PREFERRED PRACTICE PATTERN
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. http://www.accessmedicine.com. 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. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)
Log In to View More
If you don't have a subscription, please view our individual subscription options below to find out how you can gain access to this content.
Want remote access to your institution's subscription?
Sign in to your MyAccess profile while you are actively authenticated on this site via your institution (you will be able to verify this by looking at the top right corner of the screen - if you see your institution's name, you are authenticated). Once logged in to your MyAccess profile, you will be able to access your institution's subscription for 90 days from any location. You must be logged in while authenticated at least once every 90 days to maintain this remote access.
If your institution subscribes to this resource, and you don't have a MyAccess profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus.
AccessPhysiotherapy Full Site: One-Year Subscription
Connect to the full suite of AccessPhysiotherapy content and resources including interactive NPTE review, more than 500 videos, Anatomy & Physiology Revealed, 20+ leading textbooks, and more.
Pay Per View: Timed Access to all of AccessPhysiotherapy
24 Hour Subscription $34.95
48 Hour Subscription $54.95
Pop-up div Successfully Displayed
This div only appears when the trigger link is hovered over.
Otherwise it is hidden from view.