Over the past decade, the scientific information on traumatic brain injury has increased considerably. A number of models, theories and hypotheses of traumatic brain injury have been elaborated.
Despite dramatic advances in this field of medicine, traumatic brain injury, including the mild 2 Slobounov and Sebastianelli traumatic brain injury (MTBI), commonly known as a concussion, is still one of the most puzzling neurological disorders and least understood injuries facing the sport medicine world today.
Definitions of concussion are almost always qualified by the statement that loss of consciousness can occur in the absence of any gross damage or injury visible by light microscopy to the brain.
According to a recent NIH Consensus Statement, mild traumatic brain injury is an evolving dynamic process that involves multiple interrelated components exerting primary and secondary effects at the level of individual nerve cells (neuron), the level of connected networks of such neurons (neural networks), and the level of human thoughts or cognition.
The need for multidisciplinary research on mild brain injury arises from recent evidence identifying long-lasting residual disabilities that are often overlooked using current research methods. The notion of transient and rapid symptoms resolution is misleading since symptoms resolution is not indicative of injury resolution.
There are no two traumatic brain injuries alike in mechanism, symptomology, or symptoms resolution. Most grading scales are based on loss of consciousness (LOC), and post-traumatic amnesia, both of which occur infrequently in MTBI. There is still no agreement upon diagnosis and there is no known treatment for this injury besides the passage of time. LOC for instance, occurs in only 8% of concussion cases.
Overall, recent research has shown the many shortcomings of current MTBI assessments rating scales, neuropsychological assessments and brain imaging techniques.
Humans are able to compensate for mild neuronal loss because of redundancies in the brain structures that allow reallocation of resources such that undamaged pathways and neurons are used to perform cognitive and motor tasks.
Three to four weeks after conception, one of the two cell layers of the gelatin-like human embryo, now about one-tenth of an inch long, starts to thicken and build up along the middle. As this flat neural plate grows, parallel ridges, similar to the creases in a paper airplane, rise across its surface.
Within a few days, the ridges fold in toward each other and fuse to form the hollow neural tube. The top of the tube thickens into three bulges that form the hindbrain, midbrain and forebrain. The first signs of the eyes and then the hemispheres of the brain appear later.
How does all this happen? Although many of the mechanisms of human brain development remain secrets, neuroscientists are beginning to uncover some of these complex steps through studies of the roundworm, fruit fly, frog, zebrafish, mouse, rat, chicken, cat and monkey.
Knowing how the brain is put together is essential for understanding its ability to reorganize in response to external influences or to injury. These studies also shed light on brain functions, such as learning and memory.
Brain diseases, such as schizophrenia and mental retardation, are thought to result from a failure to construct proper connections during development. Neuroscientists are beginning to discover some general principles to understand the processes of development, many of which overlap in time.
