Experimental autoimmune encephalomyelitis. An anatomically-based explanation of clinical progression in rodents

R. D. Simmons, C. C A Bernard, G. Singer, P. R. Carnegie

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Abstract

Lactate accumalation was measured soon after decapitation in three adjacent lower spinal cord regions of rats with EAE. Results indicate that during EAE, and in correlation with the onset of clinical signal of both initial attack and shorth-term relapse, a differential focal increase in lactate accumulation occurs in rat spinal cord compared to Freund's Complete Adjuvant controls, with greater increase occurring in more caudal segments. A [14C]antipyrine method of estimating relative spinal cord blood flow failed to find evidence that the lactate accumulations were due to focal ischemia. Subsequent measurement of isotopic water and total protein increases in the same cord regions indicated that a slight but significant increase in vasogenic edema occurs in correlation with the increase in lactate accumulation and the onset of EAE clinical signs. The data are interpreted as lending support to a speculative theory of paralysis induced by edema during EAE, in which nerve root endoneurium is postulated as the functionally vulnerable site. More specifically, it is hypothesized that the ascending progression of clinical signs of EAE in rodents can be explained on an anatomica basis by progressive disturbance of the nodes of Ranvier in nerve root myelinated fibers.

Original languageEnglish
Pages (from-to)307-318
Number of pages12
JournalJournal of Neuroimmunology
Volume3
Issue number4
DOIs
Publication statusPublished - 1982
Externally publishedYes

Keywords

  • Edema
  • Lactic acid
  • Lewis rats
  • Myelin basic protein
  • Nerve roots

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