Struble, Laura M. PhD, GNP-BC; Sullivan, Barbara-Jean PhD, APRN-BC, NP
A common belief among healthcare professionals and the public is that aging is a downhill slope accompanied by difficulty learning new skills, rigid thinking and ultimately ending in "senility" or dementia. The old proverb, "You can't teach an old dog new tricks" is still the stereotypical view of cognition and aging in the 21st century. Although a majority of people (62%) in the United States fear the loss of mental capacity more than they fear physical disabilities (29%), negative assumptions about the capacity to grow and learn create a vicious cycle of mental inactivity and decline.1 Major research breakthroughs based on new imaging techniques have advanced science and offered a more positive view of cognitive function in older adults. Two proverbs that better explain cognitive aging are, "Older is wiser" and "If you don't use it you lose it." Although there are measurable areas of cognitive decline related to aging, they are more subtle than previously thought in healthy persons.2 This more positive image of aging must influence how advanced practice nurses educate and motivate older adults to live healthier lives.
Cognition is a combination of skills, including attention, learning, memory, language, visual spatial skills, and executive function, such as decision making, goal setting, planning, and judgment. Researchers and theorists have attempted to discover a single mechanism that controls all age-related cognitive changes to no avail. It is not that simple; cognition is influenced by the varied physiological, psychological, and social life experiences of older adults who are of the same age.3 As a result, cognitive changes in older adults are very individualized, and unfortunately this makes developing robust research designs difficult.
Degenerative brain changes in aging
Many changes occur in the brain during aging including morphologic changes in cerebral tissue, decline in cerebral blood flow in multiple regions of the brain, a decrease in some neurotransmitters or loss of their binding sites, and accumulation of lipofuscin in nerve cell bodies.4 After the age of 50, brain weight decreases approximately 2% to 3% per decade. This accelerates after the age of 80 to about 10% per decade thereafter.5 However, brain shrinkage or volumetric changes occur unequally across brain structures. In older adults there is a 12% volume decrease in the frontal lobe and 9% volume decrease in the temporal lobe. Remarkably, the parietal and occipital lobes show very little tissue loss.6 Both gray and white matter shows shrinkages during adulthood but at different rates. Gray matter (neural cell bodies) shrinks more quickly than white matter (myelinated nerve fibers) through adulthood up to age 50. The pattern then starts to reverse and more decline is seen in white matter than gray matter after age 50.7 Enlargement of the ventricles is thought to occur because of the loss of brain cells and has been studied as a short-term marker of disease progression in normal-aged controls, subjects with mild cognitive impairment (MCI) and subjects with Alzheimer disease (AD).8
In an average lifetime, a person will lose about 20 billion neocortical neurons, which calculate out to about 1 neuron per second.9 While there are extra neurons to spare, termed cognitive reserve, neuronal loss and functional consequences will add up and become noticeable in later years of life. Neurons, however, are not lost uniformly. For example, neurons in the hippocampal complex (related to memory) minimally decrease despite hippocampal volume loss from shrinkage.10 In AD, approximately 60% of neurons are lost in the CA1 region of the hippocampus while in aging the loss is minimal despite the hippocampal volume shrinkage. One theory is that aging may be a precursor to AD because of the loss of synapses and associated volume loss in the hippocampus.5,11 The accumulation of senile plaques and neurofibrillary tangles are also seen in older brains without neurogenerative disease, but these hallmark features are seen in greater numbers and distribution in AD.5
Neurogenesis and neuronal plasticity
Despite degenerative brain changes, studies have reported resilience in aging including amelioration of age-related deterioration and successful cortical remodeling.12 Cohen13 reports that in the last 20 years, "healthy older brains are often as good as or better than younger brains in a wide variety of tasks." Based on research, a more optimistic view of cognitive aging is emerging with positive aging characteristics. It is now known that neurogenesis, the birth of new neuronal cells, form throughout life into older adulthood and experience and learning enables the brain to "resculpt" itself. "Neuroplasticity" or the regeneration and structural rebuilding of lost circuits in the brain, continues with stimulation. Although research is limited, there is a clear link between brain plasticity and a rich stimulating environment that can enhance and maintain brain function in aging. Plasticity in the hippocampal region of the brain is thought to be the structural foundation in learning and memory.14 When brain cell connections are lost due to brain cell death, healthy cells are able to rebuild those connections. This enables an older individual's experience to induce learning throughout life.15,16
