Sustained neural activity during the delay phase of spatial working memory tasks is compelling evidence for the neural correlate of active storage and maintenance of spatial information, however, it does not provide insight into specific mechanisms of spatial coding. This activity may reflect a range of processes, such as maintenance of a stimulus position or a prepared motor response plan. The aim of our study was to examine neural evidence for the use of different coding strategies, depending on the characteristics (...) and demands of a spatial working memory task. Thirty-one and 44 participants performed a spatial working memory task while we measured their brain activity using fMRI in two separate experiments. Participants were asked to remember the position of a briefly presented target stimulus and, after a delay period, to use a joystick to indicate either the position of the remembered target or an indicated non-matching location. The task was designed so that the predictability of the response could be manipulated independently of task difficulty and memory retrieval process. We were particularly interested in contrasting conditions in which participants could use prospective coding of the motor response or had to rely on retrospective sensory information. Prospective motor coding was associated with activity in somatomotor, premotor, and motor cortices and increased integration of brain activity with and within the somatomotor network. In contrast, retrospective sensory coding was associated with increased activity in parietal regions and increased functional connectivity with and within secondary visual and dorsal attentional networks. The observed differences in activation levels, dynamics of differences over trial duration, and integration of information within and between brain networks provide compelling evidence for the use of complementary spatial working memory strategies optimized to meet task demands. (shrink)

Working memory (WM) deficits are pervasive co-morbidities of epilepsy. Although the pathophysiological mechanisms underpinning these impairments remain elusive, it is thought that WM depends on oscillatory interactions within and between nodes of large-scale functional networks. These include the hippocampus and default mode network as well as the prefrontal cortex and frontoparietal central executive network. Here, we review the functional roles of neural oscillations in subserving WM and the putative mechanisms by which epilepsy disrupts normative activity, leading to aberrant oscillatory signatures. (...) We highlight the particular role of interictal epileptic activity, including interictal epileptiform discharges and high frequency oscillations (HFOs) in WM deficits. We also discuss the translational opportunities presented by greater understanding of the oscillatory basis of WM function and dysfunction in epilepsy, including potential targets for neuromodulation. (shrink)