Skip Navigation LinksHome > August 2011 - Volume 43 - Issue 4 > Comorbidities and Cognitive Functioning: Implications for Nu...
Journal of Neuroscience Nursing:
doi: 10.1097/JNN.0b013e3182212a04
Article

Comorbidities and Cognitive Functioning: Implications for Nursing Research and Practice

Vance, David; Larsen, Kirsten I.; Eagerton, Gregory; Wright, Mary A.

Free Access
Article Outline
Collapse Box

Author Information

Questions or comments about this article may be directed to David Vance, PhD, at devance@uab.edu. He is an associate professor at the University of Alabama at Birmingham, AL.

Kirsten I. Larsen, BSN MS RN, is a floor nurse at UAB Hospital, University of Alabama at Birmingham, AL.

Gregory Eagerton, DNP RN NEABC, is the associate director for Patient/Nursing Service, Birmingham VA Medical Center, Birmingham, AL.

Mary A. Wright, PhD CRNP MSN, is an assistant professor at Family/Child Health and Caregiving, School of Nursing, University of Alabama at Birmingham, AL.

Collapse Box

Abstract

ABSTRACT: Optimal cognitive functioning is necessary to successfully negotiate one's environment, yet medical conditions can interfere with brain health, thus negatively impacting cognitive functioning. Such comorbidities include hypertension, heart disease, diabetes, depression, and HIV, as well as others. The physiological properties of these comorbidities can reduce one's cognitive reserve and limit one's cognitive efficiency. This article provides an overview of a few common comorbidities known to affect cognitive functioning and addresses ways in which cognitive functioning may be ameliorated and protected or mitigated in lieu of cognitive declines in such clinical populations. Implications for nursing practice and research are posited.

Cognitive functioning is an essential part of humanity that we use to define ourselves, recognize consciousness, interact with the social and physical environment, and ensure our survival. Our quality of life depends upon cognitively recognizing our strengths, limitations, aspirations, and dreams and altering our behavior to match our abilities. Many studies indicate that even subtle, nonpathological cognitive declines can impair everyday functioning (e.g., grocery shopping, preparing meals, and handling finances) and diminish quality of life (McGuire, Ford, & Arjani, 2006).

Unfortunately, cognitive health is often overlooked in medical care until it is jeopardized by serious neurological conditions such as stroke, Alzheimer disease, and traumatic brain injury. However, other "non-neurological" conditions such as hypertension, diabetes, and HIV can also negatively affect the cognitive functioning of adults by slowly taxing the physiological integrity of the brain. This physiological integrity, referred to as cognitive reserve, is needed as people grow older or are confronted with other comorbidities that also add cumulative insults to brain health and neurological functioning.

The purpose of this article is to provide a brief overview of some common comorbidities known to negatively impact cognitive reserve and, thus, cognitive functioning. From this, the role of comorbidities on cognitive reserve will be highlighted, along with strategies for protecting and improving cognitive functioning or adapting to such cognitive loss in those with such comorbidities. Table 1 and Figure 1 provide an organizational and visual representation that corresponds to the text, respectively, to guide the reader. Implications for nursing practice and research are provided.

Table 1
Table 1
Image Tools
Figure 1
Figure 1
Image Tools
Back to Top | Article Outline

Comorbidities and Cognitive Functioning

As seen in Table 1 and Figure 1, a number of comorbidities have been documented to negatively impact cognitive reserve and cognitive functioning. These comorbidities include hypertension, heart disease, diabetes, depression, and HIV, as well as a host of others. Such comorbidities exert negative effects on numerous neurological processes through direct or indirect mechanisms. Furthermore, this list of medical comorbidities does not include obvious neurological comorbidities (e.g., bipolar disorder, schizophrenia, multiple sclerosis, and posttraumatic stress syndrome) also known to be a risk factor for declines and alterations in cognitive functioning (e.g., Deckersbach et al., 2004; Neylan et al., 2004).

Back to Top | Article Outline
Hypertension and Cognition

Hypertension is one of the most common age-associated vascular conditions (Launer, Masaki, Petrovitch, Foley, & Havlik, 1995). It is particularly alarming as studies also show that hypertension affects brain health and cognitive functioning in midlife as well as in older age (Beeri, Ravona-Springer, Silverman, & Haroutunian, 2009). In a study of 580 older adults (Mage = 77.8 years), Hajjar et al. (2009) found that hypertension was independently associated with poorer reasoning and executive functioning, a type of cognitive ability. One reason for this finding is that hypertension can cause microangiographic changes in the brain, resulting in minor infarctions (Elwood, Pickering, Bayer, & Gallacher, 2002). In fact, many of these infarctions occur in the frontal lobe, the area of the brain that performs reasoning and executive functioning.

Fortunately, hypertension can be treated through diet, exercise, and medications such as beta-blockers. For example, in a recent study, Viamonte, Vance, Wadley, and Ball (2010) compared the cognitive abilities of 865 adults (age = 55 years and older) with and without hypertension. No group differences emerged; this result was surprising at first, but upon closer inspection of the data, the hypertensive participants were also prescribed medications for this condition. Thus, this study suggests that medical treatment for hypertension may be protective against cognitive loss.

