Differentiating Extensor Plantar Response in Pathological and Normal Population.

INTRODUCTION: Approximately 5%-11% of neurologically normal population has extensor plantar response (EPR). METHOD: This study is aimed to identify differentiating features of EPR between physiological and pathological population. RESULTS: A total of 43 patients with pyramidal lesions and 113 normal controls were recruited for this study. The pathological EPRs were more reproducible, with 89.4% having at least two positive Babinski responses and 91.5% having two positive Chaddock responses (vs. 14.3% and 4.8% in controls, P < 0.001). The pathological EPR was more sensitive to stimulation, in which 89.1% were elicited when the stimulation reached mid-lateral sole (vs. 11.9% in controls, P < 0.001). Most (93.6%) pathological cases had sustained big toe extension throughout stimulation (vs. 73.8% in controls, P < 0.001). As compared to those with brain lesion, the plantar responses in those with spinal lesion are less likely to have ankle dorsiflexion (5.3% vs. 25%, P < 0.05) more likely to have sustained extensor response with Babinski (94.7% vs. 71.4%, P < 0.05), Chaddock (89.5% vs. 64.3%, P < 0.05), and Schaefer (26.3% vs. 3.6%, P < 0.05) methods. A scoring system was computed using four variables, i.e., two consecutive positive Babinski or Chaddock responses, extensor response at mid-lateral sole, and sustained extension throughout stimulation. A score ≥3 is predictive of pathological origin, with sensitivity and specificity of 78.7% and 95.2%, respectively. CONCLUSION: The pathological EPR is more reproducible, sensitive to stimulation, and sustainable compared to physiological extensor response.

Altered body composition, sarcopenia, frailty, and their clinico-biological correlates, in Parkinson's disease.

INTRODUCTION: Low body weight in Parkinson's disease (PD) is poorly understood despite the associated risks of malnutrition, fractures, and death. Sarcopenia (loss of muscle bulk and strength) and frailty are geriatric syndromes that are likewise associated with adverse health outcomes, yet have received scant attention in PD. We studied body composition, sarcopenia, frailty, and their clinico-biological correlates in PD. METHODS: 93 patients and 78 spousal/sibling controls underwent comprehensive assessment of diet, clinical status, muscle strength/performance, frailty, body composition (using dual-energy X-ray absorptiometry), and serum levels of neurogastrointestinal hormones and inflammatory markers. RESULTS: PD patients were older than controls (66.0 ±â€¯8.5 vs. 62.4 ±â€¯8.4years, P = 0.003). Mean body mass index (24.0 ±â€¯0.4 vs. 25.6 ±â€¯0.5kg/m2, Padjusted = 0.016), fat mass index (7.4 ±â€¯0.3 vs. 9.0 ±â€¯0.3kg/m2, Padjusted<0.001), and whole-body fat percentage (30.7 ±â€¯0.8 vs. 35.7 ±â€¯0.9%, Padjusted<0.001) were lower in patients, even after controlling for age and gender. There were no between-group differences in skeletal muscle mass index and whole-body bone mineral density. Body composition parameters did not correlate with disease duration or motor severity. Reduced whole-body fat percentage was associated with higher risk of motor response complications as well as higher levels of insulin-growth factor-1 and inflammatory markers. PD patients had a higher prevalence of sarcopenia (17.2% vs. 10.3%, Padjusted = 0.340) and frailty (69.4% vs. 24.2%, Padjusted = 0.010). Older age and worse PD motor severity were predictors of frailty in PD. CONCLUSIONS: We found reduced body fat with relatively preserved skeletal muscle mass, and a high prevalence of frailty, in PD. Further studies are needed to understand the patho-mechanisms underlying these alterations.