Neurological Complications of Medical Illness: Critical Illness Neuropathy and Myopathy

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Critical illness neuropathy and myopathy have been commonly recognized phenomena for centuries. Patients will present will a diffuse flaccid weakness. The process appears to be mediated through inflammatory cytokines and interleukins released during sepsis. These inflammatory mediators are speculated to increase endoneural edema and affect nerve and muscle bioenergetics. The resultant decrease in nerve and muscle energy production leads to axonal loss and a functional "dying back" neuropathy. Muscle can also be directly affected. Toxic mediators affect the metabolism of myosin protein producing a characteristic myosin loss myopathy. Treatment consists of early recognition and treatment of sepsis and limitation of neuromuscular blockade. Prognosis is related to the severity and duration of sepsis. Tight glucose control and early mobilization may facilitate rehabilitation.

Original languageEnglish (US)
Title of host publicationEmergency Management in Neurocritical Care
PublisherWiley-Blackwell
Pages182-187
Number of pages6
ISBN (Print)9780470654736
DOIs
StatePublished - Apr 11 2012

Keywords

  • Axonal loss in critically ill patients
  • Complications of sepsis
  • Critical illness myopathy
  • Critical illness neuromyopathy
  • Critical illness neuropathy
  • Intensive care myopathy
  • Intensive care neuropathy
  • Neuromuscular complications of sepsis

ASJC Scopus subject areas

  • Neuroscience(all)

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