presented by Karen L. McCulloch
Financial: Karen L. McCulloch receives compensation from MedBridge for this course. There is no financial interest beyond the production of this course.
Non-Financial: Karen L. McCulloch has no competing non-financial interests or relationships with regard to the content presented in this course.
Satisfactory completion requirements: All disciplines must complete learning assessments to be awarded credit, no minimum score required unless otherwise specified within the course.
Karen L. McCulloch, PT, PhD, MS, NCS
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…Read full bio
1. Focal Lesions – Stroke as An Example
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.
2. Traumatic Brain Injury – Possible Focal and Diffuse Lesions
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.
3. Pathophysiology Associated with Degenerative and Demyelinating Disease
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.
4. Mechanisms of Recovery – Cellular Level
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.
5. Factors that Influence Plasticity
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.
6. Mechanisms of Recovery: Behavioral
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.