Medial temporal lobe lesions reduce visual working memory precision

Abstract

Classic lesion case-control studies suggest minimal involvement of the medial temporal lobe (MTL) in visual working memory (VWM), particularly for simple stimulus features like color or orientation. However, recent intracranial recordings implicate the MTL – especially the hippocampus – in supporting VWM precision by distinguishing similar visual features to reduce representational variability during short retention intervals. Meanwhile, reports that MTL activity scales with VWM set size have raised the possibility that the MTL contributes not only to the quality but also the quantity of retained VWM content – an idea motivated by models positing a unitary memory strength metric to account for behavioral expressions of both VWM quantity and quality. To clarify the extent to which MTL lesions affect VWM quality, quantity, or both, we examined VWM recall performance in 40 neurological cases with drug-resistant epilepsy before and after their brain surgery for seizure treatment. Of these, 19 had lesions involving the hippocampus, while 21 had either no lesions or lesions outside the hippocampus. Using a controlled VWM task with fixed set size and minimal non-target recall errors, we modeled participants’ recall responses to estimate recall variability as an inverse measure of VWM precision and the probability of recall success as the proportion of trials not attributable to failed, uniform recall responses. We found that lesions affecting the hippocampus in the MTL led to a significant increase in recall variability, indicating reduced VWM precision after surgery. Voxel-based lesion-symptom mapping further revealed a robust association between hippocampal damage and increased recall variability, even after controlling for overall brain lesion volume. In contrast, total lesion volume – but not hippocampal lesion extent – predicted reduced recall success rate, suggesting that broader lesion burden constrains how much content is retained, resulting in more failed recall responses. An alternative model assuming a unitary memory strength metric captured the overall performance decline with increasing total lesion volume but could not account for the MTL-specific effects. Together, these findings highlight the MTL’s role in preserving the fidelity – rather than the mere presence – of VWM representations. They challenge models that treat VWM quality and quantity as interchangeable consequences of a single underlying memory strength parameter. By identifying distinct neural correlates for each component, our results point to VWM precision as a sensitive behavioral marker – one that may be useful for tracking functional changes in individuals with memory impairment, including those with focal brain lesions.