Back to Top | Article Outline
Heart Disease and Cognition

Besides hypertension, other cardiovascular comorbidities such as heart disease exert an enormous amount of influence on cognitive reserve and brain health. In the same study by Hajjar et al. (2009), researchers found congestive heart failure to be related to poorer executive functioning. As with hypertension, heart disease can cause microangiographic changes that produce undetected minor infarctions in the brain. Furthermore, poorer vascular health from heart disease means that the brain may be experiencing less oxygenated blood and nutrients because of decreased cerebral perfusion. Likewise, conditions that produce heart disease, such as elevated cholesterol, smoking, and diabetes, can obviously intensify the negative effects of heart disease and further contribute to poorer cognitive functioning (Pressler, 2008).

Back to Top | Article Outline
Diabetes and Cognition

Studies indicate that diabetes negatively affects cognitive functioning. Ruis et al. (2009) compared the cognitive performance of 183 adults with early-stage type 2 diabetes with 69 adults without this disease. They found that modest declines in memory are already observed in those with early-stage type 2 diabetes. Nonetheless, these negative effects can grow with age and length of diagnosis. Bruehl et al. (2009) compared the brain volumes and cognitive performance of 41 middle-aged adults with type 2 diabetes (Mdiagnosed = 7 years) with 47 age-, gender-, and education-matched controls. Compared with the control group, researchers found that those with type 2 diabetes exhibited poorer cognitive functioning and reduced volume in the hippocampus (the brain structure necessary for memory formation and consolidation) and the prefrontal cortex (the brain structure necessary for executive and decision-making function). Furthermore, poorer glycemic control was associated with reduced volume in the prefrontal cortex.

All of the mechanisms involved with diabetes impacting cognitive functioning are not entirely clear; albeit, two potential mechanisms have been identified. First, diabetes can exacerbate heart disease and hypertension, both of which negatively impact brain health. Specifically, insulin resistance associated with endothelial function and vascular reactivity can impair delivery of substrates (e.g., nutrients) across the blood-brain barrier (Starr & Convit, 2007). Second, type 2 diabetes is associated with altered cortisol levels, inflammation, obesity, and hypothalamic adrenocortical axis abnormalities; these conditions are known to exert an adverse effect on brain health (Bruehl et al., 2009; Starr & Convit, 2007).

Back to Top | Article Outline
Depression and Cognition

Although some may consider depression to be neurological comorbidity, it is included as a medical comorbidity in this article because of (a) its numerous causes such as chronic stress and reaction to grief and loss, which are non-neurological in origin, and (b) its appearance as a common medical condition with nearly 20% of primary care patients presenting symptoms of depression (Zung, Broadhead, & Roth, 1993). Multiple studies show that people of all ages with depression and similar mood problems, such as anxiety, experience declines in cognitive functioning (Casteneda, Tuulio-Henriksson, Marttunen, Suvisaari, & Lönnqvist, 2008; Jeong & Cranney, 2009; Steffens, McQuoid, & Potter, 2009). The effects of depression on cognitive functioning may be more readily observed when one's cognitive reserve may already be compromised by other comorbidities or advanced aging. For example, in a cross-sectional sample of 158 community-dwelling older adults (Mage = 75 years), Vance, Wadley, Ball, Roenker, and Rizzo (2005) administered a battery of cognitive functions, depression, and other measures to these participants. Using structural equation modeling, researchers found that depression was the strongest predictor of cognitive functioning; those with higher levels of depressive symptomatology experienced poorer cognitive functioning.

There are several physiological and cognitive explanations for the effects of depression and other mood problems on decreased cognitive functioning. First, there may be a shared genetic pathogenesis between depression and cardiovascular risk factors. Lόpez-Leόn et al. (2009) administered depression, genetic, and cardiovascular measures to a large, genetically isolated population (N = 2,383). Their analysis revealed that the level of depressive symptomatology corresponded to elevated lipid levels in those with shared genetic markers, and as already mentioned, these elevated lipid levels can negatively impact brain health. Second, many suggest that depression increases cortisol levels through its effects on the central hypothalamo-pituitary-adrenal axis. Prolonged exposure to cortisol can be damaging to neurons and brain health (Carroll et al., 2007). Third, it is suggested that depression-induced stress increases cortisol levels that also increase serotonergic vulnerability. Thus, increasing serotonin through a tryptophan-rich diet has been shown to yield promising effects (Firk & Markus, 2009). Finally, a cognitive explanation for this effect is that mood problems also require cognitive ability to ruminate and dwell on such emotional states; this rumination depletes the cognitive reserves needed to perform other cognitive functions. This depletion overloads the cognitive system, resulting in poorer cognitive functioning (Beaudreau & O'Hara, 2009; Vance, Moneyham, Fordham, & Struzick, 2008).

