Events

You are here

Treating Weakness in Critically Ill Patients

EVENT: 
Weekly Seminar | Not Open to the Public
Who Should Attend: 
Researchers

Speakers

Mark Monroe Rich, M.D., Ph.D.
Professor
Department of Neuroscience, Cell Biology and Physiology
Wright State University

Abstract

Weakness induced by critical illness (intensive care unit acquired weakness) is a major cause of disability in patients and is currently untreatable. We recently identified a defect in repetitive firing of lower motor neurons as a novel contributor to intensive care unit acquired weakness. In order to develop therapy for intensive care unit acquired weakness, it was necessary to determine the mechanism underlying the defect in repetitive firing. Both computer simulation and in vivo dynamic voltage clamp of spinal motor neurons in septic rats were employed to explore potential mechanisms underlying defective repetitive firing. Our results suggested alteration in subthreshold voltage-activated currents might be the mechanism underlying defective repetitive firing. It has been shown previously that pharmacologic activation of serotonin receptors on motor neurons increases motor neuron excitability, in part by enhancing subthreshold voltage-activated inward currents. Administration of a food and drug administration approved serotonin agonist (lorcaserin) to septic rats greatly improved repetitive firing and motor unit force generation. Our findings suggest activation of serotonin receptors with lorcaserin may provide the first ever therapy for intensive care unit acquired weakness.

Mark Monroe Rich, M.D., Ph.D. Figure

Publications

Hawash AA, Voss AA, Rich MM.
Inhibiting persistent inward sodium currents prevents myotonia.
Ann Neurol. 2017 Sep;82(3):385-395. doi: 10.1002/ana.25017. Epub 2017 Sep 18.
Nardelli P, Powers R, Cope TC, Rich MM.
Increasing motor neuron excitability to treat weakness in sepsis.
Ann Neurol. 2017 Dec;82(6):961-971. doi: 10.1002/ana.25105. Epub 2017 Dec 7.
Wang X, McIntosh JM, Rich MM.
Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction.
J Neurosci. 2018 Feb 14;38(7):1725-1736. doi: 10.1523/JNEUROSCI.1789-17.2018. Epub 2018 Jan 11.

When

Tuesday, April 17, 2018 - 12:30pm

Where

Burke Medical Research Institute
785 Mamaroneck Avenue
White Plains, NY 10605
United States
Conference Room: 
Billings Building – Rosedale

More Information

Conditions & Recovery

Neurodegenerative Diseases icon
Worldwide, 50 million people are living with Alzheimer's and other dementias.