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April 06, 2015; 84 (14 Supplement) April 22, 2015

Brain temperature is elevated in relapsing-remitting relative to progressive multiple sclerosis (P5.248)

Victoria Leavitt, Alayar Kangarlu, Feng Liu, Claire Riley, James Sumowski
First published April 8, 2015,
Victoria Leavitt
3The Neurological Institute Columbia University Medical Center New York NY United States
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Alayar Kangarlu
1
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Feng Liu
5NYS Psychiatric Institute New York NY United States
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Claire Riley
2Columbia University Medical Center New York NY United States
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James Sumowski
4Kessler Foundation Research Center West Orange NJ United States
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Citation
Brain temperature is elevated in relapsing-remitting relative to progressive multiple sclerosis (P5.248)
Victoria Leavitt, Alayar Kangarlu, Feng Liu, Claire Riley, James Sumowski
Neurology Apr 2015, 84 (14 Supplement) P5.248;

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Abstract

OBJECTIVE: To compare brain temperature between patients with relapsing-remitting (RR) and progressive courses of multiple sclerosis (MS). BACKGROUND: We recently reported elevated body temperature in RRMS relative to healthy individuals and progressive MS patients in the absence of exogenous heat exposure (Sumowski & Leavitt, 2014), an observation never before reported despite the long-standing literature describing negative consequences of experimental and environmental heat exposure in MS patients (i.e., Uhthoff’s phenomenon). Elevated body temperature may result from clinically-silent brain inflammation in RRMS. If so, brain temperature should also be elevated in RRMS patients. Here, we examined brain temperature in RRMS patients versus progressive MS. METHODS: We used MR spectroscopy to derive brain temperature in 14 patients (9 RRMS, 3 SPMS, 2 PPMS). MRS permits non-invasive measurement of brain temperature because hydrogen bonding is temperature-dependent; measuring the shift in spectral position of the water signal relative to a reference metabolite (e.g., N-acetyl-aspartate) allows for derivation of brain temperature with reported accuracy of ± 0.1°C. RESULTS: Brain temperature was higher in RR than progressive patients (RRMS: 37.71 ± 1.09, progressive: 36.92 ± .93), as was body temperature measured aurally (RRMS: 36.98 ± .26, progressive: 36.59 ± .70), supporting our hypothesis that RRMS patients have higher brain temperature (likely due to brain inflammation) than progressive MS patients (consistent with previous reports of lesser brain inflammation in progressive courses of MS). In addition, brain temperature was correlated with body temperature (r=.475, p= 0.05). CONCLUSIONS: These findings provide preliminary support for body and brain temperature as biomarkers of clinically-silent brain inflammation in RRMS patients. The need for such biomarkers is critical, as the majority of active MS lesions are clinically silent, and therefore go undetected and untreated, leading to worse future disability.

Disclosure: Dr. Leavitt has nothing to disclose. Dr. Kangarlu has nothing to disclose. Dr. Liu has nothing to disclose. Dr. Riley has received personal compensation for activities with Biogen Idec, Teva Pharmaceuticals, Novartis, and Genzyme as a consultant. Dr. Riley has received personal compensation in an editorial capacity for Multiple Sclerosis (The Resource Centre an Dr. Sumowski has nothing to disclose.

Wednesday, April 22 2015, 2:00 pm-6:30 pm

  • Copyright © 2015 by AAN Enterprises, Inc.

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