44.2.2. The Essence of Brain Injury

The brain is made up of billions of cells that interconnect and communicate. The neuron is the main functional cell of the brain and nervous system, consisting of a cell body, single efferent or output part (axon), and many afferent or input parts—projections of the cell body called dendrites. The axons travel in tracts or clusters throughout the brain, providing extensive interconnections between brain areas via numerous contact synapses.

Each function of the human body and mind is based on highly organized complex neuronal networks that include numerous interrelated structures (cortices, nuclei, neuronal clusters, and pathways) located in multiple levels of the brain and spinal cord. Cooperative and synchronized work of all components of such complex networks provide optimal human performance in behavioral, cognitive, and autonomic functions. This tight integration is especially important in such complex sensory and motor functions as vision, hearing, balance, gait, and speech. Sensory-motor integration is an example of a high level neurophysiological process that needs optimal function in order to reach peak performance in critical situations, sports, and even everyday life.

There are many types of brain damage. The most typical are

• Concussion: The most minor and the most common type of TBI, involving possible brief loss of consciousness in response to a head injury, but in common language the term has come to mean any minor injury to the head or brain.

• Contusion: An area of swollen brain tissue mixed with blood released from a broken vascular system.

• Contrecoup: A contusion that occurs in response to the shaking of the brain back and forth within the confines of the skull. This injury often occurs in car accidents after high-speed stops, and in shaken baby syndrome.

• Diffuse axonal injury (shearing): Involves damage to individual nerve cells (neurons) and loss of connections among neurons. This damage causes a series of reactions that eventually leads to swelling of the axon and disconnection from the cell body of the neuron. This form of neurotrauma is frequently associated with exposure to explosive blasts.

• Hematoma: Heavy bleeding into or around the brain tissue.

• Anoxia: A condition in which there is an absence of oxygen supply to an organ’s tissues, even if there is adequate blood flow to the tissue. Without oxygen, the cells of the brain die within several minutes. This type of injury is often seen in near-drowning victims, in heart attack victims, or in people who suffer significant blood loss from other injuries that decrease blood flow to the brain.

• Neurotoxicity: Occurs when the neurons that communicate with other neurons degenerate and release toxic levels of neurotransmitters into the synapse, damaging neighboring neurons through a secondary neuroexcitatory cascade.

Neurologic changes may occur as a result of head trauma, cerebrovascular accident, or postsurgical complications, ultimately leading to a physical breakdown of overall communication among neurons in the brain and/or to neural cell death (apoptosis).

In spite of the wide spectrum of different classes of TBI and types of stroke, the residual damage to the brain and debilitation of the patient looks very similar. For example, the pattern of residual dysfunction that corresponds to a focal lesion caused by a bullet passing through the brain is similar to that caused by a similar focal lesion resulting from a stroke.

In addition to the primary brain injury, there is secondary brain damage that is frequently undetectable by all contemporary diagnostic methods, and therefore “invisible.” In secondary damage, neurons appear alive, but physical damage and structural changes in dendrites, cell body, and axons are so small that they are below the resolution of computed tomography, functional magnetic resonance imaging (fMRI), or defusion tensor imaging. The remaining neurons, even if they appear physically healthy, are nonetheless functionally damaged due to the loss of major connections, the loss of input from neighboring dead cells, or the lack of appropriate signals through broken connections. Disruption of sensory and/or motor action potentials in the complex network immediately leads to abnormalities in the supported function, disturbances in spatio-temporal interactions, and loss of sensory-motor integration (Barroso-Chinea and Bezard, 2010; D’Angelo, 2011; Price and Drevets, 2012; Watson et al., 2013; Zikopoulos and Barbas, 2013). As a result, physical manifestation of hypo- or hyper-function (dystonia or spasm and rigidity), and desynchronization and imbalance of inhibition and excitation in the neural network (tremor, seizures, oscillopsia) will occur, for which there is no corroborating evidence.

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