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Dec 13 2013

Can Gray Matter Abnormalities Occur In Mild Traumatic Brain Injury?

Posted in Community Service, Traumatic Brain Injury

Traumatic brain injuries not only cause initial damage to the Central Nervous System, but increase the risk of additional neurologic problems and dramatically impact the ongoing costs associated with caring for the patient,  says Alabama liability attorney Keith T. Belt .

birmingham brain injury lawyer

Mild Concussion Brain Imaging

Patients with mild concussions/traumatic brain injury, showed abnormal brain structural patterns that persisted long after clinical symptoms had resolved, according to recent research.

Diffusion tensor imaging in 26 patients with mild traumatic brain injury (TBI)showed increases in mean fractional anisotropy, a marker of gray matter injury, in the superior frontal cortex that persisted on the left side 4 months after the injury in the patients relative to healthy controls, according to Andrew R. Mayer, PhD, and colleagues at the Lovelace Biomedical and Environmental Research Institute in Albuquerque, N.M.

Dr. Mayer’s research systematically examines how the brain uses auditory and visual information dependent on task demands. For example, auditory signals excel at producing rapid bottom-up shifts of attention (orienting responses) whereas the visual modality is superior for making fine-grain discriminations about object location and type. He also examines how the brain processes complementary versus conflicting (selective attention) auditory and visual information.

Deficits in spatial localization and selective attention are hallmark symptoms that occur in the first weeks of mild traumatic brain injury (mTBI), a condition that affects approximately 1.4 million new patients each year. While the majority of mTBI patients will fully recover from their injury, roughly 210,000 individuals will remain symptomatic. Standard clinical scans (CT or MRI scans) are negative in the majority of cases. This promotes a common perception that residual symptoms are purely psychological, which may be akin to subsequently discredited medical views on temporal lobe epilepsy and multiple sclerosis. Indeed, emerging evidence from Dr. Mayer’s lab and others suggest subtle lesions following mTBI, including metabolic and functional abnormalities in otherwise healthy appearing tissue. The diagnosis and treatment of residual cognitive deficits in mTBI will remain woefully inadequate until we understand the underlying neural mechanisms, which is a primary focus of the lab.