In my search for the holy grail of objective proof of brain damage in those with Post Concussion Syndrome, I try to stay as current as possible on neuroimaging advances. Yesterday I focused on Dr. Randall Benson’s testimony with respect to Susceptibility Weight Imaging. Today I will focus on Diffusion Tensor Imaging, DTI.
As a professional who works exclusively in the field of brain injury I believe that DTI may offer more short term benefit in diagnosing Mild Traumatic Brain Injury (“MTBI”). The reason is that MTBI appears to be more a syndrome with attentional and processing problems which are white matter dependant functions and DTI is primarily a white matter test.
Briefly, the grey matter of the brain is primarily on the cerebral cortex of the brain and is where our memories are stored and our higher thought processes likely are centered. The white matter is the axonal fibers that connect different parts of the grey matter of different sections of the brain to each other. White matter is what allows the different brain cells to work together. A white matter injury will most often manifest itself with the attentional and processing problems easiest to prove after a concussion. Post Concussion Syndrome is far more complex than attention and processing problems, but those are the functions where there is the most consistent change across the wide range of PCS patients. For more on Diffuse Axonal Injury see http://subtlebraininjury.com/diffuse.html
Axons are extremely small. It is unlikely that neuroimaging will ever get to the point where we can see actual axonal damage in a live person. However, most axons travel through axonal pathways, which because they include tens of thousands of axons, are visible. DTI is an imaging technique that can visualize the axonal tracts. When there has been a significant disruption of any one axonal tract in the brain, DTI may show that disruption. The reason that DTI doesn’t tell us everything we want to know is that like all other imaging techniques in a live brain injured person, it is limited by the resolution of the scanner, which generally can only see pathology of as small as one millimeter.
In the image below, you can see a DTI scan with respect to the corpus callosum fiber tracts in the brain:
Dr. Benson explained DTI in his testimony this way:
Diffusion Tensor Imaging
Developed in the mid-1990’s, diffusion tensor imaging (DTI) is sensitive to the 3D flow of water inside and outside of white matter fibers (the long extensions from nerve cell bodies which connect nearby or distant cells). Closed head injuries (non-penetrating) including concussion are caused by sudden acceleration or deceleration of the head which causes local deformationsof the brain within the cranium. The anatomical and biomechanical properties of the brain are such that white matter fibers are stretched and damaged, resulting in diffuse axonal injury (DAI) which is the hallmark pathology and accounts for most of the neurological disability in TBI.
The typical cognitive deficits in TBI, i.e., slowed information processing, decreased attention and memory, and psychiatric symptoms are caused by damage to the “cables” which allow for efficient transmission of information between neurons. TBI reduces brain network efficiency resulting in decreased capacity and global functional impairment. Concussive injury such as occurs in football with high speed collisions also causes deformation of brain substance and is felt to account for many of the immediate and delayed symptoms including the post-concussive syndrome. ERP studies of sports related concussion suggest that symptomatic recovery may occur while neurologic and brain metabolic functioning continues to be impaired from weeks to months after injury.
Incurring a second concussion before neurologic recovery has been shown to worsen outcome and may begin a downward spiral culminating in chronic traumatic encephalopathy (CTE) but this is not known. Diffusion tensor imaging (DTI) is able to detect damaged white matter fibers (axons) which have altered flow of water molecules compared with healthy axons (see Figure 5). DTI, like SWI can be performed on a standard clinical scanner (1.5-3 Tesla) and is available on virtually all clinical scanners.
According to Dr. Benson, DTI is showing abnormalities in mild traumatic brain injury survivors.
Our initial investigation of DTI in 20 TBI cases found that (similar to SWI and hemorrhage) an index of DTI, fractional anisotropy (FA), is decreased uniformly in TBI compared with 14 controls (see Figure 6), and that the magnitude of the decrease in average FA for global white matter is highly correlated with TBI severity (Figure 7). Even the 6 mild TBI cases (GCS 13-15)had decreased FA compared with the controls. The separation of the milds from the controls is especially relevant to sports concussions where the great majority of injuries are mild.
In summary, DTI is able to “visualize” diffuse axonal injury from TBI. In some cases location of lesions appears to correlate with specific symptoms but generally the severity of DAI as indicated by DTI is strongly predictive of general neurocognitive disability. Since concussion produces axonal injury, particularly repetitive concussion, imaging with DTI would appear to be ideal to study NFL players. Certainly, a large scale cross-sectional study wherein head injury history, position, age, genetic risk (ApoE genotype), neuropsychological testing (focused) and possibly electrophysiological testing with EEG (ERP, qEEG) and PET are factors. In addition, a prospective study with serial scans over a player’s career, tracking concussions or hits and relating imaging to neurocognitive performance (IMPACT or similar) and other factors as in cross-sectional study. Imaging would also facilitate the evaluation of helmet and neck support designs in animal models and in the field.
In our next blog, we will focus on the value of using NFL players and other sport concussion survivors as the prototype for all concussion diagnosis and treatment.
