presented by Karen L. McCulloch
The purpose of this course is to review commonalities in physiologic mechanisms of neurologic damage through the use of key examples, including more gross processes (focal or diffuse injury that occurs suddenly) as well as degenerative changes that occur as a result of a disease process. Intrinsic and extrinsic factors that affect cellular processes that lead to improvement in function are highlighted, as well as behavioral factors that are associated with neuroplastic change. This course aims to draw parallels across conditions that are seen in adult neurologic practice and encourage therapeutic activity to drive neuroplasticity.
Karen L. McCulloch, PhD, PT, MS, NCS, is a Professor in Physical Therapy in the Division of Physical Therapy, Department of Allied Health Sciences, School of Medicine at University of North Carolina – Chapel Hill, where she has taught entry-level and advanced-level students in neurorehabilitation since 1993. She has served in multiple roles within the Academy of Neurologic Physical Therapy, including the inaugural Director of Education, and has been honored with the Service to the Section Award and the APTA Lucy Blair Service Award. Karen has cared about individuals with traumatic brain injury since beginning as a PT in clinical practice, extending from moderate to severe brain injury to a recent focus on concussion. Her research has focused on developing outcome measures and interventions to improve active movement, balance, and functional mobility, with the aim to improve quality of life. She developed the Arm Motor Ability Test (for upper limb recovery following stroke) and the Walking and Remembering Test (for dual-task performance in older adults and individuals with acquired brain injury). She served as an ORISE Fellow with the Army Office of the Surgeon General, addressing TBI issues that affect individuals in military service. Her current research efforts are focused on wounded warriors with mild traumatic brain injury as part of a team that developed the Assessment of Military Multitask Performance, a test battery of challenging dual- and multi-task activities. She is currently leading a group writing a clinical practice guideline for physical therapy management of concussion, and is involved in intervention studies that address treatment for sports and military concussion. Funding support for her research has come from the Foundation for Physical Therapy, Centers for Disease Control and Prevention, National Institutes of Health, National Football League, and Department of Defense.
Stroke is one of the most common adult neurologic conditions we encounter in the clinic. Whether the stroke occurs as a result of ischemia or hemorrhage, there are similar focal effects on brain tissue, so this will be used as an example to consider the cellular-level damage and creation of tissue that is at risk for damage in secondary injury.
Traumatic brain injury is another common condition in neurologic practice. Depending on the mechanism of injury, it is possible to have both focal and diffuse injuries occur at the onset. However, there are pathophysiologic changes associated with a “metabolic cascade” that are of concern, where additional tissue damage occurs. A hallmark of this situation is glutamate excitotoxicity that perpetuates the problem. We see this same set of symptoms in some degenerative conditions as well. We will discuss this in the context of concussion, where links between physiology and symptoms are theorized.
There are similarities in pathophysiologic processes in a number of degenerative and/or demyelination conditions, where as a result of an inflammatory process, immunologic changes occur allowing central nervous system structures to be targeted. This damage may be somewhat temporary and result in a relapse that is followed by recovery. However, over time, demyelinating changes may persist and result in axonal damage so that more longstanding deficits emerge.
Many of the strategies that show promise to improve function at the cellular level involve pharmacologic interventions that address the pathophysiologic mechanism addressed previously: to improve perfusion, to reduce excitotoxicity, to manage inflammation, or to modulate immune responses. However, activity that uses available neural structures for function can drive cellular level changes. Mechanisms of change at the cellular level will be reviewed.
There are key principles that therapists can use to improve the likelihood of neuroplasticity that improves function. These principles will be reviewed, with examples of how they may be used in clinical practice.
There are key principles that therapists can use to improve the likelihood of neuroplasticity that improves function. These principles will be reviewed with examples of how they may be used in clinical practice.