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From the Institute for Exercise & Environmental Medicine (S.L.D., C.G.C., M.J.B.), Presbyterian Hospital of Dallas, TX; Departments of Internal Medicine (S.L.D., C.G.C.), Neurology (S.L.D., T.C.F., D.A.M., O.S., E.M.F.), and Ophthalmology (E.M.F.), University of Texas Southwestern Medical Center at Dallas; New Jersey Neuroscience Institute (P.D.K.), Seton Hall University, Edison; and Neurology Section (O.S.), Medical Service, Veterans Affairs North Texas Health Care Service.
* To whom correspondence should be addressed. E-mail: Elliot.Frohman{at}UTSouthwestern.edu.
ABSTRACT
Objective: The goal of this investigation was to demonstrate that internuclear ophthalmoparesis (INO) can be utilized to model the effects of body temperature-induced changes on the fidelity of axonal conduction in multiple sclerosis (Uhthoff's phenomenon).
Methods: Ocular motor function was measured using infrared oculography at 10-minute intervals in patients with multiple sclerosis (MS) with INO (MS-INO; n = 8), patients with MS without INO (MS-CON; n = 8), and matched healthy controls (CON; n = 8) at normothermic baseline, during whole-body heating (increase in core temperature 0.8°C as measured by an ingestible temperature probe and transabdominal telemetry), and after whole-body cooling. The versional disconjugacy index (velocity-VDI), the ratio of abducting/adducting eye movements for velocity, was calculated to assess changes in interocular disconjugacy. The first pass amplitude (FPA), the position of the adducting eye when the abducting eye achieves a centrifugal fixation target, was also computed.
Results: Velocity-VDI and FPA in MS-INO patients was elevated (p < 0.001) following whole body heating with respect to baseline measures, confirming a compromise in axonal electrical impulse transmission properties. Velocity-VDI and FPA in MS-INO patients was then restored to baseline values following whole-body cooling, confirming the reversible and stereotyped nature of this characteristic feature of demyelination.
Conclusions: We have developed a neurophysiologic model for objectively understanding temperature-related reversible changes in axonal conduction in multiple sclerosis. Our observations corroborate the hypothesis that changes in core body temperature (heating and cooling) are associated with stereotypic decay and restoration in axonal conduction mechanisms.
This article has been cited by other articles:
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  A. Serra, K. Liao, M. Matta, and R. J. Leigh Diagnosing disconjugate eye movements: Phase-plane analysis of horizontal saccades Neurology, October 7, 2008; 71(15): 1167 - 1175. [Abstract] [Full Text] [PDF]
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 R. J. Fox, R. W. McColl, J.-C. Lee, T. Frohman, K. Sakaie, and E. Frohman A Preliminary Validation Study of Diffusion Tensor Imaging as a Measure of Functional Brain Injury Arch Neurol, September 1, 2008; 65(9): 1179 - 1184. [Abstract] [Full Text] [PDF]
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D. A. Mills, T. C. Frohman, S. L. Davis, A. R. Salter, S. McClure, I. Beatty, A. Shah, S. Galetta, E. Eggenberger, D. S. Zee, et al. BREAK IN BINOCULAR FUSION DURING HEAD TURNING IN MS PATIENTS WITH INO Neurology, August 5, 2008; 71(6): 458 - 460. [Full Text] [PDF]
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R. J. Leigh and A. Serra Taking the temperature of MS with INO Neurology, March 25, 2008; 70(13_Part_2): 1063 - 1064. [Full Text] [PDF]
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