Another proposed model related to plasticity and the ability of the aging brain to adapt is the scaffolding theory of aging and cognition. This theory suggests there is recruitment of additional circuitry, especially from the frontal cortex, that helps declining neural structures whose function has become inefficient.17 This "Dedifferentiation," defined as a more diffuse pattern of brain activation or cortical reorganization with aging, has been studied using functional imaging technology. Positron emission tomography and functional magnetic resonance imaging studies have shown less specificity or differentiation in brain recruitment while performing an array of cognitive tasks. The additional brain regions showing activity in older subjects are thought to reflect reorganization of function.18,19 It has been proposed that some older adults use dedifferentiation as an early compensatory response to maintain cognitive function in the initial stages of AD.20 Finally, emotional circuitry of the brain matures and becomes more balanced, and functions of the left and right hemispheres of the brain have been shown to be more integrated.4,13 While the aging brain is not completely understood, neuronal regeneration and neurogenesis does occur in 80- and 90-year-olds. The available evidence suggests that cortical structural changes can occur as a result of cognitive challenges and stimulating experiences.
Cognitive functions such as verbal ability, word knowledge, and semantic memory are preserved in older adults.21 The emerging trend in the domain of cognitive aging is to recognize the areas of cognitive decline but explore and build on the older adults' cognitive strengths. It is important to recognize that not all aspects of cognition exhibit uniform decline with aging and not all older adults experience similar levels of cognitive decline.22 Some older adults show significant cognitive deficits, but others perform as well as young adults.17
Cognitive skills and aging
Different aspects of cognition are affected in various ways over time, but research results are conflicting. Studies utilizing a longitudinal-type research design have found that cognitive decline starts to occur in the late 50s or later.23,24 However, Salthouse25 developed a cross-sectional research design and found measurable declines in early adulthood that supports the theory that age-related cognitive decline occurs in healthy educated adults in their 20s and 30s. Problems in the definition, measurement, and methodology cause disagreement about what is universal age-related cognitive deficits. The focus of this discussion will be on two common domains of cognition (attention and memory) to better understand the cognitive changes that accompany normal aging.
Attention is the ability to focus or concentrate on a task while ignoring other features in the environment. There are three different components of attention, and there are some age-related declines in two of the areas. Sustained attention is the ability to direct attention and focus on one main task over time. Examples of this ability would be reading this article or packing fragile glasses without breaking them. This simple attentional process is relatively unaffected by normal aging changes.26 Selective attention is the second component and is defined as the capacity to focus on a specific feature among a variety of stimuli. For example, watching a movie while ignoring other patrons talking and ignoring the sensations of an uncomfortable seat. Finally, the highest level of attention is called divided attention related to concurrently attending to and processing information from multiple sources. Researchers established that older adults have more difficulties with selective and divided attention than younger adults.26 Attention and cognitive slowing are also evident when there are complex tasks requiring multiple steps, especially when other stimuli are presented. When older adults try to learn in a "noisy environment" (visual, auditory, or extraneous information), this will encumber the person's ability to process information.27
Complaints of memory loss are a major concern in the older population. Even in middle-aged persons, a common worry is whether forgetting names or meetings are signs of dementia. Memory functions are vulnerable to a range of diseases; the foremost are neurodegenerative disease such as AD, but there are many other possible causes as well including stroke, head trauma, brain tumors, hypoxia, cardiac surgery, malnutrition, attention-deficit hyperactivity disorder, depression, hypoxia, medication adverse reactions, and so on. Pathology that disrupts circulation, oxygenation, or glucose utilization may impede memory. It is very important to distinguish between memory loss in aging and memory loss associated with different degenerative dementias. Memory is not a simple concept. Recently, memory has become recognized as a collection of mental abilities that depend on multiple systems within the brain. Four systems that are more clinically relevant to memory functions in normal aging are episodic memory, semantic memory, implicit memory, and working memory.28
