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Depression and Cognition: Taking a Lifespan Perspective.

Overview by Ira D. Glick, MD

In the field of psychiatry, we are beginning to focus more on the cognitive symptoms of major depressive disorder (MDD) and the effects that these symptoms have on function and, essentially, quality of life.

In patients with chronic depression of different types, the primary symptoms are lowered mood and anhedonia--ie, you can't enjoy anything. In addition, there are a variety of other symptoms, including appetite changes, sleep changes, guilt, irritability, etc. All of this is also associated with cognitive changes in depression. You can't think clearly, you can't process, and you can't organize your thoughts adequately. You don't feel like getting out, and you don't enjoy it if you do. It markedly impairs your social function and your workplace productivity.

Overall, in treating depression, I have been teaching that, ordinarily, we predominantly get partial responses to antidepressant therapies. There are very few people who get almost no response. The degree of the partial response, however, depends on the patient's genetic vulnerability, which we have not yet been able to elucidate, in part because the genes are so complicated. Genetic susceptibility and family history, then, are taken together with environmental issues, such as stressful life events, and I try to keep an eye on all of those spheres.

In this particular roundtable discussion, the focus is on the cognitive symptoms of depression - a topic that one might argue has not traditionally received enough consideration in the field of psychiatry.

What are the key considerations in addressing cognitive symptoms of major depressive disorder (MDD) in adults?

Dr Forester:

In adults, the cognitive symptoms of MDD that are commonly experienced are impairments in concentration and attention, as well as some executive function deficits related to organization, planning, and multitasking. The key deficits that we look for in this population are impairments in attention and concentration (see figure). These impairments can be evaluated at bedside using objective assessment of both cognition and how these symptoms may be impacting a person's daily functioning, in terms of social life or occupational work. These deficits often occur in the context of the depressive episode. The deficits may improve once the depression is treated effectively but may not completely normalize. Improvement of cognitive symptoms with treatment may help differentiate patients in the general adult population with depression from older adults with depression.

Dr Reynolds:

That's a great point. I think that a key principle in clinical practice is appropriate screening. In general, many clinicians prefer the Montreal Cognitive Assessment (MoCA) because it provides reasonably broad screening, including screening for executive impairments.

Something else to consider is that our experience with older adults has been that approximately half of treatment-seeking older adults with current episodes of MDD have some degree of neurocognitive impairment and often qualify for a diagnosis of some form of mild cognitive impairment (MCI).

Dr Thase:

Even in people in the age range of, say, 40-60 years, the proportions are substantially lower. But they are not negligible. You may have 5%, 10%, or even 15% of people reporting some significant difficulties with their concentration and with their memory. If they have a family history of dementia, then they are beginning to worry about whether the depression is hastening the dementia.

In the old days, we used to talk about this notion of pseudodementia, in which the more severe depression could give the appearance of cognitive impairment of dementia, but I think more recent longitudinal data suggest that depression can uncover or reveal an impending dementiform illness maybe 5 or 10 years before it clinically manifests.

Dr Reynolds:

Right. It's an interesting conversation, I think: the extent to which depression may represent a true risk factor for the subsequent onset of one or another form of dementia, and/or be a warning sign, or a kind of prodromal expression of dementia. We certainly have seen both.

My sense from the literature is that patients with longstanding depression, particularly recurrent episodes of clinical severity, are at risk for developing cognitive impairment and frank dementia--whether Alzheimer's dementia or vascular dementia.

And that, in turn, represents part of what I think of as the risk architecture for either Alzheimer's or vascular dementia later in old age. Dr Thase, I think you are absolutely correct. It's very important to take a lifespan perspective on the issue of neurocognitive impairments that we can see in people living with major depression.

Dr Forester:

I agree. Like my colleagues, I approach this initially by differentiating between 2 different groups of patients. First, there are patients who developed depression when they were in their 20s and 30s and now have aged into their 60s, 70s, and beyond. In other words, they have a lifelong history of depression, and now they are getting another episode of depression later in life. In that context, they are developing cognitive symptoms. That is one scenario that we see. Second, there are people who are developing depression for the first time later in life. In association with the depression, they are now having symptoms of cognitive impairment, whether it's attentional disturbances or executive dysfunction. When treating this group of patients, we think, "Late onset, never had this before, probably a different biological disorder, a different determinant."

Depression may be a final common pathway with many causes, and when it happens later in life, it is often due to underlying structural brain disease, including the early stages of dementia. If you think of dementia as a huge iceberg, the very tip of the iceberg--the first presenting syndrome of dementia - is sometimes depression.

As Dr Thase mentioned earlier, they used to call this pseudodementia, or the cognitive impairment syndrome of depression. If you treat these patients, and if their cognitive symptoms improve, as Dr Reynolds alluded to, after a 5-year follow-up period, half of them will then have signs of Alzheimer's disease. What that tells us is that there may be an underlying dementia syndrome -and the neuropathology of Alzheimer's disease or some other dementia--in patients who are developing depression for the first time in later life. The third syndrome of depression and dementia overlap affects patients who have no history of depression. They develop Alzheimer's disease, and, at some point during the course of their dementia syndrome, they develop depression. That's the depression syndrome of dementia. So here, the depression is secondary to the dementia because of the structural brain changes and the biochemical changes associated with dementia. These are people who already had the cognitive problems, and now they have depression on top of that. In some ways, treatment of this third group is the most complicated.

If someone scores very high on the Geriatric Depression Scale, has impairment on his or her MoCA, and is not functioning well, then you treat the depression and evaluate again after 1 month of treatment before making the leap to underlying Alzheimer's disease. It's very hard to know what someone's baseline underlying cognition is going to be while the he or she is in the midst of a depressive episode. Regardless, the bottom line for our patients being treated for depression is that it is critically important to continue to evaluate and monitor cognitive functioning.

References

Elsawy B, Higgins, KE. The geriatric assessment. Am Fam Physician. 2011;83(l):48-56.

Montreal Cognitive Assessment, http://www.mocatest.org/.Accessed June 5, 2017.

Panza F, Frisardi V, Capurso C, et al. Late-life depression, mild cognitive impairment, and dementia: possible continuum? Am J Geriatr Psychiatry. 2010;18(2):98-116.

Caption: Brent P. Forester, MD, MSc

Caption: IraD. Glick, MD

Caption: Charles F. Reynolds, III, MD

Caption: Michael E. Thase, MD

Please Note: Illustration(s) are not available due to copyright restrictions.
VAST-D Study Treatment Arms

Arms                 Interventions

Antidepressant       Current antidepressant (SSRI, SNRI,
                     or mirtazapine)
+ augmentation with  - and -
aripiprazole         Aripiprazole per protocol

Antidepressant       Current antidepressant
                     (SSRI, SNRI, or mirtazapine):
+ augmentation with  - and -
bupropion-SR         Bupropion-SR per protocol

Switching from       Switching to bupropion-SR per protocol
antidepressant
monotherapy to
bupropion-SR
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Title Annotation:EXPERT ROUNDTABLE
Publication:Internal Medicine News
Date:Nov 1, 2017
Words:1326
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