Lower cognitive control network connectivity in stroke participants with depressive features

Abstract

Around one-third of people develop depression following ischaemic stroke, yet the underlying mechanisms are poorly understood. Post-stroke depression has been linked to frontal infarcts, mainly lesions in the left dorsolateral prefrontal cortex (DLPFC). But depression is a network disorder that cannot be fully characterised through lesion-symptom mapping. Researchers of depression in non-stroke populations have successfully tapped into the cognitive control network (CCN) using the bilateral DLPFC as a seed, and found that CCN resting-state connectivity is reduced in even mildly depressed subjects, compared to healthy controls. Hence, we aimed to investigate the association between post-stroke depressive features and the CCN resting-state connectivity in a stroke population. We analysed DLPFC resting-state connectivity in 64 stroke participants, 20 of whom showed depressive features assessed with the Patient Health Questionnaire (PHQ-9) at 3 months after stroke. We directly compared groups showing symptoms of depression with those who did not, and performed a regression with PHQ-9 scores in all participants, controlling for age, gender, lesion volume and stroke severity. Post-stroke depression was associated with lower connectivity between the left DLPFC and the right supramarginal gyrus (SMG) in both group and regression analyses. Neither the seed nor the results overlapped with stroke lesions. These findings confirm an important role of the left DLPFC in post-stroke depression, but now show that large-scale network disruptions following stroke associated with depressive features occur without lesions in the DLPFC.

Neuropsychological Deficits Chronically Developed after Focal Ischemic Stroke and Beneficial Effects of Pharmacological Hypothermia in the Mouse

“…Additionally, both clinical and pre-clinical studies demonstrate the important role of reciprocal connections between the amygdala and PFC in the regulation of anxiety [25,40,42,43]. The MRI data from stroke patients provide supports that disruptions in thalamocortical and/or PFC pathways may contribute to the occurrence of PSD [44,45], and Vahid-Ansari F et al demonstrated stroke injuries in PFC led to the persistent anxiety/depression like phenotypes in lab mice [46]. In the present investigation of the focal cortical stroke model, the PFC was not a typical ischemic region and no significant cell death of TUNEL positive cells was observed in this region after stroke.…”

Left Prefrontal Connectivity Links Subthalamic Stimulation with Depressive Symptoms

“…Moreover, depressive symptoms increase gradually after left dlPFC traumatic brain injury and stroke depending on the extent of damage and network impact . Indeed, large‐scale network effects, hemispheric asymmetries, and connectivity play an important role in the development of depressive symptoms (eg, post‐stroke depression has been linked to altered dlPFC functional connectivity) . Functionally, the left dlPFC might regulate negative affect via the frontoparietal cognitive control network .…”

Lesions in the right Rolandic operculum are associated with self-rating affective and apathetic depressive symptoms for post-stroke patients

“…Network dysfunctions such as reduce d DMN within-connectivity involving left middle temporal cortex and precuneus 35 and affective network 36 have been used to predict the severity of PSD symptoms. Egorova et al 37 reported that the network dysfunction related to depressive symptoms was not necessarily associated with network lesions. This result raised a hypothesis of brain plasticity in network recovery.…”