View Entire Collection
By Clinical Topic
Diabetes – Summer 2012
Future of Nursing Initiative
Heart Failure - Fall 2011
Influenza - Winter 2011
Nursing Ethics - Fall 2011
Trauma - Fall 2010
Traumatic Brain Injury - Fall 2010
Fluids & Electrolytes
Knowing the research will help nurses aid families.
OVERVIEW: Three genes with autosomal dominant mutations have been identified that may lead to Alzheimer symptoms in carriers before they reach age 60. Genetic tests exist for Alzheimer disease, but they are considered useful only for the small number of families with a history of early-onset illness. As researchers continue to uncover evidence of genetic links to Alzheimer disease, nurses can expect to field questions from family members about genetic testing. The article presents a variety of questions nurses may be asked, as well as possible answers.
Anna Russell, director of nursing at Legacy Nursing and Rehabilitation Center, sits across the table from Allison Feldspar, who is admitting her 71-year-old mother, suffering from late-stage Alzheimer disease. (This case is fictional.) The daughter tears up frequently during the intake process, explaining that she's cared for her mother at home for seven years. Admitting that she can no longer do so is a source of pain and regret-but also relief. Russell is familiar with the conflicting emotions of caregivers and responds with reassurance, acknowledging Ms. Feldspar's feelings and inviting her to participate in her mother's care at the nursing home.
But as Russell continues with the admissions checklist, the conversation suddenly shifts focus: "There's something else that's bothering me," Ms. Feldspar says. "First it was my uncle, and now it's my mother. I'm just terrified that I'm going to end up like this some day, and I can't stand not knowing. I've heard there's a genetic test for Alzheimer disease. Can you tell me about it?"
This case illustrates the kind of encounter that nurses-whether in long-term care, acute care, or community settings-may experience. The burgeoning field of genetics is altering our understanding of the disease, as well as the care those diagnosed with it and their families need as science and technology evolve.1 Familiarity with the research and genetic testing options will be essential for nurses to respond to family members in an informed and sensitive way.
Alzheimer disease, first described by Alois Alzheimer in November 1906, is a neurodegenerative disorder that usually occurs in late life but can arise in midlife. It's characterized by dementia-a progressive deterioration in global cognitive ability resulting in impaired short- and long-term memory, abstract thinking, judgment, social and occupational performance, and other high cortical function.2 Other disorders in which irreversible dementia is often or always a feature include Huntington disease, Parkinson disease, Lewy body dementia, and frontotemporal disorders such as Pick disease. Worldwide, an estimated 25 million people had dementia in 2000, of whom 2.9 million were in the United States (in 2001).3 Prevalence increases with age; only 2% of people ages 64 to 69 have dementia, compared with nearly 25% of those over 85.3 Alzheimer disease is the most prevalent of these, accounting for as many as 65% of all irreversible dementias.4 According to estimates by Ferri and colleagues, "The number of people living with dementia will almost double every 20 years, to 42.3 million in 2020 and 81.1 million in 2040."3 According to a literature review by Bird, 1% to 6% of patients with Alzheimer disease develop symptoms before age 60; an estimated 60% of these early-onset cases are familial.5 The mean survival times after diagnosis are 4.2 years in men and 5.7 years in women.6
Clinical signs of Alzheimer disease include cognitive impairment, functional losses, and behavioral or neuropsychiatric symptoms. The cognitive losses begin with short-term memory and progress to more complex processes, such as problem solving and reasoning. Behavioral characteristics include physical and verbal restlessness, aggression, and personality changes; neuropsychiatric symptoms include depression, anxiety, delusions, and hallucinations.7, 8 Losses in function can be seen in both instrumental activities of daily living (IADLs) and activities of daily living (ADLs). IADLs are complex skills such as preparing meals, managing finances, using the telephone, and driving. (An impaired ability to perform IADLs may be an early sign of cognitive impairment.) ADLs are self-care skills such as eating, grooming, using the toilet, bathing, and dressing; impairments in the ability to perform ADLs are seen at all stages. There is no cure for Alzheimer disease; some drug and nondrug interventions have been shown to slow the progression of some symptoms, but none alters its ultimately fatal course.
