Managing Traumatic Brain Injury: Appropriate Assessment and a Rationale for Using Neurofeedback and Biofeedback to Enhance Recovery in Postconcussion Syndrome
Impairments that may result from a mild traumatic brain injury (TBI) or concussion can be both severe and long-lasting. This article will list some of the common persisting symptoms that may occur and give a brief description of the neuropathological processes that can be triggered by TBI, including diffuse axonal injury and its effects on the mitochondrial Kreb's cycle and the production of adenosine triphosphate, the brain's source of energy. This is followed by a summary of a comprehensive assessment process that includes quantitative electroencephalography, evoked potentials, heart rate variability (HRV) measures, neuropsychological testing, and blood and urine analysis. Details concerning a neurophysiological approach to effective treatment are given. These include conventional single-channel neurofeedback (NFB), also called brain-computer interface training, low-resolution electromagnetic tomography z-score neurofeedback, HRV training, and counseling on diet, sleep, and exercise. The authors expand the discussion on their treatment approach to include a neuroanatomical explanation of why the practitioner should consider combining the NFB training with HRV training.
Example of sites of injury in traumatic brain injury. Drawing by Maya Berenkey from The Companion to the Neurofeedback Book (in press) using figures by Amanda Reeves in The Neurofeedback Book.
Structure of a neuron drawn by Maya Berenkey. The terminal button is the presynaptic link to the dendrite of the next neuron. This synaptic transmission is disrupted when there is diffuse axonal injury. (Note that this figure shows a pyramidal cell. Only pyramidal cells produce the extracellular currents that summate to produce the electroencephalogram.) Figure from The Companion to the Neurofeedback Book (in press).
Schematic diagram of a synaptic junction. The figure shows, at the top, the presynaptic ending of the axon (called a “button” in Figure 2) and the postsynaptic receptor sites for glutamate: the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA), which is a glutamate receptor site, and the N-methyl-D-aspartate (NMDA) receptor site, which is initially blocked by magnesium ions. This figure is often used to explain long-term potentiation. It is illustrated here to show the synapse. Thanks are extended to Wikipedia Images; Bruno Dubuc, Website of Canadian Institutes of Health Research; Institute of Neurosciences; Mental Health and Addiction (NMHA); and to Copyleft; The content of the site The Brain from Top to Bottom is under copyleft. © is also from Nature Reviews, Neuroscience, Nature Publishing, 2005.
Steps contributing to neuronal cell death. National Institutes of Health (NIH) government document in public domain. Although originally used by the NIH to illustrate changes after a stroke, this diagram applies equally well to the energy crisis that ensues after traumatic brain injury. The next figure summarizes some of the factors that contribute to this energy crisis.
Chemical and metabolic changes after traumatic brain injury. Adapted from David A. Hovda, PhD, UCLA Brain Injury Research Center, and from a drawing in Giza and Hovda (2001).
Pre (black) and post (gray) P300 event-related potential (ERP) recordings from the same subject comparing a baseline measurement and a postinjury measure. Latency of the P3 wave is delayed in the postconcussion test, and amplitude of the P3 wave is reduced following injury. (“Big Circle” refers to the target stimulus in this ERP test that is in the program from Evoke Neuroscience.) Figure from Thompson & Hagedorn in The Companion to the Neurofeedback Book (in press).
Heart rate variability profile from a healthy adult and from a concussed athlete. From Thompson and Hagedorn (2012).
The ADD Centre logs in to CNS Vital Signs (www.cnsvs.com) to run a computerized Neuropsychological Test Report (administered through Evoke Neuroscience). This 38-year-old client presented 15 months after experiencing a brief loss of consciousness in a fall. This very bright and capable individual has a doctoral degree, yet she was plagued by memory problems and even forgot appointment times, despite e-mail reminders the day before. Given past academic and work history, one would expect consistently above-average scores, but testing corroborated self-report of memory problems continuing more than 1 year after the head injury.
Neuroguide Program diagram of progress across 17 LORETA z-score neurofeedback training sessions. At 17 sessions, this client's z-scores had moved from >4–6 standard deviations (SD) to <2 SD at all the Brodmann Area sites that were chosen to be trained. The cursor has been placed on the highest SD site for the 7th session and the message that pops up is shown in the figure. This message indicates that this site represents the SD of amplitude (AP) for Brodmann Area 13 (the insula) on the right side (R) for Beta 2 (15–18 Hz in this program). The right insula will have major effects on heart rate variability. It is also involved in affect and executive networks. Figure from The Companion to the Neurofeedback Book (in press).
Figure by Maya Berenkey after drawings by Amanda Reeves from The Companion to the Neurofeedback Book (in press). Midsagittal representation of selected central midline cortical and subcortical structures (plus the insula, which in reality is not midline but more lateral).
Schematic representation of structures to highlight the synergistic influences of neurofeedback and biofeedback–heart rate variability.
Screen from Thought Technology instruments and programs using the Thompson suite, Setting up for Clinical Success (www.BFE.org) for simultaneous neurofeedback and biofeedback training.
Michael Thompson
Lynda Thompson
Andrea Reid-Chung
James Thompson
Contributor Notes