Episodic memory. Episodic memories (autobiographical memory) are recollections actively retrieved as personal experiences framed in the person's own context, such as remembering whether you took your medication this morning. Episodic memory appears to be one of the memory systems that decline in healthy older adults.29
Semantic memory. Semantic memory refers to the general store of conceptual and factual knowledge that is not related to any specific memory, such as knowing that a dog has four legs. This is also often referred to as crystallized intelligence. It is based on facts and is rooted in the older adult's experiences. Semantic memory becomes stable and/or stronger as new knowledge and understanding accumulate throughout the years.3,4 In contrast, fluid intelligence or "native mental ability," which is the information processing system, is age sensitive. Fluid intelligence allows the person to think and reason abstractly as well as solve problems and relies on the person's inherent abilities. It has been documented that fluid intelligence peaks in adolescence and begins to decline between the age of 30 and 40.30 It is theorized that complex tasks that require taking in new information then analyzing it becomes more difficult with age.
Younger adults easily memorize large lists using rote memorization (fluid intelligence), whereas older adults with more experience make up for this (crystallized intelligence) through better developed verbal abilities and judgment.31 Older adults have a harder time memorizing because the fluid intelligence of linking the information declines with age. Older adults feel they are losing their memory functions when in fact it is a fluid intelligence problem because they are unable to connect the information.
Implicit memory. Implicit memory refers to a type of memory in which a previous experience indirectly influences an individual's behavior without intentional retrieval or conscious recollection of this experience.26 For example, recalling what you had for breakfast requires a conscious, intentional recollection of previous experiences and information (explicit memory). Knowing how to ride a bike, however, is nonintentional and does not require conscious recall of how a person was taught to ride a bike (implicit memory). Another term used frequently is "procedural memory," which is a form of implicit memory that allows a person to remember how to tie shoes or swim without consciously thinking about these activities. Implicit memory is relatively unaffected by aging compared with explicit memory.26,28
Working memory. One area of executive functioning is working memory, which refers to structures and processes used for temporarily storing and manipulating information such as the ability to remember several numbers and summing the total (for example, subtracting a dollar amount from a bill total).26 It is conceptualized as a higher order cognitive construct and requires goal-orientated active monitoring or manipulation and processing of information. Working memory should not be confused with short-term memory, which is defined as the ability to hold information in memory for a short period (for example, remembering a telephone number you just heard while dialing the number). Working memory places greater demands on cognitive abilities; therefore, it has a more significant decline with aging compared with short-term memory. To transfer information into episodic memory, the information first has to be "kept in mind" by working memory.32
Table. Tools to faci...Image Tools
Table. Tools to faci...Image Tools
The cognitive assessment process for older adults involves careful evaluation of various areas of brain function including intelligence, attention span, concentration, perception, problem solving, learning ability, judgment, orientation, memory, reaction time, social intactness, and psychomotor ability.33 Cognitive impairment is the term used to describe a range of disturbances in cognitive functioning. To accurately diagnose cognitive impairment, assessment of cognitive function and a thorough mental status exam are essential. An important part of the workup can be completed by the advanced practice nurse through physical exam (such as ruling out medical contributions to compromised cognition), the relationship with the patient, assessment of mental status during conversations, use of screening tests, family history, and development of a record of the emergence and manifestation of various symptoms. In addition, referral for a comprehensive intelligence test performed by a licensed clinical psychologist using reliable and valid tests, for example, the Wechsler Adult Intelligence Scale (WAIS), will address many of the functions described here. If major discrepancies in function are noted, often, a referral to a neuropsychologist for localization and further identification of specific functional problems is used before or along with MRI and/or CT scans.
