Chronic pain disrupts affective and motivational states, yet its impact on eating—particularly the balance between homeostatic and reward-driven intake—remains unclear. Using the spared nerve injury (SNI) model in male and female mice, we examined how persistent neuropathic pain affects feeding and reward. Fourteen days post-surgery, mice underwent a binge-eating protocol, operant conditioning for chocolate pellets, and a sucrose preference test. Daily chow intake and body weight were monitored to assess homeostatic feeding. SNI induced mechanical hypersensitivity without affecting chow intake or body weight, indicating preserved homeostatic feeding. However, male SNI mice failed to escalate high-fat diet intake, showed reduced operant responding, earned fewer rewards, and had lower sucrose preference, consistent with anhedonia. Females displayed motivational deficits but not a clear binge-eating phenotype. To explore neural correlates, we assessed nucleus accumbens activation via c-Fos after high-fat diet exposure. Although diet increased activation in both control and SNI mice, no group differences were detected. These results suggest that pain-induced changes in hedonic feeding may involve non-canonical mechanisms beyond immediate early gene activation. Overall, persistent neuropathic pain selectively impairs hedonic and motivational aspects of eating, pointing to broader affective dysfunctions linked to chronic pain.