Back to Top | Article Outline
HIV and Cognition

Second only to the immune system, HIV negatively affects the nervous system. Risk of cognitive decline is increasingly observed in asymptomatic, symptomatic, and AIDS patients. Baldewicz et al. (2004) administered cognitive measures to adults with and without HIV over 8 years; the adults with HIV were asymptomatic at baseline. Compared to the adults without HIV, researchers found that adults with HIV performed progressively worse on these cognitive measures, especially if the adults became symptomatic or progressed to AIDS. Given the growing number of older adults with HIV who are more at risk of such declines in cognitive functioning, this represents a particular problem, as people age with this disease (Vance, Childs, Moneyham, & McKie-Bell, 2009).

Several mechanisms that affect neurological functioning in adults with HIV have been noted. First, HIV is known to cross the blood-brain barrier and infect glial cells; these cells are necessary for supporting neuronal health. Second, the death of glial cells releases a by-product, quinolic acid, which damages neurons (Vance, 2004). Third, many of the HIV medications can result in or exacerbate hypertension, heart disease, liver disease, and renal disease, all of which can further contribute to declines in cognitive functioning (Vance et al., 2009).

Back to Top | Article Outline
Other Comorbidities, Related Conditions, and Cognition

A number of other comorbidities, as well as some treatments for the comorbidities, are known to negatively affect cognitive functioning. Such conditions include lupus, poor sleep hygiene and insomnia, chronic fatigue syndrome (CFS), cancer and chemotherapy, advanced aging, and polypharmacy. This list is by no means exhaustive and is intended to acknowledge other similar medical conditions to help nurses recognize such comorbidities and related conditions as risk factors for declines in cognitive functioning.

Systemic lupus erthematosus negatively impacts cognitive functioning. Thirty-one women with lupus were compared with 31 healthy women without lupus. The women with lupus reported significantly more cognitive complaints and exhibited more impaired cognitive functioning compared with those without lupus (Colazarán, López-Longo, Cruz, Brittini, & Carreño, 2009). Also, CFS is characterized by alterations in cognitive functioning. Majer et al. (2008) compared 58 adults with CFS with 104 adults without CFS on several cognitive measures. Compared with the healthy adults, those adults with CFS performed significantly worse on measures of motor speed and working memory.

Poor sleep hygiene and insomnia obviously contribute to poorer cognitive functioning as well as poorer memory consolidation. Such sleep problems increase with advancing age (Redline et al., 2004). Tworoger, Lee, and Schernhammer (2006) found that in 1,844 older women (70-81 years), those with short sleep durations (<5 hours per night) or those who experienced difficulty falling and staying asleep, exhibited poorer cognitive functioning 2 years later compared with those with no such sleep problems.

Although cancer itself may not have a direct impact on cognitive functioning, unless it is brain cancer, treating cancer with chemotherapy may produce a toxic effect on the brain, resulting in severe memory loss, confusion, disorientation, and, at times, delirium. This condition, colloquially referred to as "chemobrain," affects 17%-75% of those who undergo this treatment. Many of these cognitive declines are transient but, in some cases, may have lingering effects for years (Myers, 2009). It is well documented that advanced aging increases cognitive complaints and decreases cognitive functioning. These changes in cognitive functioning may also correspond to the rise in the prevalence of age-related comorbidities (Ball, Vance, Edwards, & Wadley, 2004).

Finally, often accompanying advanced age and age-related comorbidities, polypharmacy has been shown to negatively effect cognitive functioning. Polypharmacy is defined as taking five or more medications. Older adults, in general, have less adipose tissue and reduced liver and kidney function, making the combination of medications more problematic for the body to process, which can impair brain health and cognitive reserve (Ball et al., 2004).

Back to Top | Article Outline

Cognitive Reserve

Cognitive reserve refers to the brain's ability to successfully absorb insults from physiological sequelae, comorbidities, and lack of mental stimulation while still maintaining a level of cognitive functioning required to sustain everyday functioning (Figure 1; Vance, Viamonte, et al., 2008). Cognitive reserve depends on the number, strength, integrity, and sophistication of connections between neurons. It also refers to the brain's ability to repair damage, compensate in lieu of damage, and maintain as much cognitive functioning as possible. Thus, the more cognitive reserve one possesses, the better is one's cognitive functioning.

Cognitive reserve is thought to be maintained or depleted through two processes: positive neuroplasticity and negative neuroplasticity (Vance & Crowe, 2006). Positive neuroplasticity entails being exposed to novel and challenging stimulation that encourages the brain to adapt and, in the process, build cognitive reserves, whereas negative neuroplasticity entails lacking the exposure to novel and challenging stimuli, resulting in decreased cognitive reserve. These processes have been observed in animal and human studies.

In animal studies, Diamond (1993) explains the use of the enriched environmental paradigm in promoting neuroplasticity. Genetically similar rats were assigned to live in one of three decreasingly enriched environmental conditions: enriched, standard, and impoverished. In the enriched environmental condition, rats were placed in a large cage with other rats and toys with which to interact. In the standard environmental condition, rats were placed in a cage with two other rats with which to interact; no toys were present. In the impoverished condition, rats were placed in a cage by themselves with no toys or other rats with which to interact. Using this experimental paradigm, rats in the enriched environmental condition developed a larger brain, had more intricate connections between neurons, and performed better on maze tests compared with those in the other two conditions; likewise, rats in the standard environmental condition experienced similar gains compared with rats in the impoverished condition. In further studies, these results remained consistent despite the age of the rats or whether their brains were compromised by chemical or surgical lesioning to approximate the effects of neuroplasticity on brain damage and reduced cognitive reserve (Puurunen & Sivenius, 2002; Vance & Wright, 2009).

