In: Anatomy and Physiology
A 62-year-old woman was in a car accident and suffered severe brain damage. Will the brain be able to repair the damaged tissue to a functional level? Explain your answer.
Even the elderly can recover from a severe traumatic brain injury. Summary: Even patients over the age of 75 may recover from severe traumatic brain injury, suggests new research. This is the first study to describe the results of surgically treated elderly patients with acute subdural hematomas.
Repairing :
The inflammatory response is a subject of active debate within the neuroscience community. While some inflammation is clearly needed to limit degeneration and address the cellular debris resulting from CNS injury, there is active discussion on whether the inflammatory response should be further enhanced. Proinflammatory cytokines are released within minutes following traumatic injury, with acutely harmful effects (e.g., BBB and BSCB dysfunction, promotion of neuronal death) but are beneficial at later time points (e.g., inducing synthesis of antiinflammatory cytokines, inducing neurotrophic factor secretion, and promoting proliferation of oligodendrocyte precursor cells that may help in remyelination) . Neurons and glial cells produce chemokines and complement proteins and have corresponding receptors. In a similarly dual role, chemokines and complement proteins are involved in acute BBB and BSCB dysfunction and edema development, but these proteins eventually lead to increased growth factor production. Furthermore, complement proteins have been found to protect neurons from excitotoxicity-induced apoptosis and promote opsonization.
With respect to the cellular aspect of the inflammatory response, microglia are the first to respond (minutes to hours) by proliferating, activating, and migrating to the area of injury, where they essentially function as macrophages . Increased BBB and BSCB permeability contributes to leukocyte infiltration from the blood to the injury site, a process that is mediated by cytokines, chemokines, and complement proteins . Neutrophils infiltrate (hours to days), followed by monocytes (days) . Again, these immune cells have dual roles. The oxidative burst of neutrophils and macrophages is harmful because of the release of oxygen free radicals and neurotoxic enzymes ; however, both activated microglia and monocyte-derived macrophages aid in clearing debris from dead and damaged cells via phagocytosis
Recovery :
Brain injury will commonly be accompanied by acute swelling, which impairs function in brain tissue that remains alive. Resolution of swelling is an important factor for the individual's function to improve. The greatest factor in functional recovery after brain injury comes from the brain's ability to learn, called neuroplasticity. After injury, neuroplasticity allows intact areas of the brain to adapt and attempt to compensate for damaged parts of the brain. Although axons and the peripheral nervous system in the developing brain can regenerate, they cannot in the adult brain. This is partly because of factors produced by cells in the brain that inhibit this regeneration. Dendrites, however, will develop from intact axons, as part of the neuroplasticity process. After severe brain injury, improvement in function related to neuroplasticity is unlikely to occur without help from health professionals skilled in rehabilitation.