An important resource for beginning to distinguish between general categories of cognitive impairment is the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR).34 An advantage of the DSM-IV-TR is that it creates a common language between the multidisciplinary teams that work with older adult patients. In addition, it adds specificity to symptom descriptions including acuity and duration of symptoms that facilitates consistent reporting of behavioral signs and symptoms as well as context. The DSM-V is expected to be released in 2013.
Cognitive assessment tools
Screening tools are characterized by their brevity, speed of use by busy practitioners, and ability to screen, not diagnose clinical problems. All of the tools mentioned here, while having unique foci, are top choice screening tools. Although some may claim to be diagnostic, careful review of psychometric properties as well as a full physical, psychological, and functional assessment of the patient is essential for accuracy in the differential diagnostic process. For the purposes of focus and brevity, the tools presented will focus on overall cognitive assessment for general screening purposes followed by more specific tools related to dementia and executive dysfunction in the older population. Screening tools most frequently utilized in each category are described (see Tools to facilitate cognitive assessment in older adults). Areas that are not described here, but may also influence cognitive impairment and would be important to assess include sleep, nutrition, lifetime exercise habits, depression, mental health coping, and use and misuse of alcohol, pharmacological and illegal drugs.
Overall cognitive assessment
Since 1975, one of the primary screening tools for assessing general cognitive impairment has been the Folstein Mini Mental State Exam (MMSE).35 It takes approximately 10 minutes to complete and consists of 11 items. It addresses five general areas of cognitive function including short-term memory (recalling objects named earlier), attention and calculation (counting by sevens and spelling backward), registration (ability to name objects), language (ability to follow three-part directions), orientation (awareness of time and location, as well as perception and fine motor skill. A score of 0 is poor, while a score of 30 is normal. The MMSE serves as a good, first-line general screening tool of multiple functions. One of its drawbacks is that it has been found to be influenced by patients' levels of education and literacy, as well as culture and ethnicity.
The Clock Drawing Test (CDT) reflects frontal and temporal-parietal functioning and is easy to administer (described below as part of the Mini-Cog). It takes 2 minutes to administer and tends to be nonthreatening. A variety of scoring approaches have been studied in relation to using the scale for dementia screening. The Schulman et al approach was found to be most clinically valuable.36,37
The Montreal Cognitive Assessment (MoCA)38 was designed as a rapid screening instrument for mild cognitive dysfunction. This tool assesses different cognitive domains including attention and concentration, executive functions, memory, language, visuoconstructional skills, conceptual thinking, calculations, and orientation. It takes approximately 10 minutes to administer the MoCA. A score of 26 or above is considered normal. The total possible score is 30.
Age is the greatest risk factor of AD. Since half of the people over 85 are said to have AD and, as our elderly population rapidly increases, efficient dementia screening tools for the primary care practitioner will facilitate quick decision making about whether to refer to a psychiatric NP or neuropsychologist for a more in-depth cognitive assessment. Since dementia may be due to a variety of other medical conditions such as HIV disease, head trauma, Parkinson disease, Huntington disease, substance abuse, as well as other conditions, careful attention to medical history and history of cognitive symptoms is particularly important.
The Mini-Cog is a preferred dementia screening tool composed of a three-item recall test combined with the CDT. It takes 3 minutes to administer. In addition to speed, an advantage of this tool over the MMSE is that language, education level, culture, and ethnicity did not affect scores of older adults.39 The patient is instructed to listen carefully and remember three unrelated words and then to repeat the words. Next, the patient is asked to draw the face of a clock on a blank paper adding the numbers, and the hands of the clock to read a specific time. Finally, he is asked to repeat the 3 previously stated words. Scoring for the CDT is normal if all numbers are present in the correct sequence and position on the clock, and the hands readably display the requested time. For the word recall, one point is given for each recalled word, with a score of 0 suggesting dementia and a score of 3 as no dementia. Patients with intermediate word recall (1 to 2) are classified based on the CDT score of Abnormal or Normal.40 Because these are screening tests, more advanced neuropsychological testing would be done to further clarify diagnosis and functional capacity.