In humans, the effects of positive and negative neuroplasticity on cognitive reserve are documented in a study by Boyke, Driemeyer, Gaser, Büchel, and May (2008). These researchers recruited 69 older adults (Mage = 60 years) and taught them how to juggle using a three-ball cascade. A magnetic resonance imaging (MRI) scan was performed before teaching them to juggle, immediately after they learned to juggle, and approximately 3 months later when they no longer juggled and had lost this ability. Twenty-five of the 69 participants learned to juggle for a minimum of 1 minute. In those who learned to juggle, MRI scans revealed a significant increase in the volume of the hippocampus and nucleus accumbens immediately after learning to juggle; these brain structures are necessary for forming memory engrams. This gray matter growth epitomizes the process of positive neuroplasticity. Likewise, 3 months later, when the participants no longer practiced and lost the ability to juggle, MRI scans revealed a significant decrease in the volume of the hippocampus and nucleus accumbens; this gray matter shrinkage epitomizes the process of negative neuroplasticity. These studies reveal that cognitive reserve can be purposely increased or decreased through challenging the brain and exposing the brain to novel stimuli.

Back to Top | Article Outline

Implications for Nursing Practice

As nurses work with clients with comorbidities, holistically it is important to be aware of the possible cognitive effects disease can have on adults and the ensuing implications for nursing practice. Therefore, nurses will need to interview patients about changes in cognitive functioning; likewise, nurses may need to inquire about potential risk factors for cognitive declines. Three strategies for confronting the cognitive risks associated with certain comorbidities include lifestyle/prevention strategies, amelioration strategies, and mitigation strategies.

Back to Top | Article Outline
Lifestyle/Prevention Strategies

There are several lifestyle strategies that can prevent the onset of some comorbidities that are also neuroprotective. As health and wellness educators, nurses can convey these strategies to clients. Numerous studies indicate that physical exercise, intellectual exercise, proper nutrition including elevated levels of antioxidants, good sleep hygiene, stress reduction, moderate alcohol use, and avoidance of substance use are beneficial for physiological health and subsequently brain health (Colcombe & Kramer, 2003; Férat et al., 2009; Vance & Crowe, 2006). In fact, it has been proposed that a wellness program or an individualized cognitive prescription that incorporates these components can be used to promote cognitive health in adults as they age (Vance, Roberson, McGuiness, & Fazeli, 2010).

Back to Top | Article Outline
Amelioration Strategies

There are four amelioration strategies most commonly used. Each of these strategies involves the use of medications and/or therapies. The nurse should be familiar with each of these and support these efforts through patient education and by emphasizing the necessity of medication/therapy compliance. The first strategy is to medically treat the comorbidity. Medical treatment for many comorbidities can return one's physiological functioning to a normal, healthy homeostatic state, which also benefits brain health. Medical treatments might include appropriate use of medications. For example, statins can be prescribed for those with hypercholesterolemia, which can be neuroprotective (Green, Bachman, Benke, Cupples, & Farrer, 2003). Likewise, antidepressants have been shown to not only reduce symptoms of depression but also to reduce cortisol levels; this is important given that cortisol exerts a neurotoxic effect (Cumurcu, Ozyurt, Etikan, Demir, & Karlidag, 2009).

Second, many comorbidities affect the brain by creating an inflammatory response that can, over time, be damaging to neurons. Furthermore, many clinicians consider Alzheimer disease to be a "low-burner" inflammatory syndrome. Cyclooxygenase produces prostaglandins, which create inflammation of body tissues, including the brain. Therefore, nonsteroidal anti-inflammatory agents, which inhibit cyclooxygenases, may be considered as a supplemental treatment strategy (Vance, Keltner, McGuiness, Umlauf, & Yuan, 2010).

Third, neurotrophic medications may be a helpful strategy for some adults experiencing loss in cognitive functioning (Meyer et al., 2002). Some medications from which to choose include N-methyl-D-aspartate (NMDA) inhibitors, monamine oxidase-B inhibitors, and acetylcholine-enhancing agents. NMDA inhibitors are neuroprotective and act by preventing abnormal glutamate binding to NMDA receptors without disrupting normal glutamate neuron activation (Keltner, 2004). Because glutamate is the most plentiful excitatory neurotransmitter, this drug mechanism is important because it prevents over abundance of glutamate coupling with these receptor sites, which cause neuronal death. NMDA receptor blockade prevents excitotoxicity, which causes neuronal death; in this manner, NMDA inhibitors are considered to hinder or slow down the neurodegenerative processes (Keltner, 2004).

Monamine oxidase-B inhibitors conserve dopamine in the brain and has been observed to improve cognitive functioning in certain populations such as those with HIV (Sacktor et al., 2000). In five double-blind randomized trials, selegiline has been shown to improve cognitive functioning in adults (American Psychiatric Association, 1997). However, administering this drug can cause orthostatic hypotension, irritability, and agitation; therefore, these side effects must be taken into consideration.

