04 and r = 0.26, p = 0.01, respectively.) There was a small negative correlation between the number of documented QMs and the number of PD follow-up visits the year after the index visit (r = -0.19, p = 0.05.) No other outcome showed a statistically significant correlation with the adherence to documented QMs. Conclusions We found no clinically important improvement in patient outcomes with higher adherence levels. It is important that QM developers validate QMs to ensure that they fulfill the intended goal of improved patient outcomes. © 2019 American Academy of Neurology.Objective To quantify health care resource utilization and risk of complications in painful diabetic peripheral neuropathy (pDPN). Methods Adult patients diagnosed with diabetes mellitus or diabetic peripheral neuropathy (DPN) were identified in MarketScan from January 2010 to December 2015. Subgroups (pDPN and nonpainful DPN) were based on the use of pain medications 6 months before a new indexed diagnosis and 1 year thereafter. Health care costs were collected for up to 5 years, and complications charted for those with at least 1 and 2 years of follow-up. Complication comparisons were made using χ2 or Fisher exact tests, and a multivariable regression cost model was fit with log link function using generalized estimating equations. Results Among 360,559 patients with diabetes (62 ± 14 years; 54.3% female), 84,069 (23.3%) developed pDPN, 17,267 (4.8%) experienced nonpainful DPN, and the majority (259,223, 71.9%) were controls with diabetes without neuropathy. At baseline, costs associated with pDPN patients were 20% higher than diabetic controls (95% confidence interval [CI] [1.19, 1.21], p less then 0.001), which increased to 31% in the 5th year (95% CI [1.27, 1.34], p less then 0.001). Patients with pDPN had 200%, 356%, and 224% of the odds of using opioids, anticonvulsants, and antidepressants, respectively, compared with diabetic controls. The amputation risk in the pDPN subgroup was 16.24 times that of diabetic controls (95% CI [2.15, 122.72], p = 0.0003), and 87% more patients with pDPN experienced lower extremity infections (95% CI [1.43, 2.46], p less then 0.0001) within a year.  https://www.selleckchem.com/products/alantolactone.html  Within 2 years, 2.2% of patients with pDPN had falls and fall-related injuries compared with 1.1% of diabetic controls (p less then 0.0001). Conclusions Our study characterizes a substantial pDPN cohort in the United States, demonstrating considerable morbidity and economic costs. © 2019 American Academy of Neurology.Background Strong evidence of mitochondrial dysfunction exists for both familial and sporadic Parkinson disease (PD). A simple test, reliably identifying mitochondrial dysfunction, could be important for future stratified medicine trials in PD. We previously undertook a comparison of serum biomarkers in classic mitochondrial diseases and established that serum growth differentiation factor 15 (GDF-15) outperforms fibroblast growth factor 21 (FGF-21) when distinguishing patients with mitochondrial diseases from healthy controls. This study aimed to systematically assess serum FGF-21 and GDF-15, together with mitochondrial DNA (mtDNA) copy number levels in peripheral blood cells from patients with PD and healthy controls, to determine whether these measures could act as a biomarker of PD. Methods One hundred twenty-one patients with PD and 103 age-matched healthy controls were recruited from a single center. Serum FGF-21 and GDF-15, along with blood mtDNA copy number, were quantified using established assays. Results There were no meaningful differences identified for any of the measures when comparing patients with PD with healthy controls. This highlights a lack of diagnostic sensitivity that is incompatible with these measures being used as biomarkers for PD. Conclusion In this study, serum FGF-21, serum GDF-15, and blood mtDNA levels were similar in patients with PD and healthy controls and therefore unlikely to be satisfactory indicators of mitochondrial dysfunction in patients with PD. Classification of evidence This study provides Class III evidence that serum FGF-21, serum GDF-15, and blood mtDNA copy number levels do not distinguish patients with PD from healthy controls. There was no diagnostic uncertainty between patients with PD and healthy controls. © 2019 American Academy of Neurology.Objective To assess the role of visual measures and retinal volume to predict the risk of Parkinson disease (PD) dementia. Methods In this cohort study, we collected visual, cognitive, and motor data in people with PD. Participants underwent ophthalmic examination, retinal imaging using optical coherence tomography, and visual assessment including acuity and contrast sensitivity and high-level visuoperception measures of skew tolerance and biological motion. We assessed the risk of PD dementia using a recently described algorithm that combines age at onset, sex, depression, motor scores, and baseline cognition. Results One hundred forty-six people were included in the study (112 with PD and 34 age-matched controls). The mean disease duration was 4.1 (±2·5) years. None of these participants had dementia. Higher risk of dementia was associated with poorer performance in visual measures (acuity ρ = 0.29, p = 0.0024; contrast sensitivity ρ = -0.37, p less then 0.0001; skew tolerance ρ = -0.25, p = 0.0073; and biological motion ρ = -0.26, p = 0.0054). In addition, higher risk of PD dementia was associated with thinner retinal structure in layers containing dopaminergic cells, measured as ganglion cell layer (GCL) and inner plexiform layer (IPL) thinning (ρ = -0.29, p = 0.0021; ρ = -0.33, p = 0.00044). These relationships were not seen for the retinal nerve fiber layer that does not contain dopaminergic cells and were not seen in unaffected controls. Conclusion Visual measures and retinal structure in dopaminergic layers were related to risk of PD dementia. Our findings suggest that visual measures and retinal GCL and IPL volumes may be useful to predict the risk of dementia in PD. Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.