Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury

Abstract

Design: Cross-sectional. Objectives: (1) To determine the effects of the level of spinal cord injury (SCI) on skeletal muscle, intramuscular fat (IMF) cross-sectional areas (CSAs) and relative IMF; (2) to determine the relation, if any, of spasticity to each of these variables after incomplete SCI. Settings: In-patient study at the Shepherd Center, Atlanta, GA, USA. Methods: Thirteen individuals with incomplete SCI were classified according to their level of injury into a high level of injury group (HLI, C5-C7, n ¼ 8) and a low level of injury group (LLI, T12-L2, n ¼ 5). Spasticity was determined for thigh muscles using a modified Ashworth scale at 6 weeks post-injury. T1-weighted magnetic resonance (MR) images were taken 6 weeks post-injury to measure thigh skeletal muscle and IMF CSAs. Results: Spasticity was significantly evident in the HLI group compared to the LLI group (P ¼ 0.023). Six weeks post-injury, muscle CSA was 103718 cm 2 in the HLI group and 80720 cm 2 in the LLI group (P ¼ 0.042). Relative IMF was 3.672.0% in HLI and 7.574.0% in LLI (P ¼ 0.021). Additionally, spasticity accounted for 54% of the variability in muscle CSA for all subjects (r 2 ¼ 0.54, P ¼ 0.006). Conclusions: Spasticity may be an important factor in defending skeletal muscle size and indirectly preventing IMF accumulation early after incomplete SCI.

Oral baclofen administration in persons with chronic spinal cord injury does not prevent the protective effects of spasticity on body composition and glucose homeostasis

“…11 We were unable to accept our hypothesis because our current findings showed that a long-term administration of the same dose of oral baclofen does not interfere with the protective effects of spasticity on body composition and metabolic profile that were noted earlier. [7][8][9] Moreover, a potential protective effect was observed on glucose homeostasis.…”

“…Some patients have difficulty comprehending that the goal of treatment is spasticity control and not elimination, because a threshold level of spasticity is necessary to maintain muscle mass and enhance glucose homeostasis. 7,8 For example, those with MAS 42 have a greater skeletal muscle cross-sectional area by 420%. 7 Moreover, extensor spasticity has recently been shown to be correlated with a reduction in FM and increase in FFM after motor complete SCI.…”

“…A lower motor neuron injury is typically seen in those with an injury below T11 and leads to flaccid paralysis of the involved skeletal muscles. 7 Exclusion criteria included cardiovascular diseases, hypertension, diabetes mellitus, hyperlipidemia, cigarette smoking and pressure ulcers of Grade II or above. All SCI individuals with a BMI 435 were excluded to avoid the potentially confounding effects of a greatly expanded FM.…”

“…This statistical approach was adopted because the relationships could possibly be affected by variance in spasticity scores among participants. 7 A cutoff of 60 mg per day of oral baclofen was used to determine the effect of high-vs low-dose administration on the magnitudes of body composition and fluid (ICF, ECF and TBW). All values were presented as mean±s.d.…”

“…However, along with others, we have shown that spasticity could protect against skeletal muscle atrophy, impaired glucose tolerance and deterioration in body composition after SCI. [7][8][9] Recently, spasticity was strongly associated with increased FFM in motor complete SCI; maintenance of FFM primarily resulted in improved energy expenditure, insulin sensitivity and lipid profile. 9 In addition, spastic leg skeletal muscles have a three times higher glucose uptake than do controls.…”