For those with more severe declines in cognitive functioning, actetylcholine-enhancing agents are suggested. Studies show that they initially have a cognitive benefit in normal older adults; however, this benefit is brief and tapers off quickly (Yesavage et al., 2008). These medications are typically prescribed for those with Alzheimer disease and related dementias. Therefore, a neuropsychological assessment should also be conducted to determine if the cognitive impairment is progressing toward early-stage dementia. Likewise, these agents are not universally tolerated. For example, Cognex is associated with severe hepatic reactions, whereas Aricept is not (Keltner, 2001).

Fourth, cognitive remediation therapy has been shown to be an effective strategy in improving global cognitive functioning and specific cognitive abilities such as reasoning or speed of processing. For example, Vance et al. (2007) assigned community-dwelling older adults to either a speed of processing training condition (n = 82) or to a no-contact control group (n = 77). The speed of processing training consisted of ten 1- hour computer training sessions, whereby participants engaged in visual perception tasks designed to improve the speed in which they observe and process information. Central and peripheral visual targets were presented at a faster and faster speed on the computer screen; these exercises required the participants to respond to targets. Eventually, the presentation speed would be fast enough to reach the participants' perceptual threshold and then, through practice, stretch this cognitive ability, which epitomizes the process of positive neuroplasticity. The researchers found that the participants who received speed of processing training improved on cognitive measures of visual speed of processing compared with those who did not receive this training; it was also found that the cognitive benefits from this training were robust over a 2-year period after training occurred. This study and others like it show how cognitive remediation therapy provides a way to protect and improve cognitive functioning and mitigate cognitive loss in adults (Vance & Wright, 2009).

Back to Top | Article Outline
Mitigation Strategies

Mitigation strategies can be used to compensate for the loss of cognitive functioning and bolster everyday functioning. Although by no means exhaustive, such strategies include method of loci, chunking, spaced retrieval method, and external memory aids. All of these mitigation strategies are used to support memory needed for everyday functioning. Method of loci is a memory technique whereby the information to be remembered is visually paired with a location such as rooms of one's house or landmarks on a familiar road (Figure 2). For example, to remember a phone number of someone (e.g., 628-8807), the person may imagine each of the numbers in the sequence along the sequence of certain landmarks on a walking trail he or she is familiar with (e.g., 6-start trail, 2-playground, 8-football field, 8-campground, 8-tennis court, 0-swimming pool, 7-finish trail). Using this visual cueing technique, this paired association is highly adaptable at memorizing sequential information (Vance, Viamonte, et al., 2008).

Figure 2
Figure 2
Image Tools

Chunking is another effective memory strategy whereby the information to be learned is broken down into smaller pieces (i.e., chunks), which are more easily memorized. These smaller pieces, once learned, are reassembled to form a whole. For example, in learning a phone number, the first three digits (e.g., 6-2-8) and the last four digits (e.g., 8-8-0-7) are memorized separately; once these two chunks are successfully learned, they can be easily reassembled to form a whole. This mitigation strategy is easy to use and can be applied to a variety of venues (Vance, Viamonte, et al., 2008).

Spaced retrieval method is a particularly useful mitigation strategy to help those with more severe memory problems to learn and retain specific information. It works by presenting the target information to the person and then asking him or her to recall it over increasing intervals (e.g., 30 seconds, 1 minute, 2 minutes, 4 minutes, 8 minutes, and 16 minutes). If the person cannot recall the information at a particular interval (e.g., 8 minutes), then the information is presented again to him or her and he or she is asked to recall the information at the previous interval in which the information was successfully recalled (e.g., 4 minutes.). This process continues until the information can be successfully recalled after 16 minutes, at which point it is consolidated into one's long-term memory (Vance, Viamonte, et al., 2008). This strategy has been found to be particularly useful, especially with adults experiencing mild to moderate Alzheimer disease (Vance & Farr, 2007).

External memory aids are undoubtedly the easiest of the mitigation strategies and are used in everyday life by those without cognitive loss. Their familiarity facilitates their use in adults to mitigate the loss of cognitive functioning. These aids utilize physical reminders to cue and provide the information to be recalled; they can include lists and notes, calendars, and even family and friends (Vance, Viamonte, et al., 2008).

Back to Top | Article Outline
Consultations and Referrals

As is common in healthcare, a team approach remains the best model to gather expert advice in providing holistic, optimal care and wellbeing for the patient. Many of the strategies that involve cognitive remediation therapy as well as various mitigation strategies (e.g., chunking, spaced retrieval method) are well known to psychologists, especially neuropsychologists, cognitive psychologists, and geropsychologists. Prescribing medications to patients to improve cognitive functioning should be done so in collaboration with a neurologist or psychiatrist. Yet, nurses provide the clinical skills necessary in learning how to use, apply, and teach these cognitive strategies and techniques to patients (for more information on learning these approaches, please see Vance, Viamonte, et al., 2008).

