Working memory (WM) impairments are reported to occur in patients with Parkinson's disease (PD).However, the mechanisms are unclear. Here, we investigate several putative factors that might drive poor performance, by examining the precision of recall, the order in which items are recalled and whether memories are corrupted by random guessing (attentional lapses). We used two separate tasks that examined the quality of WM recall under different loads and retention periods, as well as a traditional digit span test. Firstly, on a simple measure of WM recall, where patients were asked to reproduce the orientation of a centrally presented arrow, overall recall was not significantly impaired.However, there was some evidence for increased guessing (attentional lapses). On a new analogue version of the Corsi-span task, where participants had to reproduce on a touchscreen the exact spatial pattern of presented stimuli in the order and locations in which they appeared, there was a reduction in the precision of spatial WM at higher loads. This deficit was due to misremembering item order. At the highest load, there was reduced recall precision, whereas increased guessing was only observed at intermediate set sizes. Finally, PD patients had impaired backward, but not forward, digit spans.Overall, these results reveal the task-and load-dependent nature of WM deficits in PD. On simple lowload tasks, attentional lapses predominate, whereas at higher loads, in the spatial domain, the corruption of mnemonic information -both order item and precision -emerge as the main driver of impairment. al., 2003). Working memory functioning is also a key index of health and is impaired in brain disorders (Baddeley et al., 1991;Christopher & MacDonald, 2005). Though, traditionally conceived as a movement disorder, it has now been established that cognitive deficits are also a core feature of Parkinson's disease (PD) (Aarsland et al., 2017;Lawson et al., 2021), with deficits in WM forming part a key component of the executive dysfunction prominent in this group (Morris et al., 1988).Deficits in short-term recall in PD are widely considered to result from the dopaminergic degeneration that characterises the disorder (Sawamoto et al., 2008). Despite this, PD patients taking dopamineenhancing medication have still been reported to display poor WM performance (Owen et al., 1992).These residual WM deficits may instead result from non-dopaminergic pathology to noradrenergic or cholinergic systems (Kehagia et al., 2010) or possibly even dopaminergic overdosing (Fallon et al., 2015;Fallon, Gowell, et al., 2019). However, the generation of pharmacological strategies to overcome this problem has been hampered by a lack of a full characterisation of medicated patients' WM deficits. Specifically, the circumstances under which impairments appear and the recall parameters that are affected have not been fully delineated.Spatial WM has been argued to be particularly vulnerable in PD (Owen et al., 1997;Postle et al., 1997). This issue has most extensively b...