Study Design: Retrospective cohort study. Objective: This study aimed to evaluate the association between nerve lengthening after adult deformity correction and motor deficits dervied from the upper lumbar plexus or femoral nerve. Summary of Background Data: Adult spinal deformity (ASD) surgery is associated with high rates of neurological deficits. Certain postoperative deficits may be related to lengthening of the upper lumbar plexus (ULP) and/or femoral nerve (FN) after correction of lumbar deformity. Methods: Patients with ASD who underwent posterior-only corrective surgery from the sacrum to L3 or above were included. The length of each lumbar nerve root (NR) was calculated geometrically using the distance from the foramen to the midpoint between the anterosuperior iliac crest and pubic symphysis on AP and lateral radiographs. The mean lengths of the L1-3 and L2-4 NRs were used to define the lengths of the ULP and FN, respectively. Pre- to postoperative changes in nerve length were calculated. Neurological examination was performed at discharge. Proximal weakness (PW) was defined as the presence of weakness compared to baseline in either hip flexors or knee extensors. Multiple linear regression analysis was used for estimating the postoperative lengthening according to the magnitude of preoperative curvature and postoperative correction angles. Results: A total of 202 sides were analyzed in 101 patients, and PW was present on 15 (7.4%) sides in 10 patients. Excluding the 10 cases with three-column osteotomies, those with PW had a significantly higher rate of pure sagittal deformity (P<.001) and greater nerve lengthening than those without PW (ULP 24 vs 15 mm, P=0.02; FN 18 vs 11 mm, P=0.05). No patient had advanced imaging showing neural compression, and complete recovery of PW occurred in 8 patients at 1-year follow-up. Conclusions: After ASD surgery, lengthening of the ULP was associated with PW. In preoperative planning, surgeons must consider how the type of correction may influence the risk for nerve lengthening, which may contribute to postoperative neurologic deficit. Level of Evidence: 3.