is the beginning of the secondary injury process. Days, or sometimes even weeks later, after this second wave of damage has passed, the area of destruction has increased—sometimes to several segments above and below the original injury. Changes in blood flow cause ongoing damage. The major reduction in blood flow to the site following the initial injury can last for as long as 24 hours and become progressively worse if there is continued compression of the cord due to swelling or bleeding. Because of the greater blood flow needs of gray matter, the impact is greater on the central cord than on the outlying white matter. Blood vessels in the gray matter also become leaky, sometimes as early as 5 minutes after injury, which initiates spinal cord swelling. Cells that line the still-intact blood vessels in the spinal cord also begin to swell, and this further reduces blood flow to the injured area. The combination of leaking, swelling, and sluggish blood flow prevents the normal delivery of oxygen and nutrients to neurons, causing many of them to die. Excessive release of neurotransmitters kills nerve cells. After the injury, an excessive release of neurotransmitters (chemicals that allow neurons to signal each other) can cause additional damage by over-stimulating nerve cells. The neurotransmitter glutamate is commonly used by axons in the spinal cord to stimulate activity in other neurons. But when spinal cells are injured, their axons flood the area with glutamate and trigger additional nerve cell damage. This process kills neurons near the injury site and the myelin-forming oligodendrocytes at and beyond the injured area. An invasion of immune system cells creates inflammation. Under normal conditions, the blood-brain barrier keeps potentially destructive immune system cells from entering the brain or spinal cord. This barrier is a naturally-occurring result of closely spaced cells along the blood vessels that prevent many substances from leaving the blood and entering brain tissues. But when the blood-brain barrier breaks down, immune system cells—primarily white blood cells—can invade the spinal cord tissue and trigger an inflammatory response. This inflammatory response can cause additional damage to some neurons and may kill others. Free radicals attack nerve cells. Another consequence of inflammation is the increased production of highly reactive forms of oxygen molecules called free radicals—chemicals that modify the chemical structure of other molecules in damaging ways, for example, damaging cell membranes. Free radicals are produced naturally as a by-product of normal oxygen metabolism in small enough amounts that they cause no harm. But injury to the spinal cord causes cells to overproduce free radicals, which destroy critical molecules of the cell. Nerve cells self-destruct. For reasons that are still unclear, spinal cord injury sets off apoptosis—a normal process of cell death that helps the body get rid of old and unhealthy cells. Apoptosis kills oligodendrocytes in damaged areas of the spinal cord days to weeks after the injury. Apoptosis can strip myelin from intact axons in adjacent ascending and descending pathways, causing the axons to become dysfunctional and disrupting the spinal cord’s ability to communicate with the brain. Scarring occurs. Following a spinal cord injury, astrocytes (star-shaped glial cells that support the brain and spinal cord) wall off the injury site by forming a scar, which creates a physical and chemical barrier to any axons which could potentially regenerate and reconnect. Even if some intact myelinated axons remain, there may not be enough to convey any meaningful information to or from the brain. Researchers are especially interested in studying the mechanisms of this wave of secondary damage because finding ways to stop it could save spinal cord tissue and thereby enable greater functional recovery. Source: ninds.nih.gov/disorders/sci/detail_sci.htm
Posted on: Sun, 25 May 2014 01:00:00 +0000
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