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TitleMuscle Weakness in Persons with Multiple Sclerosis
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LanguageEnglish
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Table of Contents
                            University of Massachusetts Amherst
[email protected] Amherst
	9-2010
Muscle Weakness in Persons with Multiple Sclerosis
	Linda Haiwon Chung
		Recommended Citation
ACKNOWLEDGMENTS
ABSTRACT
PREFACE
LIST OF TABLES
LIST OF FIGURES
CHAPTER 1
INTRODUCTION
	Multiple Sclerosis
	Factors That Influence Muscle Strength and Power
	Skeletal Muscle Weakness in Persons with MS
	Postural Control in Persons with MS
	Strength Training in Persons with MS
	Significance of Dissertation
	Study 1:  Mechanisms of Muscle Weakness in Persons with MS
	Study 2:  Resistance Training in Persons with MS
		Aim #1
		Aim #2
CHAPTER 2
LITERATURE REVIEW
	Introduction
	Sources of muscle weakness in persons with MS
		Central Nervous System
		Neuromuscular Transmission
		Muscle Size
		Contractile Function
		Spasticity
		Summary:  Sources of muscle weakness in persons with MS
	Physical Function and Postural Stability in MS
		Postural control
		Gait
		Effect of muscle strength on postural control and physical function
		Summary:  Physical function and postural stability in MS
	Effect of resistance training on motor performance in MS
		Summary:  Effect of resistance training on motor performance in MS
CHAPTER 3
PROPOSED METHODS FOR STUDY 1
	Participants
	Experimental Design
	Biodex Isokinetic Dynamometer
		Passive Torque Protocol
		Isometric Contraction Protocol
		Dynamic Contraction Protocol
		Electrical Stimulation Protocol
	Intramuscular EMG Protocol
	Magnetic Resonance Imaging (MRI) Protocol
	Data Processing
		Strength and Power
		Neuromuscular Drive
		Contractile Function
		Spasticity and Coactivation of Spastic Antagonist Muscles
	Statistical Analyses
CHAPTER 4
PROPOSED METHODS FOR STUDY 2
	Participants
	Experimental Design
	Biodex Isokinetic Dynamometer
		Isometric Contraction Protocol
		Dynamic Contraction Protocol
	Postural Control Protocol
	Intramuscular EMG Protocol
	Resistance Training Protocol
		Data Processing
	Statistical Analyses
CHAPTER 5
MECHANISMS OF MUSCLE WEAKNESS IN PERSONS WITH MULTIPLE SCLEROSIS
	Abstract
	Introduction
	Methods
		Study Design
		Group Characteristics
		Isometric Strength and Power
		Neural Factors
		Muscle Factors
		Statistical Analyses
	Results
		Group Characteristics
		Muscle Weakness in MS
		Neural Mechanisms
		Muscle Mechanisms
	Discussion
		Muscle weakness in MS
		Smaller muscles, similar specific strength, and lower specific power in MS
		No difference in the RFD during a stimulated contraction across groups
		Slower MUDR in persons with MS
		Spasticity in MS
		Voluntary RFD is not different across groups
		Future Directions
		Conclusion
	Acknowledgements
	Figure legends
CHAPTER 6
PRÉCIS OF DISSERTATION
	Novelty
	Significance and Impact
	Future Directions
APPENDIX A.
ENERGY COST OF WALKING, SYMPTOMATIC FATIGUE AND PERCEIVED EXERTION IN PERSONS WITH MULTIPLE SCLEROSIS
APPENDIX B
LIST OF MEDICATIONS
APPENDIX C
ASSOCIATIONS BETWEEN ISOMETRIC TORQUE, DYNAMIC POWER, AND PHYSICAL FUNCTION
APPENDIX D
COMPARISONS OF NEUROMUSCULAR VARIABLES BETWEEN NON-SPASTIC AND PERSONS WITH SPASTICITY
APPENDIX E
ASSOCIATIONS BETWEEN SPASTICITY AND PHYSICAL FUNCTION IN PERSONS WITH MS
APPENDIX F
ANCILLARY MEASURES TO CHAPTER 5
APPENDIX G
TABLE OF UNIT CONVERSIONS
APPENDIX H
PARTICIPANT FORMS
BIBLIOGRAPHY
                        
