title: Modeling Uhthoff's phenomenon in MS patients with internuclear ophthalmoparesis.
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 degrees 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.
authors.affiliation: Institute for Exercise & Environmental Medicine, Presbyterian Hospital of Dallas, TX, USA.
authors.forename: S L
authors.initials: SL
authors.lastname: Davis
authors.forename: T C
authors.initials: TC
authors.lastname: Frohman
authors.forename: C G
authors.initials: CG
authors.lastname: Crandall
authors.forename: M J
authors.initials: MJ
authors.lastname: Brown
authors.forename: D A
authors.initials: DA
authors.lastname: Mills
authors.forename: P D
authors.initials: PD
authors.lastname: Kramer
authors.forename: O
authors.initials: O
authors.lastname: Stüve
authors.forename: E M
authors.initials: EM
authors.lastname: Frohman
mesh_terms: D000200:Action Potentials / Q000502:physiology; D001369:Axons / Q000473:pathology; D001831:Body Temperature / Q000502:physiology*; D001933:Brain Stem / Q000473:pathology / Q000503:physiopathology*; D005334:Fever / Q000150:complications / Q000503:physiopathology; D006801:Humans; D006979:Hyperthermia, Induced; D007036:Hypothermia, Induced; D008959:Models, Neurological; D009103:Multiple Sclerosis / Q000150:complications / Q000503:physiopathology*; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D009431:Neural Conduction / Q000502:physiology*; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D015835:Ocular Motility Disorders / Q000209:etiology / Q000503:physiopathology*; D009801:Oculomotor Muscles / Q000294:innervation / Q000503:physiopathology; D011149:Pons / Q000473:pathology / Q000503:physiopathology; D012016:Reference Values; D012438:Saccades / Q000502:physiology