The current view of Alzheimer disease is that it's influenced partly by genetics, partly by environmental factors, and partly by the person's health.9, 10 Environmental factors include exposure to toxins or a history of head trauma.11, 12 Contributing health conditions include diabetes mellitus and vascular disease, including heart disease and stroke.9 Genetically, Alzheimer disease is believed to be a heterogeneous disorder, meaning that multiple genes and gene mutations can be factors in its development. Whatever the underlying etiology, the result is a loss of neurons in the brain's cerebral cortex and hippocampus. Two classic neuropathologic features are neurofibrillary tangles and amyloid (or senile) plaques. Neurofibrillary tangles occur when the protein tau, a crucial structural element of the neuron, becomes distorted and twisted. Amyloid plaques are dense deposits of the [beta]-amyloid 42 protein, which is an abnormal fragment of a larger protein called amyloid precursor protein. Both the amyloid plaques and neurofibrillary tangles disrupt neuronal communication, metabolism, and repair mechanisms, resulting in the death of neurons.
The high prevalence of Alzheimer disease, its protracted course, and the significant emotional and financial toll it takes on families and the health care system have spurred research into its etiology, pathophysiology, and treatment. Among the questions is whether Alzheimer disease results from a gene mutation. If a gene mutation is associated with a disease, then the next step is to try to understand how the mutation changes the gene's protein product. For example, is too much or too little protein made? Or is the protein shaped incorrectly so that it cannot carry out its usual cellular function? While the answers to such questions are important to the long-term goal of finding a cure, in the short term they can be used to develop diagnostic or predictive genetic tests.
Diagnostic tests are used to confirm disease in a symptomatic patient. For example, a genetic test for Huntington disease may pinpoint the reason for a patient's involuntary muscle movements. Predictive tests are used to predict the risk of future disease in an asymptomatic person. For example, an asymptomatic child of someone with Huntington disease could undergo genetic testing to determine whether she will eventually develop the disease. Whether a genetic test can predict future illness depends on the specific disease and on whether a predictive model can be built on the research that exists.
Genetic tests exist for Alzheimer disease, but they are considered useful only for the small number of families with a history of early-onset illness. Researchers have identified three genes with autosomal dominant mutations that tend to manifest in family members before age 60. Only one mutation in one of these genes is necessary to cause disease.5 The three genes are
* the amyloid precursor protein gene on chromosome 21.13
* the presenilin 1 gene on chromosome 14.14
* the presenilin 2 gene on chromosome 1.15
Predictive genetic testing is clinically available for mutations in these genes in at-risk adults. At-risk adults are those with a parent carrying the mutation or a family history showing cases of Alzheimer disease occurring before age 60 in multiple generations.
Researchers are also looking at common gene variations-called polymorphisms-to discover their influence on risk16 or Alzheimer disease's clinical presentation.17 The apolipoprotein E (APOE) gene on chromosome 19 claims the strongest and most consistent evidence for influencing Alzheimer disease risk.18 The APOE gene contains three common variations (alleles), called [varepsilon]2, [varepsilon]3, and [varepsilon]4. In studies in white subjects, the APOE [varepsilon]4 allele is consistently associated with an increased risk of developing Alzheimer disease and a decrease in the age at onset, although the latter impact is not so extreme as to classify these cases as early onset.19, 20 The APOE [varepsilon]2 allele, on the other hand, appears in whites to have a protective function, decreasing the overall risk and delaying onset.20
Ethnicity and race are emerging as important factors in the genetics of Alzheimer disease, although detailed studies of risk factors for specific racial and ethnic groups are lacking. Nevertheless, researchers have found that the frequency of APOE alleles varies among ethnic groups, as does the risk of disease associated with these alleles. But findings vary from study to study; even when allelic variations are found, their influence in individuals of specific race or ethnicity is not fully understood.13, 21-23 Therefore, in contrast to the recommendations for genetic testing when evidence exists of early-onset disease patterns, predictive testing for APOE alleles currently isn't recommended. There's even debate over whether APOE testing in symptomatic patients is useful as a diagnostic adjunct.5
Patients and their families are likely to have questions about the genetic role in Alzheimer disease and testing options as the research becomes more widely known. The best practice is to refer those at risk for early-onset inherited illness to genetics specialists. But general practice nurses still need a sufficient familiarity with the research to respond to inquiries and assess the need for referral. The following are examples of the kinds of questions that may arise and suggestions for answering them, including the rationale behind them.
