Figure 4.
Prognostic variables including MMSE in CALGB 51101. (A) Analysis of baseline clinical characteristics, adjusting for treatment arm, demonstrated that baseline MMSE was the only variable that correlated with OS. Mean baseline MMSE score for the myeloablative group was 25.7 (SD, 5.92). Mean baseline MMSE score for the nonmyeloablative group was 25.8 (SD, 6.31). Median baseline MMSE scores were 28 in each group. MMSE scores were summarized as a continuous measure as well as categorically, both as any neurocognitive impairment (MMSE, <27 vs not) as well as level of neurocognitive impairment (severe, 0-9; vs moderate, 10-20; vs mild, 21-26; vs normal, 27-30). (B) Kaplan-Meier analysis using a MMSE score of 27 as a categorical variable suggests a significant correlation between baseline neurocognitive impairment on survival in PCNSL in CALGB 51101 (P < .01). The MMSE score of 27 as a categorical variable significantly correlated with OS in patients who received myeloablative therapy (P < .02) and nonmyeloablative therapy (P < .07). We found that the negative impact of impaired neurocognition is heavily influenced by the significant impact of severe cognitive impairment (MMSE score, 0-9) on OS in relation to those with normal cognition at baseline (HR, 19.8; 95% CI, 4.94-79.0; P < .001), even after adjusting for age and treatment arm. In this same model, we found that the mild (MMSE, 21-26) and moderate (MMSE, 10-20) cognitive impairment corresponded to a tendency toward worse OS outcomes (mild HR, 2.85; 95% CI, 1.06-7.66; P = .03; moderate HR, 2.42; 95% CI, 0.62-9.43; P = .20). Furthermore, although an MMSE <27 (vs not) at baseline was not associated with worse PFS, we found that severe cognitive impairment at baseline was significantly associated with worse PFS (HR, 7.32; 95% CI, 2.09-25.6; P = .001) in relation to those with normal baseline cognition, even adjusting for age and treatment arm. Caveats with these findings are based on the fact that there were more limited numbers of patients with moderate (n = 9) and severe (n = 3) cognitive impairment at baseline. Furthermore, those with MMSE scores at baseline of at least 27 (ie, no cognitive impairment) tended to have better KPS than those with any cognitive impairment (median, 80 vs 70; P < .001); based on the nonsignificant influence of KPS on OS (P = .27), this does not appear to have any confounding effects on the influence of baseline MMSE on OS. No other baseline characteristics were significantly associated with baseline MMSE status. Baseline MMSE continuous scores as well as categorical status (eg, <27 vs ≥27) were also not significantly different between the treatment arms. (Figure 4A; supplemental Table 2). SD, standard deviation.

Prognostic variables including MMSE in CALGB 51101. (A) Analysis of baseline clinical characteristics, adjusting for treatment arm, demonstrated that baseline MMSE was the only variable that correlated with OS. Mean baseline MMSE score for the myeloablative group was 25.7 (SD, 5.92). Mean baseline MMSE score for the nonmyeloablative group was 25.8 (SD, 6.31). Median baseline MMSE scores were 28 in each group. MMSE scores were summarized as a continuous measure as well as categorically, both as any neurocognitive impairment (MMSE, <27 vs not) as well as level of neurocognitive impairment (severe, 0-9; vs moderate, 10-20; vs mild, 21-26; vs normal, 27-30). (B) Kaplan-Meier analysis using a MMSE score of 27 as a categorical variable suggests a significant correlation between baseline neurocognitive impairment on survival in PCNSL in CALGB 51101 (P < .01). The MMSE score of 27 as a categorical variable significantly correlated with OS in patients who received myeloablative therapy (P < .02) and nonmyeloablative therapy (P < .07). We found that the negative impact of impaired neurocognition is heavily influenced by the significant impact of severe cognitive impairment (MMSE score, 0-9) on OS in relation to those with normal cognition at baseline (HR, 19.8; 95% CI, 4.94-79.0; P < .001), even after adjusting for age and treatment arm. In this same model, we found that the mild (MMSE, 21-26) and moderate (MMSE, 10-20) cognitive impairment corresponded to a tendency toward worse OS outcomes (mild HR, 2.85; 95% CI, 1.06-7.66; P = .03; moderate HR, 2.42; 95% CI, 0.62-9.43; P = .20). Furthermore, although an MMSE <27 (vs not) at baseline was not associated with worse PFS, we found that severe cognitive impairment at baseline was significantly associated with worse PFS (HR, 7.32; 95% CI, 2.09-25.6; P = .001) in relation to those with normal baseline cognition, even adjusting for age and treatment arm. Caveats with these findings are based on the fact that there were more limited numbers of patients with moderate (n = 9) and severe (n = 3) cognitive impairment at baseline. Furthermore, those with MMSE scores at baseline of at least 27 (ie, no cognitive impairment) tended to have better KPS than those with any cognitive impairment (median, 80 vs 70; P < .001); based on the nonsignificant influence of KPS on OS (P = .27), this does not appear to have any confounding effects on the influence of baseline MMSE on OS. No other baseline characteristics were significantly associated with baseline MMSE status. Baseline MMSE continuous scores as well as categorical status (eg, <27 vs ≥27) were also not significantly different between the treatment arms. (Figure 4A; supplemental Table 2). SD, standard deviation.

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