Principal Investigators //
- Vince Calhoun, PhD >
- Arvind Caprihan, PhD >
- Zikuan Chen, PhD >
- Vince Clark, PhD >
- Eric D. Claus, PhD >
- Carla Harenski, PhD >
- Kent Hutchison, PhD >
- Kent A. Kiehl, PhD >
- Jeffrey D. Lewine, PhD >
- Jingyu Liu, PhD >
- Andrew R. Mayer, PhD
- John Phillips, MD >
- Sergey Plis, PhD >
- Matthew Shane, PhD >
- Julia M. Stephen, PhD >
- Jing Sui, PhD >
- Jessica Turner, PhD >
Andrew R. Mayer, PhD
Associate Professor of Translational Neuroscience, The Mind Research Network
Adjunct Assistant Professor of Neurology, University of New Mexico Health Science Center
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. Our work suggests that unisensory cortex can be up- (increased signal) or down- (decreased signal) regulated during bimodal stimulation during demanding attentional tasks.
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.
For more information on Dr. Mayer, please refer to his Curriculum Vitae.
Selected Publications //
- A fMRI study of auditory orienting and inhibition of return in pediatric mild traumatic brain injury >
- A Longitudinal Proton Magnetic Resonance Spectroscopy Study of Mild Traumatic Brain Injury >
- Auditory orienting and inhibition of return in schizophrenia: A functional magnetic resonance… >
- Biomarkers of increased diffusion anisotropy in semi-acute mild traumatic brain injury… >
- Functional Imaging of the Hemodynamic Sensory Gating Response in Schizophrenia >
- Evoked and Intrinsic Asymmetries during Auditory Attention: Implications for the Contralateral… >
- A practical approach to incidental findings in neuroimaging research >
- Functional connectivity in mild traumatic brain injury >
- Modeling Conflict and Error in the Medial Frontal Cortex >
- Enhanced cue reactivity and fronto-striatal functional connectivity in cocaine use disorders. >
- The Effects of Stimulus Modality and Frequency of Stimulus Presentation on Cross-modal Distraction >
Consequences of mTBI
Almost all of us will get “hit in the head” at some point in our lives. “How hard” we get hit will likely determine whether we have a life altering experience or just walk away from it. However, emerging evidence suggests that even mild TBI can have prolonged consequences, affecting how we perform at work and make critical daily decisions for months. More importantly, particularly for athletes or soldiers, repeat injuries may make us more vulnerable for experiencing long-term negative outcomes. Unfortunately, mild TBI is not detected using routine clinical brain imaging techniques, nor do we have sufficient understanding of its long-term effects on behavior.
In the Mild TBI Project at MRN, lead by Dr. Andrew Mayer, we are investigating the subtle structural and biochemical consequences of mild TBI using state-of-the-art neuroimaging techniques. Our preliminary findings have shown that mild TBI causes alterations in the brain’s structure, function and chemistry. We are exploring how these alterations correlate with neurobehavioral symptoms, and how these may change as a function of recovery.
Attentional Bias Modification (ABM)
Cocaine abuse and dependence are chronic, relapsing disorders for which there are few effective treatments. Changes in frontal and sub-cortical neural circuitry following prolonged drug exposure can last for years after cessation and may compromise an addict’s ability to suppress drug seeking when exposed to drug-related cues. Attentional Bias Modification (ABM) training purportedly reduces the attentional response to salient drug stimuli and has been shown to be efficacious in treating alcohol dependence; however, the efficacy of ABM in treating individuals with cocaine addiction has yet to be empirically determined. Previous research suggests that chronic cocaine users also exhibit a decreased neuronal response during inhibitory control in addition to the enhanced neuronal response to salient drug cues. Although extensive evidence of these two neuronal abnormalities exists, to date we are not aware of a study that has directly compared the differential validity of these two metrics (i.e., enhanced cue reactivity and decreased inhibitory control) for predicting relapse. Additionally, our preliminary data provides evidence of increased intrinsic neuronal activity (functional connectivity; fcMRI) within a frontal sub-cortical circuit in CCA relative to controls. Therefore, our current study has two primary objectives that are both clinically significant and highly innovative. First, we will investigate the efficacy and mechanism of action of ABM in treating cocaine addiction (Aim 1). Second, we will determine which of the three neuronal abnormalities (i.e., enhanced cue reactivity or abnormalities in inhibitory control or increased fcMRI) are more predictive of relapse and drug utilization (Exploratory Aim 1).
Mild Traumatic Brain Injury (mTBI)
Mild traumatic brain injury (mTBI) is associated with neurobehavioral deficits in a majority of patients during the semi-acute injury phase, with a minority of patients remaining symptomatic for months to years post-injury. Routine clinical imaging scans (MRI and CT) are usually negative, suggesting that alternative neuroimaging techniques such as fMRI, DTI and 1H-MRS are well-positioned to provide unique information about the putative “silent lesions” of mTBI and their impact on neurobehavioral functioning. To this end, published data from my lab provides preliminary evidence of tissue-specific dysfunction and self-reported neuropsychiatric disturbances in both children and adults following mTBI. These injuries include increased fractional anisotropy in white matter, likely resulting from cytotoxic edema, secondary inflammatory processes, and potential structural alterations in neurofilaments and myelin. The brain’s ability to respond to external stimuli also appears to be reduced in the semi-acute stage of mTBI, with individual brain networks failing to communicate properly with each other. An increased understanding of the mechanisms underlying these injuries and how/when they recover represents the crucial next step for determining when patients can safely resume physical activities.