Energy Costs of Spasticity in Spinal Cord Injury: A Pilot Investigation
| Status: | Terminated |
|---|---|
| Conditions: | Hospital, Neurology |
| Therapuetic Areas: | Neurology, Other |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 4/21/2016 |
| Start Date: | January 2008 |
| End Date: | July 2010 |
The purpose of this study is to determine if there is a relationship between spasticity and
relative changes in Basal Energy Expenditure in persons with spinal cord injury.
relative changes in Basal Energy Expenditure in persons with spinal cord injury.
Obesity is at epidemic proportions in the population with spinal cord injury (SCI), and is
likely the mediator of the metabolic syndrome in this special population. Recent literature
reviews have suggested that obesity is present in > 67% of persons with SCI. Additionally,
recent studies have demonstrated the causal relationship between adipose tissue accumulation
and vascular inflammation, dyslipidemia, insulin resistance / glucose intolerance,
hypertension and thromboemboli.
Obesity in SCI occurs because of acute and ongoing positive energy balance, i.e., greater
caloric intake than energy expenditure. Total Daily Energy Expenditure (TDEE) in SCI is
reduced primarily because of muscular atrophy and diminished muscular contraction;
pharmacological treatment of spasticity possibly reduces energy expenditure (EE) even
further, but has not been evaluated to date. TDEE is comprised of three components: Basal
Energy Expenditure (BEE), Thermic Effect of Activity (TEA) and Thermic Effect of Food (TEF).
Of the three, BEE contributes the greatest amount (65-75% TDEE) and is the most sensitive to
changes in spasticity.
Dampening spasticity has been reported to increase weight gain and necessitate reduced
caloric intake in a child with spastic quadriplegia. Similarly, athetosis in patients with
cerebral palsy increased resting metabolic rate (RMR) as compared to control subjects with
no athetotic movements. Although several studies have reported energy requirements for
persons with neurodevelopmental disabilities, and even SCI, however, none have attempted to
measure the metabolic effect of spasticity.
likely the mediator of the metabolic syndrome in this special population. Recent literature
reviews have suggested that obesity is present in > 67% of persons with SCI. Additionally,
recent studies have demonstrated the causal relationship between adipose tissue accumulation
and vascular inflammation, dyslipidemia, insulin resistance / glucose intolerance,
hypertension and thromboemboli.
Obesity in SCI occurs because of acute and ongoing positive energy balance, i.e., greater
caloric intake than energy expenditure. Total Daily Energy Expenditure (TDEE) in SCI is
reduced primarily because of muscular atrophy and diminished muscular contraction;
pharmacological treatment of spasticity possibly reduces energy expenditure (EE) even
further, but has not been evaluated to date. TDEE is comprised of three components: Basal
Energy Expenditure (BEE), Thermic Effect of Activity (TEA) and Thermic Effect of Food (TEF).
Of the three, BEE contributes the greatest amount (65-75% TDEE) and is the most sensitive to
changes in spasticity.
Dampening spasticity has been reported to increase weight gain and necessitate reduced
caloric intake in a child with spastic quadriplegia. Similarly, athetosis in patients with
cerebral palsy increased resting metabolic rate (RMR) as compared to control subjects with
no athetotic movements. Although several studies have reported energy requirements for
persons with neurodevelopmental disabilities, and even SCI, however, none have attempted to
measure the metabolic effect of spasticity.
Inclusion Criteria:
- C1-T10 SCI at least 1 year post injury
- Spasticity in the legs
- Veteran
Exclusion Criteria:
- Recent increase in spasticity
- Botox within 6 months
- Phenol within 2 years
- Prior surgery for spasticity
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