Cognitive impairment and fMRI in major depression

Abstract

Cognitive impairment in depression may be one of the more practically important aspects of the illness, responsible for much of its morbidity. It also is at the heart of its psychopathology, may contribute to strategies of treatment, and may give us a more easily quantifiable measure of impaired function to correlate with brain activity. Functional magnetic resonance imaging (fMRI) is ideally suited to examine brain function in depression. It has the correct time window to repeatedly sample cognitive task performance; it does not require exposure to radioactive tracers and can therefore be repeated many times; it also can be linked with high resolution structural images acquired in the same imaging session that help identify the regions of activation and support the spatial transformation necessary to compare the scans of different subjects. fMRI has already produced a series of consistent results in depression, identifying increased activity of rostral anterior cingulate and other medial prefrontal structures during effortful tasks and on occasion also increased dorsolateral prefrontal activity, suggesting increased possibly compensatory activity to maintain task performance. Investigating the interplay between limbic (orbitomedial) and 'cognitive' dorsolateral structures clearly has the potential to clarify important illness mechanisms of depressive illness.

Specifying the Neuropsychology of Affective Disorders: Clinical, Demographic and Neurobiological Factors

“…The findings indicate that structural abnormalities that relate to cognitive function are-besides of the hippocampus-primarily found in the dorsolateral prefrontal cortex (DLPFC). This is consistent with what could be expected given the putative functions of these regions and the impaired cognitive outcomes with which they are associated, namely executive function, attention/ ↑a (Melcher et al 2008;Wagner et al 2006;Ebmeier et al 2006;Harvey et al 2005;Steele et al 2004) RVPFC: ↓a (Melcher et al 2008;Kronhaus et al 2006;Blumberg et al 2003;Strakowski et al 2002) Caudal ACC: ↓a ( working memory, and declarative memory. Furthermore, some correlational studies demonstrated associations between neuropsychological deficits and structural abnormalities of the orbital frontal cortex (Taylor et al 2003) left cingulate cortex (Yuan et al 2008), and the basal ganglia (Naismith et al 2002) as well as white matter lesions (Hickie et al 2007) in patients with MDD.…”

Cortical-limbic regions modulate depression and anxiety factors in functional dyspepsia: a PET-CT study

“…Van Oudenhove [23,24] used H 2 O 15 -PET in hypersensitive FD patients to explore the neurobiological mechanism of visceral hypersensitivity, and discovered that bilateral somatosensory cortexes (SI/SII) and the ventrolateral prefrontal cortex were activated in hypersensitive FD patients compared to controls. Taken together, former studies found the response of the cerebral cortex to FD or depression or anxiety was mainly located in the prefrontal cortex [20][21][22][23][24][25][26][27][28]. In the current study, cerebral activities were not just contained in the frontal cortex, but they were also located in the temporal, parietal and occipital regions as observed in FD patients with depression and anxiety factors.…”

“…Zhao et al [26] observed deactivation in the medial prefrontal cortex and posterior cingulate cortex in anxiety patients relative to controls. Taken together, the responses of the limbic system to depression or anxiety were mainly in the anterior or posterior cingulate gyrus, striatum, amygdala, caudate nucleus and parahippocampal gyrus [20][21][22][25][26][27][28]. Van Oudenhove et al [29] found that the bilateral ventral posterior cingulate cortex was activated in normosensitives relative to hypersensitives.…”

Working‐memory fMRI reveals cingulate hyperactivation in euthymic major depression

“…Modern neuroimaging methods indicate that dysfunction of cortico-limbic networks plays an important role in the pathophysiology of both affective and cognitive symptoms in MDD (Dougherty and Rauch, 2007). In the acute episode of depression, brain metabolism is significantly altered, with pathological changes in the dorsolateral prefrontal and limbic cortex at rest and during cognitive activation (Drevets, 2001;Ebmeier et al, 2006;Fitzgerald et al, 2006;Greicius et al, 2007). Much less is known about brain function when depressed patients reach the euthymic mood state.…”