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Function follows structure. The central (CNS) and peripheral (PNS) nervous system matrix is a rich resource for learning and for retraining. This chapter begins with the structural framework of interconnected neural components that contribute to motor control for walking, reaching, and grasping, and to cognition and mood. I then review what we know about cellular mechanisms that may be manipulated by physical, cognitive, and pharmacologic therapies to lessen impairments and disabilities. These discussions of functional neuroanatomy provide a map for mechanisms relevant to neural repair, functional neuroimaging, and theory-based practices for neurologic rehabilitation.

Injuries and diseases of the brain and spinal cord damage clusters of neurons and disconnect their feedforward and feedback projections. The victims of neurologic disorders often improve, however. Mechanisms of activity-dependent learning within spared modules of like-acting neurons are a fundamental property of the neurobiology of functional gains. Rehabilitation strategies can aim to manipulate the molecules, cells, and synapses of networks that learn to represent some of what has been lost. This plasticity may be no different than what occurs during early development, when a new physiologic organization emerges from intrinsic drives on the properties of neurons and their synapses. Similar mechanisms drive how living creatures learn new skills and abilities.

Activity-dependent plasticity after a CNS or PNS lesion, however, may produce mutability that aids patients or mutagenic physiology that impedes functional gains.

Our understanding of functional neuroanatomy is a humbling work in progress. Although neuroanatomy and neuropathology may seem like old arts, studies of nonhuman primates and of man continue to reveal the connections and interactions of neurons. The brain's macrostructure is better understood than the microstructure of the connections between neurons. It is just possible to imagine that we will grasp the design principles of the 100,000 neurons and their glial supports within 1 mm3 of cortex, but almost impossible to look forward to explaining the activities of the 10 billion cortical neurons that make some 60 trillion synapses.1 Aside from the glia that play an important role in synaptic function, each cubic millimeter of gray matter contains 3 km of axon and each cubic millimeter of white matter includes 9 meters of axon. The tedious work of understanding the dynamic interplay of this matrix is driven by new histochemical approaches that can label cells and their projections, by electrical microstimulation of small ensembles of neurons, by physiological recordings from single cells and small groups of neurons, by molecular analyses that localize and quantify neurotransmitters, receptors and gene products, and by comparisons with the architecture of human and nonhuman cortical neurons and fiber arrangements.

Functional neuroimaging techniques, such as positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and transcranial magnetic stimulation (TMS) allow comparisons between the findings from animal research and the functional neu-roanatomy of people with and without CNS lesions. These computerized techniques offer insights into where the coactive assemblies of neurons lie as they simultaneously, in parallel and in series, process information that allows thought and behavior. Neuroimaging has both promise and limitations (see Chapter 3).

What neuroscientists have established about the molecular and morphologic bases for learning motor and cognitive skills has become more critical for rehabilitationists to understand. Neuroscientific insights relevant to the restitution of function can be appreciated at all the main levels of organization of the nervous sys tem, from behavioral systems to interregional and local circuits, to neurons and their dendritic trees and spines, to microcircuits on axons and dendrites, and most importantly, to synapses and their molecules and ions. Experience and practice lead to adaptations at all levels. Knowledge of mechanisms of this activity-dependent plasticity may lead to the design of better sensorimotor, cognitive, phar-macologic, and biologic interventions to enhance gains after stroke, traumatic brain and spinal cord injury, multiple sclerosis, and other diseases.

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