Is genetic testing appropriate for me and other members of my family?
Response: Most families in which someone has Alzheimer disease have little to gain from genetic testing. But in families with two or more affected relatives who developed symptoms before age 60, genetic tests may identify gene mutations that predict the likelihood of disease.
Rationale: Currently, genetic testing is recommended only in families in which a parent or two or more second-degree family members have had early-onset symptoms and autosomal dominant patterns of inheritance.24 Most families will not benefit from genetic testing because the majority of Alzheimer disease cases are sporadic and late in onset. When in doubt, the nonspecialist nurse should refer patients for specialized genetics services.
How is genetic testing done, and where can I obtain it?
Response: Genetic tests for Alzheimer disease usually require blood samples or cheek swabs that are sent for analysis to specialized laboratories. It can take as long as six weeks for results to be available. The tests are performed by specialists in genetic testing, and they're the ones who'll explain the results to you. Over-the-counter tests and other home genetic tests are not recommended.
Rationale: Genetic testing, especially for predictive purposes, should be accompanied by counseling, preferably by advanced practice nurses credentialed in genetics, certified genetics counselors, or physician geneticists practicing at specialized clinics.
How much does genetic testing cost?
Response: The cost of genetic testing varies, depending upon the laboratory method used and whether specific gene mutations have already been identified in the candidate's family. Costs can run as high as several thousand dollars. On top of testing costs, there are fees for pre- and posttest genetics counseling. Health insurance doesn't always cover these tests. The genetics specialists can help you find out whether your insurance will pay for the tests.
Rationale: Genetic testing involves molecular studies of varying complexity. Only a limited number of laboratories have the equipment and expertise. To reduce costs, the family member with Alzheimer disease should be tested first to see if there is a gene mutation. Then tests on family members can be limited to that specific mutation. Otherwise, testing will be a more involved and costly process. Genetics specialists can discuss testing costs and payment options with clients. Some clients may choose to pay for testing out of pocket to protect their privacy. Privacy protections vary from state to state and among types of insurers (health, life, and long-term care). Discussion of these issues is an integral part of genetics counseling.25
What will genetic testing tell me?
Response: If you are in the small subset of families showing early-onset disease and autosomal dominant inheritance, genetic testing can help you gauge your risk of future disease. If the same gene mutation present in the Alzheimer patient is found in a family member, the latter's risk of disease is nearly 100%, although the test cannot pinpoint the age of onset.5 A negative result means the family member's risk is the same as for people in the general population.
Rationale: Predictive genetic testing can clarify an at-risk person's chances of developing disease. There are three possible results: negative, positive, and inconclusive. A negative result means the person doesn't have the disease-causing mutation, making her risk of Alzheimer disease the same as that of people in the general population. A positive result means a person is found to have a disease-causing mutation. Inconclusive findings are those in which genetic abnormalities are found but their clinical significance is unknown. Even when results are positive, genetic tests cannot predict the age at which an individual will develop symptoms or how the disease will progress. Interpretation of test results is best provided by genetics specialists.26
Why is my family history so important?
Response: A detailed family history helps identify possible inherited patterns of Alzheimer disease that could warrant genetic testing. An important element of the history is age of onset of Alzheimer symptoms or memory problems in relatives, preferably for three generations.
