The role of left insula in executive set-switching: Lesion evidence from an acute stroke cohort

Abstract

Impairments in executive functions are common in stroke survivors, both in the acute and in the chronic phase. However, little is known about the underlying lesion neuroanatomy of these deficits. This study aimed to elucidate the pattern of brain damage underlying executive dysfunction in a large and acute stroke cohort. Executive set-switching deficits were evaluated by a shape-based analogue of the Trail Making Test (from the Oxford Cognitive Screen) in a consecutive sample of 144 stroke patients (age: 70 ± 15 years, examination: 5 ± 4 days post-stroke; brain imaging: 1.7 ± 2.9 days post-stroke). A voxelwise lesion-symptom mapping analysis was performed by combining executive set-switching accuracy scores with manually delineated lesions on computerized tomography or magnetic resonance imaging scans. The analysis showed that lesions within the left insular cortex and adjacent white matter predicted poorer executive set-switching. Further analyses confirmed that the lesion effect in the left insula survived correction for the low-level visuospatial and motor component processes of executive set-switching. In conclusion, the study provides lesion-based evidence for the role of the left insular cortex in flexible switching of attention. The findings are consistent with emergent models of insular function postulating the role of this region in regulatory aspects of goal-directed behaviour.

Neural signatures of Trail Making Test performance: Evidence from lesion-mapping and neuroimaging studies

“… 37 ± 11 years Chronic (3 ± 3 years) Standard TMT VLSM of TMT-B raw completion time. Left dorsomedial prefrontal Varjacic et al (2017) 144 Stroke (ischemic and haemorrhagic) Left (N = 47); Right (N = 60); Bilateral (N = 37). 71 ± 15 years Acute (5 ± 4 days) TMT analogue from Oxford Cognitive Screen (OCS) VLSM of accuracy score on the set-switching condition Left insula …”

“…An association was found between circumscribed lesion sites within the right dorsolateral prefrontal cortex and TMT-B sequencing and shifting errors, respectively. In the second VLSM study, acute stroke patients without hemi-spatial neglect ( Varjacic et al, 2017 ) performed the TMT analogue of the Oxford Cognitive Screen (OCS, Demeyere et al, 2015 ), which is an optimised test battery for the cognitive assessment of stroke patients. Specifically, participants were asked to connect large-to-small target shapes embedded in an array of non-target shape distractors (baseline condition, analogous to TMT-A) and to connect large-to-small target shapes in an alternating fashion (set-switching condition, analogous to TMT-B).…”

Brain-predicted age difference score is related to specific cognitive functions: A multi-site replication analysis

“…Task-based fMRI studies have shown significantly increased activation during TMT B versus TMT A within the left precentral gyrus (Moll, Oliveira-Souza, Moll, Bramati, & Andreiuolo, 2002) and the insula (Zakzanis, Mraz, & Graham, 2005). Additionally, a voxel-based lesion-symptom mapping study reported a negative association between lesions within the left insular cortex and a TMT task accuracy score, which like the TMT B minus A score attenuates the influence of processing speed and reflects cognitive flexibility (Varjačić et al, 2018). Like the TMT B score, the TMT B minus A is also correlated with atrophy of the bilateral medial temporal lobes (Oosterman et al, 2010).…”

Cognitive Reserve Proxies Do Not Differentially Account for Cognitive Performance in Patients with Focal Frontal and Non-Frontal Lesions

“…While grouping patients with different aetiologies is likely to suffer from potential confounds, it remains necessary to obtain large groups of patients to investigate cognitive impairments (for similar approaches see Aridan, Pelletier, Fellows, & Schonberg, 2019;Aron, Monsell, Sahakian, & Robbins, 2004;Gläscher et al, 2012;Roca et al, 2010;Stamenova et al, 2017;Stuss et al, 2005;Thompson-Schill et al, 1998;Urbanski et al, 2016). Some other studies favour the use of a single aetiology (e.g., Baldo, Schwartz, Wilkins, & Dronkers, 2006;Campanella et al, 2016;Sperber & Karnath, 2017;Varjačić et al, 2018). However, there is no consensus in the field of neuropsychology regarding what is the best approach to adopt.…”