Back to Top | Article Outline

Implications for Nursing Research

There are three primary research vectors for nurse scientists to investigate how to prevent, ameliorate, or mitigate the loss of cognitive functioning in adults with comorbidities. First, the physiological mechanisms of these comorbidities and related conditions on cognitive reserve needs further study in order for them to be identified and targeted for intervention (e.g., cortisol levels, decreased cerebral perfusion, disease correlates). Second, methods for preventing and effectively treating such comorbidities must continue to be developed. This research vector is fundamental in preventing the loss of cognitive reserves needed to support cognitive functioning. Finally, the development of cognitive wellness programs that take into consideration all of the factors related to optimal cognitive functioning (e.g., physical and intellectual exercise, nutrition, and stress reduction) should be examined. This vector entails mixing and matching different strategies to synergistically protect and improve cognitive functioning. For example, Vance, Roberson, et al. (2010) recently provided step-by-step instructions for creating an individualized cognitive prescription that is adaptable for preventing cognitive loss and ameliorating or mitigating loss in cognitive functioning.

Back to Top | Article Outline

Conclusion

Cognitive functioning is important for negotiating one's environment, interacting with others, and enjoying life. Unfortunately, comorbidities and sometimes even the medications used to treat them may contribute to poorer cognitive functioning. Nurses need to be aware of the potential risks of the cognitive decline of their clients, especially if they have more than one comorbidity or are advancing in age when many comorbidities are more prevalent. Likewise, given their proximity to patients, nurses are in a superb position to observe and assess cognitive changes in patients. Similarly, as educators, nurses can teach patients strategies to maintain or improve and protect their cognitive abilities. As shown, there are a variety of techniques and opportunities to improve one's cognitive reserve and maintain cognitive function or protect against cognitive decline immediately and over the life span. Such an approach has the potential to improve their quality of life and may benefit the overall health of patients.

Back to Top | Article Outline

Acknowledgments

We appreciate the comments and feedback of Steven Antonson and Paul Durham in writing this article.

Back to Top | Article Outline

References

American Psychiatric Association. (1997). Practice guideline for treatment of patients with Alzheimer's disease. Washington, DC: American Psychiatric Association.

Baldewicz, T. T., Leserman, J., Silva, S. G., Pettito, J. M., Golden, R. N., Perkins, D. O., et al. (2004). Changes in neuropsychological functioning with progression of HIV-1 infection: Results of an 8-year longitudinal investigation. AIDS and Behavior, 8(5), 345-355. doi: 10.1023/B:AIBE.0000044081.42034.54.

Ball, K. K., Vance, D. E., Edwards, J. E., & Wadley, V. W. (2004). Aging and the brain. In M. Rizzo & P. J. Eslinger (Eds.), Principles and Practice of Behavioral Neurology and Neuropsychology (pp. 795-809). Philadelphia: Saunders.

Beaudreau, S. A., & O'Hara, R. (2009). The association of anxiety and depressive symptoms with cognitive performance in community-dwelling older adults. Psychology and Aging, 24(2), 507-512. doi: 10.1037/a0016035.

Beeri, M. S., Ravona-Springer, R., Silverman, J. M., & Haroutunian, V. (2009). The effects of cardiovascular risk factors on cognitive compromise. Dialogues in Clinical Neuroscience, 11(2), 201-212.

Boyke, J., Driemeyer, J., Gaser, C., Büchel, C., & May, A. (2008). Training-induced brain structure changes in the elderly. Journal of Neuroscience, 28, 7031-7035. doi: 10.1523/JNEUROSCI.0742-08.2008.

Bruehl, H., Wolf, O. T., Sweat, V., Tirsi, A., Richardson, S., & Convit, A. (2009). Modifiers of cognitive function and brain structure in middle-aged and elderly individuals with type 2 diabetes mellitus. Brain Research, 1280, 186-194. doi: 10.1016/j.brainres.2009.05.032.

Carroll, B. J., Cassidy, F., Naftolowitz, D., Tatham, N. E., Wilson, W. H., Iranmanesh, A., et al. (2007). Pathophysiology of hypercortisolism in depression. Acta Psychiatric Scandinavia Supplmentia, 433, 90-103. doi: 10.1111/j.1600-0447.2007.00967.x.

Casteneda, A. E., Tuulio-Henriksson, A., Marttunen, M., Suvisaari, J., & Lönnqvist, J. (2008). A review on cognitive impairments in depressive and anxiety disorders with a focus on young adults. Journal of Affective Disorders, 106(1-2), 1-27. doi: 10.1016/j.jad.2007.06.006.

Colazarán, J., López-Longo, J., Cruz, I., Bittini, A., & Carreño, L. (2009). Cognitive dysfunction in systemic lupus erythematosus: Prevalence and correlates. European Neurology, 62(1), 49-55. doi: 10.1159/000215879.

Colcombe, S., & Kramer, A. F. (2003). Fitness effects on the cognitive function of older adults: A meta-analytic study. Psychological Science: A Journal of the American Psychological Society, 14, 125-130. doi: 10.1111/1467-9280.t01-1-01430.

Cumurcu, B. E., Ozyurt, H., Etikan, I., Demir, S., & Karlidag, R. (2009). Total antioxidant capacity and total oxidant status in patients with major depression: Impact of antidepressant treatment. Psychiatry and Clinical Neuroscience, 63(5), 639-645. doi: 10.1111/j.1440-1819.2009.02004.x.

