Amyotrophic Lateral Sclerosis: Pathophysiology and Implications for Physical Therapy

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Amyotrophic Lateral Sclerosis: Pathophysiology and Implications for Physical Therapy This work will provide a basic overview of the pathophysiology for amyotrophic lateral sclerosis (ALS) as well as the medical interventions used in treatment of the disease. Physical therapy interventions for ALS and therapeutic exercise recommendations are the major focus of this study, and will be discussed in greater detail in the later portion.
Amyotrophic lateral sclerosis, or Lou Gehrig's disease as it is commonly called, is described by the ALS association (ALSA, 2010) as “a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord.” Amyotrophic is described by Porth and Matfin (2009) as muscle
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In very few cases, ALS progression has ceased and, in still fewer, it has reversed. Military veterans are a unique population who show a higher risk of developing ALS, and those deployed during the Gulf War are twice as likely to develop the disease. Pathophysiology
In and of itself, ALS should not be described as a single disease. ALS is a clinical diagnosis which includes many different pathologies that lead to the same physiological conditions. There are many different forms of this disease which can be generally categorized as familial (hereditary) or spontaneous (caused by unknown factors); benign and juvenile forms are rare. This collection of pathologies follows the same general sequence of systematic destruction to motor neurons. ALS degrades motor neurons in three locations: the lower motor neuron cells of the anterior horn, the motor nuclei of the brainstem (hypoglossal in particular), and the upper motor neurons of the cerebral cortex (Porth & Matfin, 2009). ALS most often progresses by first affecting peripheral muscles and eventually, those of the trunk including the muscles required for respiration. People who develop ALS often become paralyzed. Most die from respiratory failure, malnutrition or dehydration (Lescher, 2011).
The nature of the destruction of neural tissue in ALS is not known; it is however suspected that it is caused by excitotoxicity of the neurotransmitter glutamate.

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