Amyotrophic Lateral Sclerosis Physical Therapy Interventions: An Attempt to Limit Debilitating Symptoms

Amyotrophic Lateral Sclerosis Physical Therapy Interventions: An Attempt to Limit Debilitating Symptoms
Jennifaye V. Brown, PhD, PT, NCS
June 30, 2016

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 Amyotrophic Lateral Sclerosis Physical Therapy Interventions: An Attempt to Limit Debilitating Symptoms.The participant will be able to accurately describe the pathophysiology of ALS.The participant will be able to differentiate between at least two major types and subtypes of ALS.The participant will be able to correctly describe at least three common impairments that are a result of ALS.The participant will be able to independently identify at least three specific physical therapy treatment interventions used to alleviate or dissipate symptoms depending on disease progression.Background of ALS HistoryJean-Martin Charcot is a French neurologist, but he was trained as a pathologist. He is known as the father of neurology. In his findings, he and his colleagues were able to discover lesions in 2 distinct places. The first place was the lateral column of the spinal cord and the outcomes presented as progressive paralysis, contractures, but no atrophy. Then they found lesions in the anterior horn of the spinal cord and the outcomes were paralysis, no contracture, but atrophy. ALS was termed in 1874 when Dr. Charcot's lectures were compiled as Oeuvres Completes. However, in some parts of the world, ALS is still termed Charcot's Disease. It become very commonplace to call ALS after a famous baseball player named Lou Gehrig. He was the first baseman for the New York Yankees from 1923 to 1939. He was forced to retire in 1939 after being diagnosed with ALS. He died 2 years later. I want you to remember this timing of 2 years because it is going to become significant after we talk about the different ALS-related diagnoses. Defining ALSWhen we define ALS, it is easy to look at the parts of the words and see what they mean. “A “means without. “Myo” is pertaining to muscle. “Trophic” pertains to growth and nourishment of structures by efferent innervation. This is a disease process of motor neurons, which provides efferent innervation. “Lateral” means pertaining to the side and “sclerosis” is hardening of nervous tissue due to degeneration. Overall, ALS is primarily considered a disease of the central nervous system. The central nervous system is everything pertaining to the brain and the spinal cord. What you see is progressive weakness and/or paresis leading to death in a few years from respiratory compromise. There are people out there who have diagnoses of ALS and have lived 5 to 10 years, but they have a different version of the disease that is in a category now known as ALS-related motor neuron diseases.EtiologyIt has been a very long time since Jean-Martin Charcot determined what he called was ALS, but due to different and updated imaging and genetic studies, the etiology of ALS is determined by the pathophysiology and the associated clinical classifications. Now you are going to see a broad spectrum of ALS-related diseases, but the true ALS as we know it, will have a point of death within 1 to 2 years. Pathophysiological MechanismsALS is a multi-system disease process. It has various pathophysiologic determinates of origin. When we look at the pathophysiology, due to our new genetic and imaging studies, there are 6 ways the origins of ALS can come about. I am going to give you the definitions of them, but we are not going to go through the process of how the etiology comes about. We are not pathologists, but we need to know what they are so we can better explain it to our patients. First.  The first is oxidative stress. Oxidative stress simply means that the motor neuron cells are going to have impaired performance because there are too many oxygen molecules in them. Second.  The second is mitochondrial damage. We all know that the mitochondria is the energy factory. It provides the energy needed for cells to survive and it produces about 90% of that energy. When there is mitochondrial damage, your cells do not get the energy needed to properly function and that contributes to one of the pathophysiological mechanisms seen in ALS. Third.  The third is protein accumulation. We have these various proteins that our cells need to operate.   The first being superoxide dismutase 1 and when there is a shape change or, for a better term, a mutation, in SOD1, it can contribute to motor neuron death. They have also found a mutation of the protein TDP-43 in cases of ALS. When you have an accumulation of these proteins in a mutant form, it contributes to the pathological processes seen in ALS. Forth.  The next is cytoskeletal interruption. Let’s review of the motor neuron.  Figure 1 depicts a nerve cell.  The center of the blue is the cell body. This is where you would find the mitochondria and it is known as the perikaryon. It's like the brain of the motor neuron. Then the long blue stem is the axon. All the impulses travel down the axon to your effector cell, which is the muscle. The impulses travel along the myelin sheath in the nodes of Ranvier. Inside this longitudinal structure (axon) you have a skeleton.  A mutation of profilin, PFN1, which is a gene needed for the growth and development of that cytoskeleton can cause cytoskeletal interruption.  When you do not have that cytoskeleton, the structure loses its strength and the ability to transmit information is lost.  A tree can grow tall and strong with its external bark. When you lose that bark, the tree starts to bend and it cannot grow and produce leaves and fruit. The same thing happens with this axon. It cannot send the necessary impulses and the information to the muscle. When there is a mutation of profilin, this gene is unable to participate in the growth and the development of the cytoskeleton of the nerve axons. Figure 1 Nerve Cell Fifth.  The fifth is glutamate and neuronal toxicity. Glutamate is an excitatory neurotransmitter. It is used in learning and in memory. In the central nervous system, it causes a release of calcium. When you have high levels of glutamate, it causes nerve cells to die. This glutamate toxicity causes calcium to stay in the cell. High...