Rationale: The family history offers a window on patterns of movement of a disease or trait within a family.24 This information helps the generalist determine the appropriateness of referral to genetics specialists. Criteria for referral include an onset of symptoms before age 60 and autosomal dominant inheritance. Referral isn't warranted when disease patterns show random cases of Alzheimer disease in family members older than 65.
Family members need specific information about genetic testing, but equally pressing is the need for psychosocial support. Once a family member is identified as a candidate for genetic testing, nurses should explore her reasons for wanting genetic testing and whether she needs nursing or other support through the process. Some are troubled by not knowing whether they will develop Alzheimer disease and want to know their risk. Others may pursue testing for family planning purposes, to understand the risks their children will carry, or to plan financially and otherwise for the future.27-29 Nurses also should explore clients' knowledge of genetics and their ability to cope with the genetic testing experience. Do they have realistic expectations of the tests? How do they handle stress and uncertainty? Do they have a supportive network of family and friends?
For people whose family history suggests inherited risk, nurses should use open-ended statements such as, "I see that you have several close relatives with Alzheimer disease and that the symptoms seem to begin fairly early in your family" may prompt the client to reveal her concerns and desire (or lack of desire) to pursue genetic testing. Health professionals should not actively recommend genetic testing, but they can suggest referral to genetics specialists.
Not everyone for whom referral to a genetics specialist is indicated pursues that course. Reasons vary; patients may simply not want to know the likelihood of future illness. At the other extreme are family members so worried about inherited illness, despite reassuring family histories, that referral for genetics counseling is warranted. Nurses undertaking the initial assessment act as bridges between family members and the genetics counselor. For this reason, knowledge of local genetics resources and relationships with specialists are an important part of the job.
Nurses working in tertiary care facilities may have genetics specialists in house. Nurses in other settings, however, generally have to build relationships with genetics specialists at other facilities. Most regional health care facilities have specialty genetics services, and some may also have outreach programs in local clinics. State health departments are a good source of information on available genetics services; there may even be a state coordinator of genetics services. Useful Web sites include those of the International Society of Nurses in Genetics (http://www.isong.org) and the National Society of Genetic Counselors (http://www.nsgc.org). The next step is to make a call to a nearby specialist or identify a nurse at one's facility who can act as liaison for the staff.
Preparing clients for genetics services is another important role for nurses. For example, genetics specialists typically contact clients by phone before the appointment in order to obtain a comprehensive family history, including detailed medical information on the family member with Alzheimer disease. They may also try to ascertain what family members hope to learn from counseling or testing. At the first clinic appointment, a team of genetics specialists usually meets with family members to discuss the risks and benefits of testing. There may also be discussion of the feasibility of testing the afflicted family member, which may require the participation of family members or the legal representative of the person with Alzheimer disease if she is unable to give informed consent.30
Even if family members are found to be candidates for testing, the process is a lengthy one, sometimes taking several months. Obtaining informed consent and collecting blood samples generally take place during the second appointment. A third visit is then scheduled to discuss the test results; follow-up to assess how the person is coping with the new information is also warranted. Sometimes clients are asked to bring someone with them to support them throughout the process. As more evidence is obtained about the long-term effects of predictive genetic testing and the effectiveness of existing protocols, these scenarios may change.
In 1995, at age 61, the painter William Utermohlen received a diagnosis of Alzheimer disease. An established artist for more than three decades, Utermohlen used his artistic skill to investigate, as the illness progressed, the ways in which his mental capacity diminished and his identity distorted. In a variety of mediums-pencil, watercolors, oils-Utermohlen's self-portraits poignantly illustrate one man's struggle to remain recognizable to himself despite the gradual yet inexorable erosion of language, independence, and creative will. Utermohlen continued to paint, at a nurse's urging, for five years after his diagnosis.
In this painting, Self-Portrait (with Easel-Yellow and Green), made a year after his diagnosis, the easel appears to bolster and confine the artist, who looks out in defiance and dread. Works in subsequent years show a gradual deterioration in his talent (see page 42).
Allele: an alternate form of a particular gene.