The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) is often used as a supplement with the MMSE or Mini-Cog because it helps determine onset, duration, and the impact of the cognitive impairment on function. This questionnaire elicits information from a person with a close relationship with the patient.41 This person can be particularly helpful in determining the patient's duration of memory impairment, which is necessary for distinguishing between delirium and dementia. Utilization of this questionnaire (IQCODE) as well as naturally occurring conversations and observations, a common practice in nursing, provides very useful information for accurate assessment of a patient's cognitive functioning.
More so than memory abilities, "executive functions" are highly predictive of a person's ability to function independently.42 According to DSM-IV-TR, executive dysfunction involves impairment in the ability to plan, sequence, initiate, self-monitor, think abstractly, and be flexible with unexpected changes. While executive dysfunction may be an element of impairment in both vascular dementia and AD, it may also occur without dementia, or when memory is intact. In part, this may be due to the fact that while working memory is most often associated with prefrontal cortex function, other kinds of memory are associated with temporal lobe (for example, hippocampal) function.28 Accordingly, even when dementia is not present and memory appears to be intact, executive dysfunction can explain other kinds of cognitive dysfunction essential to the patient's daily functioning. Detection of executive dysfunction is particularly important with respect to patient independence and safety. In fact, according to some neuropsychological studies, memory impairment may be less reliable in prediction of loss of independence or autonomy than executive dysfunction.40 Importantly, these factors play a decisive role in discharge planning for elderly patients who live alone or may not be fully able to care for themselves.43 The two most helpful screening tools in this regard are:
Trail Making Test: The oral test has two parts. In part A, the patient is asked to count from 1 to 25. In part B, the patient pairs numbers and letters in a sequence. For assessment of executive function, only Part B is scored. (Both correct and incorrect pairings are discretely scored.) Two or more errors in the 13 number-letter pairings indicates possible impairment.44,45
COWAT (Controlled Oral Word Association Test)46: For this test, the patient is told a letter from the alphabet and is asked for 1 minute, to name all the words beginning with that letter. The same procedure continues with two additional letters. All the words are recorded, observing for repetitions, loosing track of self, and so on. In scoring the COWAT, correct answers (that is, words starting with the correct letter) receive one point. Variants of previously used words (for example, plurals, or other tenses) receive zero points. (People with executive dysfunction often repeat and insert errors.) A score of 30 or more indicates no impairment.46
Approaches to enhance learning
Once screening and differential diagnosis decisions are completed, developing approaches to enhance existing cognitive capacities is essential. When working with older adults, patient educational opportunities arise in numerous ways and in a variety of settings (see Promoting cognitive wellness in older adults by way of health education).
A key component to teaching older adults is to personalize the information presented. Communicate the information in a nondistracting environment and in a way that the person can utilize his or her many years of knowledge to process it.31 This strategy relies more on crystallized intelligence, which is embedded in past experiences. Instructional challenges occur in the areas related to fluid intelligence. Approaches that would enhance learning include pacing the task, use of memory aids, elaborate on the subject, and have a well-planned out approach to the learning session.3,47 Memory problems are common especially in the ability to move new information into long-term memory, and linking information together. Memory training programs that use imagery, categorization, analysis of written material, and practice are useful tools for learning and improvements in mental performance.3
In conclusion, the literature supports the idea that older adults are very capable of learning well into their 90s. Although it has long been assumed that cognitive decline is inevitable in old age, recent studies demonstrate the potential of plasticity in the aging brain. Advanced NPs have the ability to break negative stereotypes related to cognition and aging. Conveying positive beliefs and developing individualized patient education interactions will allow the older adult to enjoy later life learning and educational opportunities.
2. Albert MS, Killiany R. Age-related cognitive change and brain-behavior relationships. In: Birren JE, Schaie KW, eds. Handbook of the Psychology of Aging. San Diego: Academic Press; 2001:161–185.
3. Saxon SV, Etten MJ, Perkins EA. The Nervous System. A Guide for the Helping Professions: Physical Change & Aging. 5th ed. New York: Springer; 2010:65–88.
