Spatial Memory Impairment in Opioid Use Disorder During Buprenorphine Treatment: Evidence from a Spatial Navigation Task – UROP Symposium

Spatial Memory Impairment in Opioid Use Disorder During Buprenorphine Treatment: Evidence from a Spatial Navigation Task

Lyndsey Kim

Research Mentor: Negin Nadvar
Mentor Department: Department of Psychiatry, Medicine
Author(s): Lyndsey Kim, Aml Almamri, Madeline Vincent, Negin Nadvar
Session: Session 3 (11:00 AM – 11:50 AM)
Presentation Type: Poster 83

Abstract

Opioid use disorder (OUD) has been associated with structural and functional alterations in the hippocampus (Herlinger, 2022; Bechara, 2019), impairing allocentric spatial memory: the ability to construct and retrieve cognitive maps using external landmarks (Ekstrom, 2023; Kühn, 2014; Hampstead, 2014). Yet few studies have examined whether these deficits persist during buprenorphine-assisted treatment or what constitutes vulnerable spatial memory processes. We examined spatial navigation in 8 individuals with OUD receiving buprenorphine and 14 healthy controls. We hypothesize that OUD results in impairment of allocentric but not egocentric navigation, consistent with hippocampal vulnerability to chronic opioid exposure. Three conditions were assessed. The allocentric cued condition required free reconstruction of a target’s exact location with no response options, measured as total spatial error in pixels (px). The allocentric recognition condition offered structured response choices, measured as percent correct. Egocentric navigation, relying on striatal rather than hippocampal memory, served as the low-demand reference, also measured as percent correct. Welch’s t-tests were run at p < 0.05 to compare group performance. The OUD group showed significantly larger spatial error (M = 8,673.74 px) compared with controls (M = 5,524.52 px) in the allocentric cued condition (t = 3.12, p = 0.007, d = 1.34). Group differences for allocentric recognition (t = -2.01, p = 0.063, d = 0.88) and egocentric (t = -1.79, p = 0.094, d = 0.79) performance were not significant. Impairment was greatest in the cued condition, likely because it placed greater demand on hippocampal spatial encoding than recognition-based formats (Xu, 2025). Non-significant but large effect sizes likely reflect Type II error from limited sample size. This graded pattern provides preliminary evidence that buprenorphine may not fully restore hippocampal-dependent cognitive map formation; future research should examine whether hippocampal-targeted cognitive rehabilitation improves spatial memory and reduces relapse risk in OUD. References: Bechara, A., Berridge, K. C., Bickel, W. K., Morón, J. A., Williams, S. B., & Stein, J. S. (2019). A neurobehavioral approach to addiction: Implications for the opioid epidemic and the psychology of addiction. Psychological Science in the Public Interest, 20(2), 96–127. Ekstrom, A. D., & Hill, P. F. (2023). Spatial navigation and memory: A review of the similarities and differences relevant to brain models and age. Neuron, 111(7), 1037–1049. Hampstead, B. M., Brown, G. S., & Hartley, J. F. (2014). Transcranial direct current stimulation modulates activation and effective connectivity during spatial navigation. Brain stimulation, 7(2), 314-324. Herlinger, K., & Lingford-Hughes, A. (2022). Opioid use disorder and the brain: A clinical perspective. Addiction, 117(2), 495–505. Kühn, S., & Gallinat, J. (2014). Segregating cognitive functions within hippocampal formation: A quantitative meta-analysis on spatial navigation and episodic memory. Human Brain Mapping, 35(4), 1129–1142. Xu, X., & Mao, D. (2025). Dissociation and transformation between recognition memory and spatial navigation representations. Trends in Neurosciences

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