Autosomal dominant: a pattern of Mendelian inheritance. Autosomal means that a gene mutation is located on one of the autosomes (chromosomes 1 to 22). Dominant means that only one copy of the gene mutation is needed to result in the associated phenotype. People with autosomal dominant diseases have a 50% chance of passing the gene mutation on to each of their children.
Cerebral cortex: the outer layer of the brain's cerebral hemispheres, it plays a role in higher-order thinking and reasoning.
Gene: a segment of DNA. Most genes carry the instructions for making a specific protein.
Genotype: a person's genetic makeup at the level of DNA sequence.
Hippocampus: part of the limbic system of the brain and one of several structures involved with emotion, memory, and learning.
Mendelian inheritance: predictable patterns of transmission of genes or traits from parent to offspring, consistent with the observations of 19th-century plant biologist Gregor Mendel. The most common Mendelian patterns in humans are autosomal dominant, autosomal recessive, and X-linked recessive inheritance.
Mutation: a change in DNA sequence. This change may or may not alter the production of the protein coded for by the gene.
Nucleotide: a structural component of DNA and RNA consisting of a base (one of four chemicals: adenine [A], thymine [T], guanine [G], and cytosine [C]) plus one sugar molecule and one phosphoric acid molecule.
Phenotype: physical or clinical traits that reflect the expression of genes or their interactions with environmental factors.
Polymorphism: any change in DNA sequence that is present in more than 1% of the population.
Susceptibility gene: a change in DNA sequence that increases a person's risk of developing a disease or disorder.
A talking glossary of genetics terms is available online through the National Institutes of Health at http://www.genome.gov/glossary.cfm.
A series of Webcasts designed to improve multidisciplinary care.
This is the last article in the series A New Look at the Old; over the course of the series 15 free Webcasts have run, created through the collaboration of AJN, the Gerontological Society of America, and Trinity Healthforce Learning and sponsored in part through a grant from Atlantic Philanthropies. AJN will continue publishing articles on the nursing care of older adults, and videos based on the series will continue to be produced, including one on this article. For information on the schedule or to view an archive of previous Webcasts, go to http://www.nursingcenter.com/AJNolderadults.
1. Schutte DL. The evolving role of genomics in shaping care for persons with dementia. Nurs Clin North Am 2004;39(3):581-92. [Context Link]
2. American Psychological Association. Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed. Washington, DC: The Association; 1994. [Context Link]
3. Ferri CP, et al. Global prevalence of dementia: a Delphi consensus study. Lancet 2005;366(9503):2112-7. [Context Link]
4. Launer LJ, et al. Rates and risk factors for dementia and Alzheimer's disease: results from EURODEM pooled analyses. EURODEM Incidence Research Group and Work Groups. European Studies of Dementia. Neurology 1999;52(1):78-84. [Context Link]
5. Bird TD. Alzheimer disease overview. Seattle: University of Washington; 2005 Feb. http://www.geneclinics.org/profiles/azheimer/details.html. [Context Link]
6. Larson EB, et al. Survival after initial diagnosis of Alzheimer disease. Ann Intern Med 2004;140(7):501-9. [Context Link]
7. Cummings JL, McPherson S. Neuropsychiatric assessment of Alzheimer's disease and related dementias. Aging (Milano) 2001;13(3):240-6. [Context Link]
8. Payne JL, et al. Incidence, prevalence, and outcomes of depression in residents of a long-term care facility with dementia. Int J Geriatr Psychiatry 2002;17(3):247-53. [Context Link]
9. National Institute of Aging. Progress report on Alzheimer's disease 2004-2005: new discoveries, new insights: U.S. Department of Health and Human Services; 2006 Nov. NIH Pub. No. 05-5724. http://www.nia.nih.gov/NR/rdonlyres/E601F872-FE6D-4930-9724-9D826DA37208/0/Progr. [Context Link]
