Arson, figure 4 A) and GCIP thickness (p = 0.0141, r = 0.35, Pearson, figure 4 B). The mean macular thickness of Wilson’s disease patients correlated positively with the thickness of 
all of the macular layers except for the OPL (all p,0.05, GCIP: p,0.0001, r = 0.67; INL: p = 0.0008, r = 0.51; ONL: p = 0.0008; r = 0.47, Pearson, figure 4 C ). For the manually segmented paramacular layers, we observed weak but significant positive correlations between the thickness of the GCIP and INL (p = 0.0398, r = 0.32, Pearson, 
figure 4 F) and between the INL and ONL (p = 0.0389, r = 0.33, Pearson, figure 4 G). A Methionine enkephalin site thinner RNFL, macular thickness and GCIP appeared to be associated with longer P100 and N75 latencies and lower VEP amplitudes. However, only ONL thickness and N75 latency were significantly correlated (p = 0.0073, 76932-56-4 buy BI 78D3 Pearson r = 0.50, figure 4 H) and the correlation was actually positive. Of note is that the ONLwas not altered in Wilson’s disease patients compared with controls. We observed no significant correlation between the clinical Wilson score or the time since diagnosis of the disease and the thickness of any retinal layer or with any VEP parameter. Additionally, the Wilson score did not correlate with the time since diagnosis (Spearman). An analysis of the laboratory parameters of our patients revealed weak positive correlations of both the N75 latency and the P100 latency with the concentrations of copper and caeruloplasmin in serum (N75: p = 0.0046 and p = 0.0188 respectively, both r = 0.52, Pearson, figure 5 A+B; P100: p = 0.0052 and, p = 0.0207 respectively, Pearson r = 0.52 and r = 0.45 respectively figure 5 C+D). As all correlations of VEP parameters were very much influenced by one outlier with a N75 latency of 109 ms and a P100 latency of 130 ms, 18055761 we recalculated the correlations again after removing this patient from the analysis (dotted lines in figure 4 H and 5 A ). Without the outlier, the correlations with VEP parameters were not significant whereas P100 and N75 still differed significantly 
in the group comparison between Wilson’s disease and controls (t-test, p = 0.0019 and p = 0.0182, respectively). The mean OPL thickness was weakly but significantly correlated with the concentrations of copper (p = 0.0181, r = 0.36, Pearson Figure 5 E) and caeruloplasmin in serum (p,0.05, r = 0.32, Pearson, figure 5 F). The copper MedChemExpress 3PO concentration in 24 h urine showed a weak positive correlation with the clinical Wilson score (p = 0.0402, r = 0.37, Spearman, figure 5 G) and a stronger positive correlation with the caeruloplasmin concentration in serum (p,0.0001, r = 0.86, Pearson, Figure 5 H).Optical Coherence Tomography in Wilsons’s Disease(p,0.0024), INL (p = 0.0192), and ONL (p = 0.0192) and of copper in urine with caeruloplasmin in serum (p,0.0024) remained significant. The clinical and laboratory parameters may influence VEPand OCT parameters. We therefore performed a multivariate correlation analysis adjusting for age, sex, the clinical disease score and the concentrations of caeruloplasmin in serum and of copper in serum and urine. When controlling for these variables, macular thickness was significantly correlated with RNFL (p = 0.002, r = 0.67), GCIP (p = 0.001, r = 0.72), INL (p = 0.020, r = 0.50) and ONL (p = 0.025, r = 0.51). RNFL was correlated with GCIP (p = 0.005, r = 0.611), INL (p = 0.028, r = 0.50) and ONL (p = 0.025, r = 0.511). To test if any of the clinical parameters had influence on the retinal changes observed, we p.Arson, figure 4 A) and GCIP thickness (p = 0.0141, r = 0.35, Pearson, figure 4 B). The mean macular thickness of Wilson’s disease patients correlated positively with the thickness of all of the macular layers except for the OPL (all p,0.05, GCIP: p,0.0001, r = 0.67; INL: p = 0.0008, r = 0.51; ONL: p = 0.0008; r = 0.47, Pearson, figure 4 C ). For the manually segmented paramacular layers, we observed weak but significant positive correlations between the thickness of the GCIP and INL (p = 0.0398, r = 0.32, Pearson, figure 4 F) and between the INL and ONL (p = 0.0389, r = 0.33, Pearson, figure 4 G). A thinner RNFL, macular thickness and GCIP appeared to be associated with longer P100 and N75 latencies and lower VEP amplitudes. However, only ONL thickness and N75 latency were significantly correlated (p = 0.0073, Pearson r = 0.50, figure 4 H) and the correlation was actually positive. 
