MSK Consequences of SCI

Mechanisms of bone loss due to SCI

imbalance in bone formation and reabsorption, loss of loading and normal muscle pull, bone/fat relationships

when is bone loss greatest in SCI?

first 6 months with rapid decline continuing for first 2 years

what changes in bone are seen in the first 2 years post SCI?

cortical thinning, decreased trabecular bone

most common fracture sites for people with SCI

distal femur and proximal tibia (falls out of wheelchair and transfer twisting injuries)

is spine bone mineral density affected by SCI

not significantly

how does fracture risk change post SCI?

increases up to 46%, more non-traumatic occurrences, increased complications and hospital stays

posible complications of fractures in SCI population

pressure ulcers, respiratory illness, UTI, AD, spasticity, delirium. nonunion, mortality, decreased mobility/independence

how do bone and muscle impact each other?

muscle pulls on bone to impact geometry, muscle CSA and bone density are related, muscle functions as endocrine tissue to regulate glucose metabolism

what factors influence muscle mass?

genetics, activity, age, neurologic factors/motor unit health, metabolic factors, endocrine function, inflammation/chronic disease

how long does it take for muscle atrophy to occur after SCI

very quick (depends on the muscle but can be 10-20% decline by 25 weeks)

what changes are seen in muscle after SCI?

atrophy, fatty deposits, slow to fast fiber transition, becomes more fatiguable

metabolic consequences of decreased muscle mass

reduced energy expenditure, increased adiposity, intramuscular adipose tissue doubles, increased visceral adipose tissue

how common is overweight/obesity in SCI?

66%

BMI and waist circumference both _____ obesity in SCI. Why?

underestimate, because people with SCI lose muscle an gain fat

gold standard for assessing obesity in SCI

fat mass over 20%

potential complications of increased adiposity due to SCI

hyperglycemia, dislipidemia, insulin resistance, diabetes, metabolic syndrome, CV disease

how common is metabolic syndrome in chronic SCI?

55%

how common is insulin resistance in chronic SCI?

60%

how common is diabetes in chronic SCI?

50%

what components make up metabolic syndrome?

hyperglycemia, dyslipidemia, hypertension, abdominal obesity

how much higher is the risk of CAD in people with paraplegia?

70% higher

how much higher is the risk of CV disease in people with tetraplegia?

5x higher

what is the primary cause of death in people with chronic SCI?

CV disease

Treatment options to mitigate MSK impacts of SCI

e-stim for strengthening, FES

Potential benefits of e-stim

improved body composition (muscle to fat), bone, CV/metabolism, pumonary, spasticity, functional, QOL

contraindications/precautions to e-stim

bone density/fracture history (use clinical judgement), pacemaker, uncontrolled AD, uncontrolled hyper/hypotension, open skin, thrombosis, pregnancy, cancer, ROM limits that impact activity

how does FES/NMES resistance training impact muscle?

increased muscle size/CSA, stops or reverses atrophy , improves body composition and metabolism, increased power output and strength, increased muscle health

how does FES/NMES resistance training impact fat?

less effect than on muscle, some studies showed modest changes

how does FES/NMES resistance training impact CV/metabolism?

decreased intra-muscular fat, increased plasma glucose/muscle glucose uptake, improved CV/metabolic outcomes

what is needed in an e-stim intervention to produce changes in bone?

strong visible contractions, resistance, at least 1 year of intervention (takes more time to change)

how does FES/NMES resistance training impact bone?

lower level evidence- may prevent bone mineral density decline and partially reverse bone mineral loss (long intervention period and resistance are needed)

challenges with the literature on e-stim interventions

Inconsistent methodology makes comparison hard, inadequate dosing may explain the lack of effects or decreased effects

consideration when using HR to measure intensity in the SCI population

autonomic dysfunction

Measures of intervention intensity

RPE, VO2, power output, loading, HR

key point when using NMES intervention

a strong contraction must be elicited

FES and NMES have a greater effect on _____ than on ______

muscle, bone

how can FES/NMES intervention effect fiber type

reverse the fiber type change by increasing the amount of slow/intermediate fibers→ makes muscles less fatiguable and increases VO2

how is muscle impacted in the stroke population?

preferential atrophy of type II (fast) fibers and hypertrophy of type I fibers

how is bone impacted in the stroke population?

1.82x higher risk of osteoporosis

how is muscle impacted in the MS population?

increased fast twitch fibers

how is bone impacted in the MS population?

decreased BMD (secondary to immobility or meds)

how is muscle impacted in the Parkinson’s Disease population?

Type I (slow) fiber hypertrophy and Type II fiber atrophy in some cases

how is bone impacted in the Parkinson’s Disease population?

higher incidence of osteoporosis

how is bone impacted in the TBI population?

decreased BMD and HO→ pituitary and hypothalamic nuclei play role in regulation of bone remodeling