This report builds on a highly valued predecessor, the 1994 Institute of Medicine (IOM) report entitled Reducing Risks for Mental Disorders: Frontiers for Preventive Intervention Research. That report provided the basis for understanding prevention science, elucidating its then-existing research base, and contemplating where it should go in the future. This report documents that an increasing number of mental, emotional, and behavioral problems in young people are in fact preventable. The proverbial ounce of prevention will indeed be worth a pound of cure: effectively applying the evidence-based prevention interventions at hand could potentially save billions of dollars in associated costs by avoiding or tempering these disorders in many individuals. Furthermore, devoting significantly greater resources to research on even more effective prevention and promotion efforts, and then reliably implementing the findings of such research, could substantially diminish the human and economic toll.

Preventing Mental, Emotional, and Behavioral Disorders Among Young People: Progress and Possibilities

Synaptic plasticity in adult neural circuits may involve the strengthening or weakening of existing synapses as well as structural plasticity, including synapse formation and elimination. Indeed, long-term in vivo imaging studies are beginning to reveal the structural dynamics of neocortical neurons in the normal and injured adult brain. Although the overall cell-specific morphology of axons and dendrites, as well as of a subpopulation of small synaptic structures, are remarkably stable, there is increasing evidence that experience-dependent plasticity of specific circuits in the somatosensory and visual cortex involves cell type-specific structural plasticity: some boutons and dendritic spines appear and disappear, accompanied by synapse formation and elimination, respectively. This Review focuses on recent evidence for such structural forms of synaptic plasticity in the mammalian cortex and outlines open questions.

Experience-dependent structural synaptic plasticity in the mammalian brain.

Reductions in blood flow to the brain of sufficient duration and extent lead to stroke, which results in damage to neuronal networks and the impairment of sensation, movement or cognition. Evidence from animal models suggests that a time-limited window of neuroplasticity opens following a stroke, during which the greatest gains in recovery occur. Plasticity mechanisms include activity-dependent rewiring and synapse strengthening. The challenge for improving stroke recovery is to understand how to optimally engage and modify surviving neuronal networks, to provide new response strategies that compensate for tissue lost to injury.

Plasticity during stroke recovery: from synapse to behaviour.

Human brain imaging has identified structural changes in gray and white matter that occur with learning. However, ascribing imaging measures to underlying cellular and molecular events is challenging. Here we review human neuroimaging findings of structural plasticity and then discuss cellular and molecular level changes that could underlie observed imaging effects. Greater dialog between researchers in these different fields would help to facilitate cross-talk between cellular and systems level explanations of how learning sculpts brain structure.

Plasticity in gray and white: neuroimaging changes in brain structure during learning

Although previous work has shown that extensive training in the complex visuo-motor skills involved in juggling results in adult gray-matter changes, it is unclear whether such practice can produce similar changes in adult white matter. This paper now uses diffusion tensor imaging to demonstrate structural white-matter changes when adults practice juggling.

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Training induces changes in white-matter architecture

Previously, we showed that the ventral premotor cortex (PMv) underwent neurophysiological remodeling after injury to the primary motor cortex (M1). In the present study, we examined cortical connections of PMv after such lesions. The neuroanatomical tract tracer biotinylated dextran amine was injected into the PMv hand area at least 5 months after ischemic injury to the M1 hand area. Comparison of labeling patterns between experimental and control animals demonstrated extensive proliferation of novel PMv terminal fields and the appearance of retrogradely labeled cell bodies within area 1/2 of the primary somatosensory cortex after M1 injury. Furthermore, evidence was found for alterations in the trajectory of PMv intracortical axons near the site of the lesion. The results suggest that M1 injury results in axonal sprouting near the ischemic injury and the establishment of novel connections within a distant target. These results support the hypothesis that, after a cortical injury, such as occurs after stroke, cortical areas distant from the injury undergo major neuroanatomical reorganization. Our results reveal an extraordinary anatomical rewiring capacity in the adult CNS after injury that may potentially play a role in recovery.

https://www.jneurosci.org/content/jneuro/25/44/10167.full.pdf

Extensive cortical rewiring after brain injury.

astrocytoma included, yielding 22 total patients. The tumor was resected in 18 patients and un-resected in 4. A random number generator was used to select comparison groups of 26 stroke patients and 20 traumatic brain injury (TBI) patients who were admitted during the same period. Interventions: Not applicable. Main Outcome Measures: Functional independence measure (FIM) change between admission and discharge, FIM efficiency, percentage of therapy days that 3-hour rule was not met, major complication rate, and rate of transfer out of acute rehabilitation unit. Results: Average FIM change by group was GBM 16.5, stroke 22.6 (P1⁄4.116), and TBI 24.8 (P1⁄4.048). FIM efficiency by group was GBM 1.04, stroke 1.62 (P1⁄4.089), TBI 2.24 (P1⁄4.003). Percent of therapy days that 3-hour rule was not met by group was GBM 28.3%, stroke 13.2% (P1⁄4.014), TBI 15.3% (P1⁄4.042). Major complication rate by group was GBM 0.59, stroke 0.27 (P1⁄4.094), and TBI 0.65 (P1⁄4.808). Rate of transfer out of rehabilitation unit was 0.23 for GBM group, 0.25 for stroke (P1⁄4.777), and 0.15 for TBI (P1⁄4.812). Conclusions: GBM patients demonstrated functional improvement during acute rehabilitation; however, their rate and magnitude of improvement was significantly less than TBI patients and trended towards significance compared to stroke patients. Additionally, the participation of GBM patients was significantly less than stroke and TBI patients. This may be helpful for providers, therapists, and patients when guiding expectations. In addition, decisions regarding delay of chemotherapy treatments for pursuit of an acute rehabilitation course may be made with a better understanding of potential functional outcomes. Level of Evidence: Level III

Daofen Chen

Papers

Extensive cortical rewiring after brain injury.

Effects of Forced Use on the Ventral Premotor Cortex Distal Forelimb Representation After Ischemic Infarct in Primary Motor Cortex.