Of note is that the ONLwas not altered in Wilson’s disease patients compared with controls. We observed no significant correlation between the clinical Wilson score or the time since diagnosis of the disease and the thickness of any retinal layer or with any VEP parameter. Additionally, the Wilson score did not correlate with the time since diagnosis (Spearman). An analysis of the laboratory parameters of our patients revealed weak positive correlations of both the N75 latency and the P100 latency with the concentrations of copper and caeruloplasmin in serum (N75: p = 0.0046 and p = 0.0188 respectively, both r = 0.52, Pearson, figure 5 A+B; P100: p = 0.0052 and, p = 0.0207 respectively, Pearson r = 0.52 and r = 0.45 respectively figure 5 C+D). As all correlations of VEP parameters were very much influenced by one outlier with a N75 latency of 109 ms and a P100 latency of 130 ms, 18055761 we recalculated the correlations again after removing this patient from the analysis (dotted lines in figure 4 H and 5 A ). Without the outlier, the correlations with VEP parameters were not significant whereas P100 and N75 still differed significantly in the group comparison between Wilson’s disease and controls (t-test, p = 0.0019 and p = 0.0182, respectively). The mean OPL thickness was weakly but significantly correlated with the concentrations of copper (p = 0.0181, r = 0.36, Pearson Figure 5 E) and caeruloplasmin in serum (p,0.05, r = 0.32, Pearson, figure 5 F). The copper concentration in 24 h urine showed a weak positive correlation with the clinical Wilson score (p = 0.0402, r = 0.37, Spearman, figure 5 G) and a stronger positive correlation with the caeruloplasmin concentration in serum (p,0.0001, r = 0.86, Pearson, Figure 5 H).Optical Coherence Tomography in Wilsons’s Disease(p,0.0024), INL (p = 0.0192), and ONL (p = 0.0192) and of copper in urine with caeruloplasmin in serum (p,0.0024) remained significant. The clinical and laboratory parameters may influence VEPand OCT parameters. We therefore performed a multivariate correlation analysis adjusting for age, sex, the clinical disease score and the concentrations of caeruloplasmin in serum and of copper in serum and urine. When controlling for these variables, macular thickness was significantly correlated with RNFL (p = 0.002, r = 0.67), GCIP (p = 0.001, r = 0.72), INL (p = 0.020, r = 0.50) and ONL (p = 0.025, r = 0.51). RNFL was correlated with GCIP (p = 0.005, r = 0.611), INL (p = 0.028, r = 0.50) and ONL (p = 0.025, r = 0.511). To test if any of the clinical parameters had influence on the retinal changes observed, we p.Arson, figure 4 A) and GCIP thickness (p = 0.0141, r = 0.35, Pearson, figure 4 B). The mean macular thickness of Wilson’s disease patients correlated positively with the thickness of all of the macular layers except for the OPL (all p,0.05, GCIP: p,0.0001, r = 0.67; INL: p = 0.0008, r = 0.51; ONL: p = 0.0008; r = 0.47, Pearson, figure 4 C ). For the manually segmented paramacular layers, we observed weak but significant positive correlations between the thickness of the GCIP and INL (p = 0.0398, r = 0.32, Pearson, figure 4 F) and between the INL and ONL (p = 0.0389, r = 0.33, Pearson, figure 4 G). A thinner RNFL, macular thickness and GCIP appeared to be associated with longer P100 and N75 latencies and lower VEP amplitudes. However, only ONL thickness and N75 latency were significantly correlated (p = 0.0073, Pearson r = 0.50, figure 4 H) and the correlation was actually positive. Of note is that the ONLwas not altered in Wilson’s disease patients compared with controls. We observed no significant correlation between the clinical Wilson score or the time since diagnosis of the disease and the thickness of any retinal layer or with any VEP parameter. Additionally, the Wilson score did not correlate with the time since diagnosis (Spearman). An analysis of the laboratory parameters of our patients revealed weak positive correlations of both the N75 latency and the P100 latency with the concentrations of copper and caeruloplasmin in serum (N75: p = 0.0046 and p = 0.0188 respectively, both r = 0.52, Pearson, figure 5 A+B; P100: p = 0.0052 and, p = 0.0207 respectively, Pearson r = 0.52 and r = 0.45 respectively figure 5 C+D). As all correlations of VEP parameters were very much influenced by one outlier with a N75 latency of 109 ms and a P100 latency of 130 ms, 18055761 we recalculated the correlations again after removing this patient from the analysis (dotted lines in figure 4 H and 5 A ). Without the outlier, the correlations with VEP parameters were not significant whereas P100 and N75 still differed significantly in the group comparison between Wilson’s disease and controls (t-test, p = 0.0019 and p = 0.0182, respectively). The mean OPL thickness was weakly but