Deckersbach, T., Savage, C. R., Reilly-Harrintgton, N., Clark, L., Sachs, G., & Rauch, S. L. (2004). Episodic memory impairment in bipolar disorder and obsessive-compulsive disorder: The role of memory strategies. Bipolar Disorder, 6(3), 233-244. doi: 10.1111/j.1399-5618.2004.00118.x.

Diamond, M. (1993). An optimistic view of the aging brain. Generations, 17, 31-33.

Elwood, P. C., Pickering, J., Bayer, A., & Gallacher, J. E. J. (2002). Vascular disease and cognitive function in older men in the Caerphilly Cohort. Age and Ageing, 31, 43-48. doi: 10.1093/ageing/31.1.43.

Férat, C., Samieri, C., Rondeau, V., Amieva, H., Portet, F., Dartigues, J. F., et al. (2009). Adherence to a Mediterranean diet, cognitive decline, and risk of dementia. Journal of the American Medical Association, 302(6),638-648. doi: 10.1001/jama.2009.1146.

Firk, C., & Markus, C. R. (2009). Mood and cortisol responses following tryptophan-rich hydrolyzed protein and acute stress in healthy subjects with high and low cognitive reactivity to depression. Clinical Nutrition, 28(3), 266-271. doi: 10.1016/j.clnu.2009.03.002.

Green, R. C., Bachman, D. L., Benke, K. S., Cupples, L. A., & Farrer, L. A. (2003). MIRAGE Study Group Comparison of Alzheimer's disease risk factors in White and African American families. Neurology, 60(8), 1372-1374.

Hajjar, I., Yang, F., Sorond, F., Jones, R. N., Milberg, W., Cupples, L. A., et al. (2009). A novel aging phenotype of slow gait, impaired executive function, and depressive symptoms: Relationship to blood pressure and other cardiovascular risks. Journal of Gerontology: Medical Sciences, 64A(9), 994-1001. doi: 10/1093/Gerona/glp075.

Jeong, J. M., & Cranney, J. (2009). Motivation, depression, and naturalistic time-based prospective remembering. Memory, 27, 1-10. doi:10.1080/09658210903074673.

Keltner, N. (2001). Drugs used for cognitive symptoms of Alzheimer's disease. Perspectives in Psychiatric Care, 37(1), 31-34.

Keltner, N. (2004). Memantine: A new approach to Alzheimer's disease. Perspectives in Psychiatric Care, 40(3), 123-124. doi: 10.1111/j.1744-6163.2004.tb00007.x.

Launer, L. J., Masaki, K., Petrovitch, H., Foley, D., & Havlik, R. J. (1995). The association between midlife blood pressure levels and late-life cognitive function. The Honolulu-Asia Aging Study. Journal of the American Medical Association, 274(23), 1846-1851. doi: 10.1001/jama.274.23.1846.

Lόpez-Leόn, S., Aulchenko, Y. S., Tiemeier, H., Oostra, B. A., van Duijn, C. M., & Janssens, A. C. (2009). Shared genetic factors in the co-occurrence of symptoms of depression and cardiovascular risk factors. Journal of Affective Disorders. Epub ahead of print.

Majer, M., Welberg, L. A., Capuron, L., Miller, A. H., Pagnoni, G., & Reeves, W. C. (2008). Neuropsychological performance in person with chronic fatigue syndrome: Results from a population-based study. Psychosomatic Medicine, 70(7), 829-836. doi: 10.1097/PSY.0b013e31817b9793.

McGuire, L. C., Ford, E. S., & Ajani, U. A. (2006). Cognitive functioning as a predictor of functional disability in later life. American Journal of Geriatric Psychiatry, 14(1), 36-42. doi: 10.1097/01.JGP.0000192502.10692.d6.

Meyer, J. S., Li, Y., Xu, G., Thornby, J., Chowdhury, M., & Quach, M. (2002). Feasibility of treating mild cognitive impairment with cholinesterase inhibitors. International Journal of Geriatric Psychiatry, 17, 586-588.

Myers, J. S. (2009). Chemotherapy-related cognitive impairment. Clinical Journal of Oncology Nursing, 13(4), 413-421. doi: 10.1188/09.CJON.413-421.

Neylan, T. C., Leonoci, M., Rothlind, J., Metzler, T. J., Schuff, N., Du, A. T., et al (2004). Attention, learning, and memory in posttraumatic stress disorder. Journal of Traumatic Stress, 17(1), 41-46. doi: 10.1023/B:JOTS.0000014675.75686.ee.

Pressler, S. J. (2008). Cognitive functioning and chronic heart failure: A review of the literature (2002-July 2007). Journal of Cardiovascular Nursing, 23(3), 239-249. doi: 10.109/01.JCN0000305096.09/10.ec.

Puurunen, K., & Sivenius, J. (2002). Influence of enriched environment on spatial learning following cerebral insult. Reviews in the Neurosciences, 13(4), 347-364.