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jennifaye v brown

Jennifaye V. Brown, PhD, PT, NCS

Jennifaye V. Brown, PT, PhD, NCS has a BA-Psychology (Emory University), a MS- Physical Therapy (University of Miami-FL) and a PhD-Exercise Science (University of South Carolina).  Dr. Brown has 27 years of clinical experience focused in neurorehabilitation across the continuum of care and has presented numerous continuing education courses on adult neurologic assessment and treatment intervention for acquired brain injury.  Dr. Brown’s special interests and extensive clinical background include gait analysis and training.  Her approach to effective gait analysis and treatment is to know the lesion site, understand neuroanatomical functions and along with past medical history, environmental, psychosocial and cultural factors, determine prognosis and devise realistic goals reflective of the client and caregiver’s lived experiences.  She is the creative force behind the Stroke Gait Center, which is a collaborative effort to partner with healthcare professionals to fabricate AFOs (specializing in accommodating ladies’ footwear) utilizing 3D printing based on a full spectrum gait-related physical therapy evaluation. Her current research agenda explores the perceptions and opinions of individuals with stroke regarding their experiences with AFO fabrication, modification and maintenance. As an Advanced Credentialed Clinical Instructor by the Clinical Instructor Education Board and a three 10-year term board certified neurologic clinical specialist by the American Board of Physical Therapy Specialties (ABPTS) of the APTA, Dr. Brown has taught at PT and PTA programs in Georgia and South Carolina (SC). She is a member of the APTA, Neurology Section of the APTA, SC Chapter of the APTA, American Heart Association/American Stroke Association, Aerobics & Fitness Association of America, and the Neuro-Developmental Treatment Association.  Dr. Brown is currently an Assistant Clinical Professor at Ohio University in the Physical Therapy Program.



Related Courses

ALS: Physical Therapy Interventions in Attempt to Limit Debilitating Symptoms
Presented by Jennifaye V. Brown, PhD, PT, NCS
Recorded Webinar
Course: #23842 Hours
The purpose of the course is to provide information regarding pathology and different types of ALS and how the approach for physical therapy interventions should change base on disease progression. A patient-centered approach will be used to describe treatment interventions taking into consideration the social determinants of health that impact patients, caregivers and the provisions of care in rehabilitation. This course is directly related to the practice of physical therapy and is therefore appropriate for Physical Therapists and Physical Therapist Assistants. This course is open captioned.

GBS: GoodBye Symptoms via Physical Therapy Interventions
Presented by Jennifaye V. Brown, PhD, PT, NCS
Recorded Webinar
Course: #24582 Hours
The purpose of the course is to provide information regarding etiology and pathology regarding the different types of Guillain-Barre syndrome (GBS). Medical management and physical therapy interventions will be discussed based on disease progression and regression taking into consideration patient and caregiver perspectives. This course is directly related to the practice of physical therapy and is therefore appropriate for the PT and PTA.

Neurologic Gait Analysis, Treatment, and Measurement: Case-Based Interventions for the PTA, Part I: Lesions of the Cortex
Presented by Jennifaye V. Brown, PhD, PT, NCS
Recorded Webinar
Course: #27132 Hours
The purpose of this course is to review typical stroke lesions of the cortex and describe resulting impairments that may be observed during gait. Using a systems approach, the PTA will be instructed how to formulate interventions within their scope of practice and the established plan of care to improve gait impairments. The presentation will utilize a case-based approach to demonstrate and summarize application of the material. This course is directly related to the practice of physical therapy and is therefore appropriate for the PT and PTA.

Neurologic Gait Analysis, Treatment, and Measurement: Case-Based Interventions for the PTA, Part II: Lesions of the Subcortex
Presented by Jennifaye V. Brown, PhD, PT, NCS
Recorded Webinar
Course: #27142 Hours
The purpose of this course is to review typical stroke lesions of the subcortex and describe resulting impairments that may be observed during gait. Using a systems approach, the PTA will be instructed how to formulate interventions within their scope of practice and the established plan of care to improve gait impairments. This course is directly related to the practice of physical therapy and is therefore appropriate for the PT and PTA.

Neurologic Gait Analysis, Treatment, and Measurement: Case-Based Interventions for the PTA, Part III: Lesions of the Cerebellum
Presented by Jennifaye V. Brown, PhD, PT, NCS
Recorded Webinar
Course: #27102 Hours
The purpose of this course is to review typical stroke lesions of the cerebellum and describe resulting impairments that may be observed during gait. Using a systems approach, the PTA will be instructed how to formulate interventions within their scope of practice and the established plan of care to improve gait impairments. The presentation will utilize a case-based approach to demonstrate and summarize application of the material. This course is directly related to the practice of physical therapy and is therefore appropriate for the PT and PTA.