4. Miller CA. Promoting Wellness in Psychosocial Function in Nursing for Wellness in Older Adults. 5th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2009:185–199.
5. Drachman DA. Aging of the brain, entropy, and Alzheimer disease. Neurology. 2006;67(8):1340–1352.
6. DeCarli C, Massaro J, Harvey, et al. Measures of brain morphology and infarction in the Framingham Heart Study: establishing what is normal. Neurobiol Aging. 2005;26(4):491–510.
7. Esiri MM, Hyman BT, Beyreuther DO, Masters CL. Aging and dementia. In: Granham DI, Lantos LS, eds. Greenfield's Neuropathology. 6th ed. London: Arnold; 1997:153–234.
8. Nestor SM, Rupsingh R, Borrie M, et al. Ventricular enlargement as a possible measure of Alzheimer's disease progression validated using the Alzheimer's disease neuroimaging initiative database. Brain. 2008;131(pt 9):2443–2454.
9. Pakkenberg B, Pelvig D, Marner L, et al. Aging and the human neocortex. Exp Gerontol. 2003;38(1–2):95–99.
10. Scahill RI, Frost C, Jenkins R, Whitewell JL, Rossor MN, Fox NC. A longitudinal study of brain volume changes in normal aging using serial registered magnetic resonance imaging. Arch Neurol. 2003;60(7):989–994.
11. Davis DG, Schmitt FA, Wekstein DR, Marksbery WR. Alzheimer neuropathologic alterations in aged cognitively normal subjects. J Neuropathol Exp Neurol. 1999;58(4):376–388.
12. Dinse HR. Cortical reorganization in the aging brain. Prog Brain Res. 2006;157:57–80.
13. Cohen GD. The Mature Mind: The Positive Power of the Aging Brain. New York: Basic Books; 2005.
14. Klempin F, Kempermann G. Adult hippocampal neurogenesis and aging. Eur Arch Psychiatry Clin Neurosci. 2007;257(5):271–280.
15. Cotman CW. Synaptic plasticity, neurotrophic factors, and transplantation in the aged brain. In: Schneider EL, Rowe JW, eds. Handbook of the Biology of Aging. San Diego: Academic Press; 1990.
16. Merzenich MM, Jenkins WM. In: Levy-Reiner S, ed. The Adaptable Brain. Vol II. Washington, DC: Library of Congress; 1999:37–50.
17. Park DC, Reuter-Lorenz P. Aging and neurocognitive scaffolding. Annu Rev Psychol. 2009;60:173–196.
18. Beason-Held LL, Kraut MA, Resnick SM. Longitudinal changes in aging brain function. Neurobiol Aging. 2008;29(4):483–496.
19. Cabeza R, Anderson ND, Locantore JK, McIntosh AR. Aging gracefully: compensatory brain activity in high-performing older adults. Neuroimage. 2002;17(3):1394–1402.
20. Buckner RL. Memory and executive function in aging and AD: multiple factors that cause decline and reserve factors that compensate. Neuron. 2004;44(1):195–208.
21. Caserta MT, Bannon Y, Fernandez F, Giunta B, Schoenberg MR, Tan J. Normal brain aging: clinical immunological, neuropsychological, and neuroimaging features. Intern Rev Neurobiol. 2009;84:1–19.
22. Langley LK. Cognitive assessment of older adults. In: Kane RL, Kane RA, eds. Assessing Older Persons: Measures, Meaning, and Practical Applications. New York: Oxford University Press; 2000:65–128.
23. Aartsen MJ, Smith CH, van Tilburg T, Knipscheer KC, Deeg DJ. Activity in older adults: cause or consequence of cognitive functioning? A longitudinal study on everyday activities and cognitive performance in older adults. J Gerontol B: Psychol Sci Soc Sci. 2002;57(2):P153-P162.
24. Ronnlund M, Nyberg L, Backman L, Nilsson LG. Stability, growth, and decline in adult life span development of declarative memory: cross-sectional and longitudinal data from a population-based study. Psychol Aging. 2005;20(1):3–18.
