We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
(1) To delineate whether cognitive flexibility and inhibitory ability are neurocognitive markers of passive suicidal ideation (PSI), an early stage of suicide risk in depression and (2) to determine whether PSI is associated with volumetric differences in regions of the prefrontal cortex (PFC) in middle-aged and older adults with depression.
Design:
Cross-sectional study.
Setting:
University medical school.
Participants:
Forty community-dwelling middle-aged and older adults with depression from a larger study of depression and anxiety (NIMH R01 MH091342-05 PI: O’Hara).
Measurements:
Psychiatric measures were assessed for the presence of a DSM-5 depressive disorder and PSI. A neurocognitive battery assessed cognitive flexibility, inhibitory ability, as well as other neurocognitive domains.
Results:
The PSI group (n = 18) performed significantly worse on cognitive flexibility and inhibitory ability, but not on other neurocognitive tasks, compared to the group without PSI (n = 22). The group with PSI had larger left mid-frontal gyri (MFG) than the no-PSI group. There was no association between cognitive flexibility/inhibitory ability and left MFG volume.
Conclusions:
Findings implicate a neurocognitive signature of PSI: poorer cognitive flexibility and poor inhibitory ability not better accounted for by other domains of cognitive dysfunction and not associated with volumetric differences in the left MFG. This suggests that there are two specific but independent risk factors of PSI in middle- and older-aged adults.
Late life suicide is an international public health crisis, yet the mechanisms underlying late life suicide risk are far less understood compared to younger age groups. Executive dysfunction is widely documented in late life depression (LLD), and cognitive flexibility and inhibition are specifically hypothesized as vulnerabilities for suicide risk. There is some evidence that LLD patients with suicidal ideation or attempt suicide have worse executive dysfunction than LLD patients that do not; however, it is unknown whether these differences exist in Passive Suicidal Ideation (PSI), which may be an important early stage of suicide risk. Delineating the mechanisms of risk for PSI in LLD is a crucial direction for late life suicide research. The purpose of our study was to examine whether cognitive flexibility and inhibitory ability are neurocognitive markers of PSI. The secondary purpose of our study was to determine if neurocognitive differences due to PSI are mediated by volumetric differences in the prefrontal cortex.
Methods:
Forty community-dwelling middle- and older-aged adults with LLD (18 with PSI, 22 without) completed a neurocognitive battery that assessed cognitive flexibility, inhibitory ability, as well as other neurocognitive domains, and underwent structural neuroimaging.
Results:
The PSI group performed significantly worse on cognitive flexibility and inhibitory ability, but not on other neurocognitive tasks which included other measures of executive function. The PSI group had a larger left mid-frontal gyrus (LMFG) than those without PSI, but there was no association between LMFG and cognitive flexibility or inhibitory ability, nor was there statistical evidence of mediation.
Conclusions:
Our findings implicate a unique neurocognitive signature in LLD with PSI: poorer cognitive flexibility and poorer inhibitory ability not better accounted for by other domains of cognitive dysfunction and not mediated by volumetric differences in the prefrontal cortex. Volumetric brain differences in the LMFG appear unrelated to differences in cognitive flexibility and inhibitory ability, which suggests two specific but independent risk factors for PSI in middle- and older-aged adults.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.