Document Text Contents
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University of Massachusetts Amherst
[email protected] Amherst

Open Access Dissertations

9-2010

Muscle Weakness in Persons with Multiple
Sclerosis
Linda Haiwon Chung
University of Massachusetts Amherst, [email protected]

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MUSCLE WEAKNESS IN PERSONS WITH MULTIPLE SCLEROSIS








A Dissertation Presented


by


LINDA H. CHUNG










Submitted to the Graduate School of the
University of Massachusetts Amherst in partial fulfillment

of the requirements for the degree of


DOCTOR OF PHILOSOPHY



September 2010


Kinesiology

Page 99

factors, such as lower MUDR, were likely explaining lower peak power production in

MS.

No difference in the RFD during a stimulated contraction across groups

The maximum RFD elicited by electrical stimulation has been used in previous

studies as a measure of the rate of cross-bridge cycling (28; 30; 113). We observed no

difference in the RFD in the KE between persons with and without MS, suggesting that

the rate of cross-bridge cycling was similar across groups. De Haan et al. (28) have

observed no differences in RFD between MS and control, using a current intensity to

elicit 30% MVIC in the KE. The lack of difference in RFD between groups may be

that the current intensity used to elicit submaximal torque was insufficient to recruit all

muscle fibers. However, using a supramaximal stimulus, de Ruiter et al. (30) showed

similar RFD across groups in the adductor pollicis muscle, whereas Sharma et al. (113)

showed lower RFD in the ankle dorsiflexors in MS compared with control. At the

single fiber level, cross-bridge kinetics were not different between persons with MS and

controls (17; 44), supporting our observations. Thus, cross-bridge kinetics are likely

not a mechanism for muscle weakness in persons with MS.

Slower MUDR in persons with MS

We observed that persons with MS had ~20% slower maximal MUDR in the

vastus lateralis muscle compared with controls. Only one other study has examined

MUDR during a MVIC and observed ~ 46% lower maxMUDR in a small group of 4

ambulatory persons with MS compared with 16 controls (106). Notably, motor unit

discharge variability during a maximal voluntary contraction was not different between

groups, suggesting that the pattern of motor unit discharges is similar between MS and

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control. No studies have examined motor unit discharge variability during maximal

contractions in persons with MS compared with control. However, Dorfman et al. (33)

observed increased motor unit discharge variability in MS compared with control

during submaximal contractions in various muscle groups (brachial biceps, brachial

triceps, anterior tibial).

Slower rate-coding may be a consequence of demyelination in MS, generating

prolonged motor conduction (12; 43; 123) and after-hyperpolarization period (10; 12) in

persons with MS. Redistribution of sodium channels in the demyelinated areas of the

axon (25) may explain the slowed recovery of the motor neuron (10; 12). Maximal

MUDR may account for ~31% and 26% of the variance in isometric strength and

power, respectively, indicating the importance of rate-coding on both contraction

modes. In addition, maximal MUDR was shown to explain 25% of the variance in

specific power, suggesting that rate-coding may be one mechanism of specific power.

Spasticity in MS

Spasticity can be a significant problem in persons with MS. Spasticity in an

antagonist muscle is a potential mechanism for power loss in an agonist muscle,

because of the antagonist’s resistance to passive movement due to a hyperexcitable

stretch reflex (64). Antagonist co-activation may slow the velocity of a dynamic

contraction and, thus, decrease the power generated by an agonist muscle. This

phenomenon could explain some of the muscle weakness in MS, particularly during

high-velocity contractions. Using the dynamometer, we showed no difference in KF

passive torque during knee extension between persons with MS and controls. The

percentage of KF passive-to-KE voluntary torque was slightly higher in persons with

83

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