25. Salthouse TA. When dose age-related cognitive decline begin? Neurobiol Aging. 2009;30(4):507–514.
26. Drag LL, Bieliauskas LA. Contemporary review 2009: cognitive aging. J Geriatr Psychiatr Neurol. 2010;23(2):75–93.
27. Capaezuti EA, Siegler, EL, Mezey, MD, eds. The Encyclopedia of Elder Care: The Comprehensive Resource on Geriatric and Social Care. New York: Springer; 2008:148–150.
28. Budson AE, Price BH. Current concepts: memory dysfunction. N Engl J Med. 2005;352(7):692–696.
29. Nilsson LG. Memory function in normal aging. Acta Neurol Scand Suppl. 2003;179:7–13.
30. Horn JL, Hofer S. Major abilities and development in the adult period. In: Sternberg RJ, Berg CA, eds. Intellectual Development. New York: Cambridge University Press; 1992:44–99.
31. Merriam SB. The New Update on Adult Learning Theory. San Francisco: Jossey-Bass; 2001.
32. Fletcher PC, Henson RNA. Frontal lobes and human memory: insights from functional neuroimaging. Brain. 2001;124(pt 1):849–881.
33. McDougall GJ Jr. Cognitive interventions among older adults. Ann Rev Nurs Res. 1999;17:219–240.
34. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed., text revision. Washington, DC: Author; 2000.
35. Folstein MF, Folstein SE, McHugh PR. "Mini-mental state": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189–198.
36. Schulman K, Shedletsky R, Silver I. The challenge of time. Clock drawing and cognitive function in the elderly. Int J Geriatr Psychiatry. 1986;1:135–140.
37. Brodaty H, Moore CM. The Clock Drawing Test for dementia of the Alzheimer's type: a comparison of three scoring methods in a memory disorders clinic. Int J Geriatr Psychiatry. l997;12(6):619–627.
38. Nasreddine ZS, Phillips NA, Bedirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695–699.
39. Brodaty H, Low LF, Gibson L, Burns K. What is the best dementia screening instrument for general practitioners to use? Am J Geriatr Psychiatry. 2006;14(5):391–400.
40. Borson S, Scanlan J, Brush M, Vitaliano P, Dokmak A. The Mini-Cog: a cognitive 'vital signs' measure for dementia screening in multi-lingual elderly. Int J Geriatr Psychiatry. 2000;15(11):1021–1027.
41. Cole MG, McCusker J, Bellavance F, et al. Systematic detection and multidisciplinary care of delirium in older medical inpatients: a randomized trial. Can Med Assoc J. 2002;167(7):753–759.
42. Royall DR, Lauterbach EC, Kaufer D, et al. The cognitive correlates of functional status: a review from the Committee on Research of the American Neuropsychiatric Association. J Neuropsychiatry Clin Neurosci. 2007;19(3): 249–265.
43. Cooney LM Jr, Kennedy GJ, Hawkins KA, Hurme SB. Who can stay at home? Assessing the capacity to choose to live in the community. Arch Intern Med. 2004;164(4):357–360.
44. Grober E, Hall C, McGinn M, et al. Neuropsychological strategies for detecting early dementia. J Int Neuropsychol Soc. 2008;14(1):130–142.
45. Ricker JH, Axelrod BN. Analysis of an oral paradigm for the Trail Making Test. Assessment. 1994;1(1):47–52.
46. Ardila A, Ostrosky-solís F, Bernal B. Cognitive testing toward the future: the example of Semantic Verbal Fluency (ANIMALS). Int J Psychology. 2006;41 (5):324–332.
47. Touhy TA. Cognition and caring for persons with cognitive impairments. In: Ebersole P, Hess P, Touhy TA, Jett K, Luggen AS, eds. Toward Healthy Aging. 7th ed. St. Louis: Mosby Elsevier; 2008:548–581.
© 2011 Lippincott Williams & Wilkins, Inc.