Personal mobility is typically achieved through bipedal locomotion. When neurological disorders limit movements, there is potentially a downward spiral. Deconditioning further threatens a person’s capacity to meet the elevated energy demands of paretic or spastic gait. Deconditioning leads to abnormal metabolic function and gross atrophy, reducing muscular strength and endurance. This chain of events compromises walking and Activities of Daily Living (ADL) performance. Metabolic changes that occur in immobile muscle propagate the insulin-resistance syndrome linked to increased cardiovascular risk. Although many of the physiological sequelae are reversible with exercise, such exercise is often impossible because of disabling neurological conditions. In addition to adverse long-term physiological sequelae, immobility profoundly limits access across the social and physical environments, often impeding participation in substantial gainful activity long-term. This introduction of the symposium presents the stage for later segments by:
This model begins with the measurement of metabolic parameters associated with paretic or spastic gait during mobility and ADL performance inside and outside the laboratory, and ends with the expression of social and physical environmental facilitators and barriers to mobility. Strategies for developing technologies to increase mobility need to encompass all levels of this model. Whether biotechnologies are placed inside (functional and electrical stimulation), or outside the person (mobility enhancing aids that climb over architectural barriers), the objectives are to reduce the pathological sequelae of inactivity and to increase the ecological niche or range of activity sites where persons with mobility limitations can function.
Speakers:Kenneth Manton, Ph.D. - Demographics and Scope of the ProblemRichard Macko, M.D. - Secondary Physiological ChangesDavid B. Gray, Ph.D. - Where Does Mobility Get You?