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  • Lou Gehrig disease

  • Amyotrophic lateral sclerosis (ALS)

  • Motor neuron disease


  • 728.2 Muscular wasting and disuse atrophy not elsewhere classified


  • M62.50 Muscle wasting and atrophy, not elsewhere classified, unspecified site


  • 5E: Impaired Motor Function and Sensory Integrity Associated with Progressive Disorders of the Central Nervous System1


In home health, the physical therapist sees a 51-year-old man who is transitioning from moderate to severe ALS. Following examination the physical therapist determines that he is no longer capable of safe ambulation; he tolerates sitting upright but only with full support. He reports he is having increased difficulty with his coughing and his chest feels heavy. His care giver is getting increasingly concerned about his skin and would like advice on how to manage him better. Presently he is able to communicate verbally, but the activity is fatiguing and his oxygen saturation drops to 83% during conversation. On muscle testing he demonstrates gross strength of 2+/5 in bilateral upper extremities and 3/5 in bilateral lower extremities. Sensation is intact.


Amyotrophic lateral sclerosis. Axial T2-weighted MRI scan through the lateral ventricles of the brain reveals abnormal high signal intensity within the corticospinal tracts (red arrows). This MRI feature represents an increase in water content in myelin tracts undergoing Wallerian degeneration secondary to cortical motor neuronal loss. This finding is commonly present in ALS, but can also be seen in AIDS-related encephalopathy, infarction, or other disease processes that produce corticospinal neuronal loss in a symmetric fashion. (From Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)


Monosynaptic muscle stretch reflex with descending control via inhibitory interneurons. Primary Ia afferents (green) from muscle spindles, activated when the muscle is stretched rapidly, synapse directly on motor neurons (blue) going to the stretched muscle, causing it to contract and resist the movement. Pyramidal upper motor neurons (aqua) from the cerebral cortex suppress spinal reflexes and the lower motor neurons indirectly by activating the spinal cord inhibitory interneuron pools (red). When the pyramidal influences are removed, the reflexes are released from inhibition and become more active, leading to hyperreflexia and spasticity. Baclofen acts to restore the lost inhibition by stimulating postsynaptic GABA receptors. Tizanidine acts presynaptically to stimulate GABA release from spinal cord inhibitory interneuron. (From Brunton LL, Chabner BA, Knollmann BC. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)

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