Unipolar depressives seem apt to show neuropsychological impairment, particularly involving executive function and memory. Yet, not all depressed patients show such deficits. Major depressive illness shares a high rate of comorbid anxiety disorder, and anxiety disorders also tend to correspond with cognitive difficulties. Consequently, depressed individuals with comorbid anxiety disorders may be inclined to demonstrate greater neuropsychological dysfunction than those without anxiety disorders.
We compared nonpsychotic depressed inpatients with (n=22) and without comorbid anxiety disorders (n=30) to a group of control subjects (n=38) on a brief but broad battery of neuropsychological tests. Patients were tested during an inpatient admission, and data were collected retrospectively from available records.
Both groups of depressed patients showed worse memory function than the controls. Yet, executive dysfunction and psychomotor slowing were specific to the depressed group with comorbid anxiety. The comorbid anxiety group also had more impaired scores than either the nonanxious depressed group or the control group. The depressed group without a comorbid anxiety disorder demonstrated no significant slowing compared to the control group.
Major depressive disorder corresponds with significant memory impairment, regardless of comorbid anxiety disorder. Yet, presence of a comorbid anxiety disorder coincides with deficits involving executive function and psychomotor slowing. Clinical and theoretical relevance of the data is discussed.
"After adjusting for age, clinical depression without anxiety is not associated with executive dysfunction in older or younger adults (Thomas et al., 2008). Episodic memory deficits, however, may be unique to depression, as they are associated with depressive disorder alone in younger adults (Basso et al., 2007). Even after adjusting for age differences, late-life major depression is also associated with greater impairment in episodic memory compared with depression in the young to middle adult years (Thomas et al., 2008). "
"In addition, several studies suggest greater cognitive impairment among adults with OCD and depressive disorders (Moritz et al., 2001) as well as suggesting added executive functioning difficulties in adults with anxiety disorders (Basso et al., 2007). Other studies (in non-OCD youth) suggest that neurocognitive impairment may be compounded by the burden of multiple comorbidities (Sukhodolsky et al., 2010; Vloet et al., 2010). "
[Show abstract][Hide abstract] ABSTRACT: Preliminary research suggests neuropsychological deficits in youth with obsessive-compulsive disorder (OCD) similar to those in adults; however, small samples and methodological confounds limit interpretation. We aimed to examine the rates and clinical correlates of cognitive sequelae in youth with OCD, focusing on executive functioning and memory abilities. Youth ages 7–17 years with OCD (N=96) completed a hypothesis-driven neuropsychological battery (including the Rey-Osterreith Complex Figure, California Verbal Learning Test, and subtests of the Delis-Kaplan Executive Function System and Wide Range Assessment of Memory and Learning) that primarily assessed executive functioning, memory and processing speed. Cognitive sequelae were identified in 65% of youth (37% using a more stringent definition of impairment). Magnitude of cognitive sequelae was not associated with OCD severity or age; however, greater neuropsychological impairments were found amongst youth prescribed atypical neuroleptics and those diagnosed with comorbid tic disorders. Comorbidity burden was associated with presence of neuropsychological impairment, but was not specific to any single tests. Findings suggest that the presence of cognitive sequelae is prevalent amongst treatment-seeking youth with OCD. Deficits were found in executive functioning and non-verbal memory performance but these impairments were not associated with OCD severity.
"There is also debate over how other symptoms such as anxiety are related to subtype (Angst et al., 2007; Coryell, 2007; Gold and Chrousos, 2002; Parker, 2000; Parker et al., 1995). Anxiety has been shown to impact upon neuropsychological task performance in depression (Basso et al., 2007). Interestingly, MDD without co-morbid anxiety displays impaired immediate recall of new information but not retrieval or retention of information , whereas MDD with co-morbid anxiety displays impaired recall and recognition memory (immediate and delayed) (Kizilbash et al., 2002) but not working memory deficits (Basso et al., 2007). "
[Show abstract][Hide abstract] ABSTRACT: Objective:
Depressed patients display a variety of deficits in neuropsychological function, and contradictory findings in the literature may be due to disorder heterogeneity. The aim of this study was to examine the impact of severity, subtype and symptoms on cognitive control.
Neuropsychological function across a range of cognitive control tasks was examined in melancholic (n = 65) and non-melancholic depressed patients (n = 59) relative to controls (n = 124). The relationship between subtype (melancholia vs non-melancholia) and anxiety was also examined.
Melancholia was characterised by attention and working memory deficits typically associated with the dorsolateral prefrontal cortex, while non-melancholia was characterised by verbal memory recall deficits indicative of left frontal lobe and medial temporal lobe function. The severity of anxious arousal and psychomotor disturbance contributed to cognitive impairment more than the severity of depression symptoms and anxious apprehension.
Findings highlight a differential impact of depression subtype and severity, and suggest that anxious arousal and psychomotor disturbance may contribute to poorer performance on neuropsychological tasks associated with dorsolateral prefrontal cortex function.
Australian and New Zealand Journal of Psychiatry 11/2012; 46(11):1079-88. DOI:10.1177/0004867412461383 · 3.41 Impact Factor
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