10. Van Duijn CM, et al. Interaction between genetic and environmental risk factors for Alzheimer's disease: a reanalysis of case-control studies. EURODEM Risk Factors Research Group. Genet Epidemiol 1994;11(6):539-51. [Context Link]
11. Almeida OP, et al. Smoking as a risk factor for Alzheimer's disease: contrasting evidence from a systematic review of case-control and cohort studies. Addiction 2002;97(1):15-28. [Context Link]
12. Ikonomovic MD, et al. Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury. Exp Neurol 2004;190(1):192-203. [Context Link]
13. Goate A, et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 1991;349(6311):704-6. [Context Link]
14. Mullan M, et al. A locus for familial early-onset Alzheimer's disease on the long arm of chromosome 14, proximal to the alpha 1-antichymotrypsin gene. Nat Genet 1992;2(4):340-2. [Context Link]
15. Levy-Lahad E, et al. Candidate gene for the chromosome 1 familial Alzheimer's disease locus. Science 1995;269(5226):973-7. [Context Link]
16. Myers AJ, Goate AM. The genetics of late-onset Alzheimer's disease. Curr Opin Neurol 2001;14(4):433-40. [Context Link]
17. Schutte DL, et al. A LRPAP1 intronic insertion/deletion polymorphism and phenotypic variability in Alzheimer disease. Res Theory Nurs Pract 2003;17(4):301-19. [Context Link]
18. Pericak-Vance MA, et al. Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage. Am J Hum Genet 1991;48(6):1034-50. [Context Link]
19. Breitner JC, et al. APOE-[varepsilon]4 count predicts age when prevalence of AD increases, then declines: the Cache County Study. Neurology 1999;53(2):321-31. [Context Link]
20. Corder EH, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science 1993;261(5123):921-3. [Context Link]
21. Evans DA, et al. Incidence of Alzheimer disease in a biracial urban community: relation to apolipoprotein E allele status. Arch Neurol 2003;60(2):185-9. [Context Link]
22. Graff-Radford NR, et al. Association between apolipoprotein E genotype and Alzheimer disease in African American subjects. Arch Neurol 2002;59(4):594-600. [Context Link]
23. Tang MX, et al. The APOE-[varepsilon]4 allele and the risk of Alzheimer disease among African Americans, whites, and Hispanics. JAMA 1998;279(10):751-5. [Context Link]
24. Schutte DL, et al. Evidence-based protocol: identification, referral, and support of older adults with genetic conditions. J Gerontol Nurs 2002;28(2):6-14. [Context Link]
25. Rothstein MA. Predictive genetic testing for Alzheimer's disease in long-term care insurance. Georgia Law Rev 2001;35(2):707-33. [Context Link]
26. International Society of Nurses in Genetics, American Nurses Association. Statement on the scope and standards of genetics clinical nursing practice. Washington, DC: American Nurses Association; 1998. ANA Pub. No. 9807ST. [Context Link]
27. Roberts JS, et al. Who seeks genetic susceptibility testing for Alzheimer's disease? Findings from a multisite, randomized clinical trial. Genet Med 2004;6(4):197-203. [Context Link]
28. Williams JK, et al. Adults seeking presymptomatic gene testing for Huntington disease. Image J Nurs Sch 1999;31(2):109-14. [Context Link]
29. Steinbart EJ, et al. Impact of DNA testing for early-onset familial Alzheimer disease and frontotemporal dementia. Arch Neurol 2001;58(11):1828-31. [Context Link]
30. Eaton ML. Surrogate decision making for genetic testing for Alzheimer disease. Genet Test 1999;3(1):93-7. [Context Link]
Go tohttp://www.nursingcenter.com/CE/ajnand receive a certificate within minutes.
GENERAL PURPOSE: To provide nurses with the latest evidence-based information about genetic links to Alzheimer disease.
LEARNING OBJECTIVES: After reading this article and taking the test on the next page, you will be able to
* review Alzheimer disease, including incidence, characteristics, and manifestations.
* discuss the implications of genetic testing for Alzheimer disease.
* describe the appropriate instructions and information to share with families considering genetic testing.
To take the test online, go to our secure Web site athttp://www.nursingcenter.com/CE/ajn.