significantly correlated with the concentrations of copper (p = 0.0181, r = 0.36, Pearson Figure 5 E) and caeruloplasmin in serum (p,0.05, r = 0.32, Pearson, figure 5 F). The copper concentration in 24 h urine showed a weak positive correlation with the clinical Wilson score (p = 0.0402, r = 0.37, Spearman, figure 5 G) and a stronger positive correlation with the caeruloplasmin concentration in serum (p,0.0001, r = 0.86, Pearson, Figure 5 H).Optical Coherence Tomography in Wilsons’s Disease(p,0.0024), INL (p = 0.0192), and ONL (p = 0.0192) and of copper in urine with caeruloplasmin in serum (p,0.0024) remained significant. The clinical and laboratory parameters may influence VEPand OCT parameters. We therefore performed a multivariate correlation analysis adjusting for age, sex, the clinical disease score and the concentrations of caeruloplasmin in serum and of copper in serum and urine. When controlling for these variables, macular thickness was significantly correlated with RNFL (p = 0.002, r = 0.67), GCIP (p = 0.001, r = 0.72), INL (p = 0.020, r = 0.50) and ONL (p = 0.025, r = 0.51). RNFL was correlated with GCIP (p = 0.005, r = 0.611), INL (p = 0.028, r = 0.50) and ONL (p = 0.025, r = 0.511). To test if any of the clinical parameters had influence on the retinal changes observed, we p.Arson, figure 4 A) and GCIP thickness (p = 0.0141, r = 0.35, Pearson, figure 4 B). The mean macular thickness of Wilson’s disease patients correlated positively with the thickness of all of the macular layers except for the OPL (all p,0.05, GCIP: p,0.0001, r = 0.67; INL: p = 0.0008, r = 0.51; ONL: p = 0.0008; r = 0.47, Pearson, figure 4 C ). For the manually segmented paramacular layers, we observed weak but significant positive correlations between the thickness of the GCIP and INL (p = 0.0398, r = 0.32, Pearson, figure 4 F) and between the INL and ONL (p = 0.0389, r = 0.33, Pearson, figure 4 G). A thinner RNFL, macular thickness and GCIP appeared to be associated with longer P100 and N75 latencies and lower VEP amplitudes. However, only ONL thickness and N75 latency were significantly correlated (p = 0.0073, Pearson r = 0.50, figure 4 H) and the correlation was actually positive. Of note is that the ONLwas not altered in Wilson’s disease patients compared with controls. We observed no significant correlation between the clinical Wilson score or the time since diagnosis of the disease and the thickness of any retinal layer or with any VEP parameter. Additionally, the Wilson score did not correlate with the time since diagnosis (Spearman). An analysis of the laboratory parameters of our patients revealed weak positive correlations of both the N75 latency and the P100 latency with the concentrations of copper and caeruloplasmin in serum (N75: p = 0.0046 and p = 0.0188 respectively, both r = 0.52, Pearson, figure 5 A+B; P100: p = 0.0052 and, p = 0.0207 respectively, Pearson r = 0.52 and r = 0.45 respectively figure 5 C+D). As all correlations of VEP parameters were very much influenced by one outlier with a N75 latency of 109 ms and a P100 latency of 130 ms, 18055761 we recalculated the correlations again after removing this patient from the analysis (dotted lines in figure 4 H and 5 A ). Without the outlier, the correlations with VEP parameters were not significant whereas P100 and N75 still differed significantly in the group comparison between Wilson’s disease and controls (t-test, p = 0.0019 and p = 0.0182, respectively). The mean OPL thickness was weakly but significantly correlated with the concentrations of copper (p = 0.0181, r = 0.36, Pearson Figure 5 E) and caeruloplasmin in serum (p,0.05, r = 0.32, Pearson, figure 5 F). The copper concentration in 24 h urine showed a weak positive correlation with the clinical Wilson score (p = 0.0402, r = 0.37, Spearman, figure 5 G) and a stronger positive correlation with the caeruloplasmin concentration in serum (p,0.0001, r = 0.86, Pearson, Figure 5 H).Optical Coherence Tomography in Wilsons’s Disease(p,0.0024), INL (p = 0.0192), and ONL (p = 0.0192) and of copper in urine with caeruloplasmin in serum (p,0.0024) remained significant. The clinical and laboratory parameters may influence VEPand OCT parameters. We therefore performed a multivariate correlation analysis adjusting for age, sex, the clinical disease score and the concentrations of caeruloplasmin in serum and of copper in serum and urine. When controlling for these variables, macular thickness was significantly correlated with RNFL (p = 0.002, r = 0.67), GCIP (p = 0.001, r = 0.72), INL (p = 0.020, r = 0.50) and ONL (p = 0.025, r = 0.51). RNFL was correlated with GCIP (p = 0.005, r = 0.611), INL (p = 0.028, r = 0.50) and ONL (p = 0.025, r = 0.511). To test if any of the clinical parameters had influence on the retinal changes observed, we p.