Concussion Science Overview

Simulating 1 second of human brain activity requires 82,944 processors and takes over 40 minutes.  It is estimated we all carry 80-100 billion nerve cells, or about as many stars as there are in the Milky Way.

There is a reason scientists with super-computing power at their disposal have not been able to duplicate all that the human brain can do in a mere 3 pound sphere. So, when damaged the results can be complex, confusing, long-lasting and life-altering if not properly identified and treated.

Three major areas of the brain can be damaged in a concussion. They include the Cerebral Cortex which contains the Frontal Lobe, Parietal Lobe, Temporal Lobe, and Occipital Lobe which communicate with the Basal Ganglia. The Cerebellum which has more neurons than all the other parts of the brain combined and the Brain Stem, critical to supporting the involuntary activity of life itself.

Concussion causes neurons in these brain regions to become damaged both physically and chemically by impact stretching and twisting leading to a confusing myriad of symptoms. Unless doctors can verify and understand that a concussion has occurred much time, energy and money can be wasted chasing the causes of these seemingly disparate symptoms.

Symptoms of concussion can be evidenced in the cardiovascular system, digestive tract, balance, coordination, sight, hearing,depression, anxiety, speech, memory, attitude, anger, focus, sleep disturbance and much more.

EEG Findings in Traumatic Brain Injury

This brief summary will discuss the various EEG findings seen in head injury when it results in a brain injury, though any given head injury may or may not result in traumatic brain injury.  When an injury is incurred by the brain there are a few varieties of findings seen in the EEG, ranging from spectral changes associated with either white or gray matter damage, to the changes in “connectivity”, seen as changes in coherence or correlation measured across the cortex, or between more distant functionally related areas.

Damage is seldom restricted to merely being exclusively either white or gray matter, and mixed findings are seen commonly.  There are studies showing the correlation of quantitative EEG findings with quantitative MRI findings that are instructive in identifying the nature of the effect on the EEG of the different types of damage.

The EEG changes following brain injury are spectrally different between white and gray matter damage, which helps when evaluating the nature of the damage with the EEG.  The white matter is a high speed relay system that innervates the cortex, both with primary sensory input relayed from the thalamus, and with cortical-cortical input via various fasciculi.

When the cortex has decreased innervation, delta content emerges, according to the IFCN’s position paper on the basic mechanisms of cerebral rhythmic EEG**.  Thus, traumatic brain injury resulting in white matter damage is associated with slower spectral increases in the areas cortically where decreased innervation is present.  These slow spectral increases are seen primarily as delta, and may also be seen as a slower band including theta, especially with larger increases in the slow spectra.

White matter also carries signals across the cortex, and from the cortex through subcortical structures to other cortical locations, resulting in the neural network’s “connectivity”.  There has been a small case series showing that in some direct frontal injuries, there is a decrease in correlation from the left to the right frontal lobe, seen as decreased spectral correlation, also referred to as co-modulation (M.B. Sterman and D. Kaiser’s SKIL software).  This is identical to the changes seen with damage to the anterior portions of the corpus callosum following surgery.  This data was presented by Dr. Sterman, and published by the Journal of Neurotherapy as a technical paper describing their co-modulation metric.

Coherence changes may also be seen with head injury, with both hypercoherence and hypocoherence reported, depending on the nature of the specific case’s damage.  Isolated areas may become hypercoherent due to the lack of input, though separated areas will be hypocoherent due to the damage to their connective network.

Damage may be seen in gray matter, which is highly “plastic”, unlike white matter, where damage persists.  The neural plasticity allows for regeneration of the cortical gray matter following injury, so the spectral changes associated with gray matter damage may change over time, from the more acute stages, through a transition phase into a static phase, which may allow for re-integration into functional relationships with neural network activity.

The immediate changes seen spectrally with gray matter injury is a decrease in the function of the thermo-cortical neural network activity, seen spectrally as decreased alpha and beta, as well as decreased gamma in the affected gray matter.  These changes last for the period of the healing, commonly seen across a period from 6 months to a year.

As the gray matter heals, but is not integrated into the neural network function, the idling rhythm in alpha may return and even be seen as an excessive value in database comparisons, since the cortical area is not “working”.  The beta and gamma remain low during this phase, since they are not seen at normal levels in the idled cortical areas.  Beta is generated in local gray matter network activity, and gamma is seen in functionally bound and active networks only.

Once the neural network of the local gray matter is re-integrated into the functional processing, the alpha will then be reduced, and the faster activity seen associated with local function will also be seen as returning to more normal levels.  This may not happen spontaneously, and may require specific interventions, such as neurofeedback, physical therapy, and/or various cognitive-behavioral interventions.

The work of Dr. Kirtley Thornton showed that the gamma and beta remain low, even when the alpha return has occurred.  These faster patterns returned following successful clinical therapy to re-integrate the neural tissue into the functional neural network of the cortical gray matter and white matter.