To use the form provided in this issue,
* record your answers in the test answer section of the CE enrollment form between pages 64 and 65. Each question has only one correct answer. You may make copies of the form.
* complete the registration information and course evaluation. Mail the completed enrollment form and registration fee of $24.95 to Lippincott Williams and Wilkins CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723, by December 31, 2008. You will receive your certificate in four to six weeks. For faster service, include a fax number and we will fax your certificate within two business days of receiving your enrollment form. You will receive your CE certificate of earned contact hours and an answer key to review your results. There is no minimum passing grade.
DISCOUNTS and CUSTOMER SERVICE
* Send two or more tests in any nursing journal published by Lippincott Williams and Wilkins (LWW) together, and deduct $0.95 from the price of each test.
* We also offer CE accounts for hospitals and other health care facilities online at http://www.nursingcenter.com. Call (800) 787-8985 for details.
LWW, the publisher of AJN, will award 3 contact hours for this continuing nursing education activity. LWW is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. This activity is also provider-approved by the California Board of Registered Nursing, Provider Number CEP 11749, for 3 contact hours. LWW is also an approved provider by the American Association of Critical-Care Nurses (AACN 00012278, CERP Category A), Alabama #ABNP0114, Florida #FBN2454, and Iowa #75. LWW home study activities are classified for Texas nursing continuing education requirements as Type 1. Your certificate is valid in all states.
The late self-portraits of William Utermohlen.
The subject of a traveling exhibition that came to the New York Academy of Medicine at the end of October, William Utermohlen's self-portraits seem fairly traditional; still, they make for difficult, even painful, viewing. Utermohlen, an American who has lived in London for more than four decades, now has Alzheimer disease; most of the works in this exhibition were created between 1995, when he was diagnosed, and 2000, when he stopped painting. The paintings and drawings from this period form a record of his struggle against increasing debilities of perception, cognition, memory, and artistic skill.
The earliest work in the show is a self-portrait from his student days in the mid-1950s, and there's another from the mid-1960s, when he was at the height of his powers as a draftsman. Both works show a lean young man with a high forehead who gazes at the viewer with large, dark, somewhat anxious eyes. The pictures convey an immediate presence; there's no question that the artist feels compelled to communicate himself, confidently baring his strengths and flaws and idiosyncrasies.
Utermohlen was always a figurative painter; abstraction held little fascination for him. Over the next three decades he produced paintings consistent with a style popular in mid-century Britain: a somber realism mixed with an exuberant, at times surrealistic, expressionism. Yet the late works present various human distortions that result not from artistic decisions so much as compromises negotiated with a disease.
A nurse's encouragement. Utermohlen was given a diagnosis of probable Alzheimer disease at the Institute of Neurology in London; he then enrolled in a clinical trial of a cholinesterase inhibitor. According to his wife, the art historian Patricia Utermohlen, "We used to have to keep going to the Institute for Bill to get tested and we always saw the most extraordinary man, a nurse called Ron Isaacs. He became very instrumental in supporting Bill through this rather difficult period." Isaacs took great interest in Utermohlen's painting and encouraged him to continue working. He visited the Utermohlen home to photograph the paintings and later travelled to Paris for an exhibition at Utermohlen's gallery. Isaacs also coauthored a case report on Utermohlen that traced the artist's cognitive and perceptual decline and provided a view of how the progressive illness affected the artist's creative activity.1 (Isaacs succumbed to cancer about two years later.)
Ms. Utermohlen emphasizes her belief that dementia is no more shameful than any other illness, and she offered some characteristically British advice to those in the early stages: "Bill, bless him, always used to say, 'I've got Alzheimer's.' I would urge your nurses to tell people the same thing. You must tell everybody what's wrong with you. There's no use hiding and being silly." -James M. Stubenrauch, senior editor
1. Crutch SJ, et al. Some workmen can blame their tools: artistic change in an individual with Alzheimer's disease. Lancet 2001;357(9274):2129-33. [Context Link]
Back to Top