Redline, S., Kirchner, H. L., Quan, S. F., Gottlieb, D. J., Kapur, V., & Newman, A. (2004). The effects of age, sex, ethnicity, and sleep-disordered breathing on sleep architecture. Archives of Internal Medicine, 164, 406-418.

Ruis, C., Biessels, G. J., Gorter, K. J., Donk, M. V. D., Kappelle, L. J., & Rutten, G. E. H. M. (2009). Cognition in the early stage of type 2 diabetes. Diabetes Care, 32(7), 1261-1265. doi: 10/2337/dc08-2143.

Sacktor, N., Schifitto, G., McDermott, M. P., Marder, K., McArthur, J. C., & Kieburtz, K. (2000). Transdermal selegiline in HIV-associated cognitive impairment: Pilot, placebo-controlled study. Neurology, 54(1), 233-235.

Starr, V. L., & Convit, A. (2007). Diabetes, sugar-coated but harmful to the brain. Current Opinion in Pharmacology, 7(6), 638-642. doi: 10.1016/j.coph.2007.10.007.

Steffens, D. C., McQuoid, D. R., & Potter, G. G. (2009). Outcomes of older cognitively impaired individuals with current and past depression in the CDODE study. Journal of Geriatric Psychiatry and Neurology, 22(1), 52-61. doi: 10.1177/0891988708328213.

Tworoger, S. S., Lee, S., Schernhammer, E. S., & Grodstein, F. (2006). The association of self-reported sleep duration, difficulty sleeping, and snoring with cognitive function in older women. Alzheimer's Disease and Associated Disorders, 20(1), 41-48. doi: 10.1097/01.wad.0000 201850. 52707.80.

Vance, D. E. (2004). Cortical and subcortical dynamics of aging with HIV infection. Perceptual and Motor Skills, 98, 647-655. doi: 10.2466/PMS.98.2.647-655.

Vance, D. E., Childs, G., Moneyham, L., & McKie-Bell, P. (2009). Barriers to successful aging with HIV: A brief overview for nursing. Journal of Gerontological Nursing, 24, 19-25. doi: 10.3928/00989134-20090731-04.

Vance, D. E., & Crowe, M. (2006). A proposed model of neuroplasticity and cognitive reserve in older adults. Activities, Adaptation and Aging, 30(3), 61-79. doi: 10.1300?J016v30n03_04.

Vance, D. E., Dawson, J., Wadley, V., Edwards, J., Roenker, D., Rizzo, M., et al. (2007). The Accelerate Study: The longitudinal effect of speed of processing training on cognitive performance of older adults. Rehabilitation Psychology, 52(1), 89-96. doi: 10.1037/0090-5550.52.1.89.

Vance, D. E., & Farr, K. (2007). Spaced retrieval for enhancing memory: Implications for nursing practice and research. Journal of Gerontological Nursing, 33(9), 46-52.

Vance, D. E., Keltner, N. L., McGuiness, T., Umlauf, M. G., & Yuan, Y. Y. (2010). The future of cognitive remediation training in older adults. Journal of Neuroscience Nursing, 42, 255-264. doi: 10.1097/JNN.0b013e3181ecb003.

Vance, D. E., Moneyham, L., Fordham, P., & Struzick, T. C. (2008). A model of suicidal ideation in adults aging with HIV. Journal of the Association of Nurses in AIDS Care, 19(5), 375-384. doi: 10.1016/j.jana.2008.04.011.

Vance, D. E., Roberson, A. J., McGuiness, T., & Fazeli, P. L. (2010). Protecting cognitive functioning across the lifespan: A multifactorial perspective on neuroplasticity and cognitive reserve. Journal of Psychosocial Nursing and Mental Health Services, 48, 23-30. doi: 10.3928/02793695-20100302-01.

Vance, D. E., Viamonte, S., Foote, A., Webb, N., Marceaux, J., & Ball, K. K. (2008). Mental stimulation, neural plasticity, and aging: Directions for nursing practice and research. Journal of Neuroscience Nursing, 40(4), 241-249.

Vance, D. E., Wadley, V. G., Ball, K. K., Roenker, D. L., & Rizzo, M. (2005). Physical activity and sedentary behavior on cognitive health in older adults. Journal of Physical Activity in the Elderly, 13, 294-313.

Vance, D. E., & Wright, M. A. (2009). Positive and negative neuroplasticity: Implications for promotion of cognitive health in aging. Journal of Gerontological Nursing, 35(6), 11-17. doi: 10.9999/00989134-20090428-02.

Viamonte, S., Vance, D., Wadley, V., & Ball, K. (2010). Driving-related cognitive performance in older adults with pharmacologically-treated cardiovascular disease. Clinical Gerontologist, 33, 109-123.

Yesavage, J. A., Friedman, L., Ashford, J. W., Kraemer, H. C., Mumenthaler, M. S., Noda, A., et al. (2008). Acetylcholinesterase inhibitors in combination with cognitive training in older adults. Journal of Gerontology: Psychological and Social Science, 63(5), 288-294.

Zung, W. W., Broadhead, W. E., & Roth, M. E. (1993). Prevalence of depressive symptoms in primary care. Journal of Family Practice, 37, 337-344.

© 2011 American Association of Neuroscience Nurses

Login

Article Level Metrics