CASE STUDYAllie, a 72 year old lady was brought to see aneuropsychologist for an evaluation of memory lossof a progressive nature. The symptoms had beenpresent for years and were getting worse. Hermemory loss originally took the form of a tendencyto repeat questions and ideas. As the symptomsprogressed, her son, reported that her mother washaving trouble reasoning and was disoriented withregards to time, day, month and year. Frequently,Allie did not understand were she was when outsideof home.
CASE STUDYHer son described that his mother is stillexperiencing anxiety and depression, which wassignified a personality change in her mother despitemultiple courses of medication for depression. Sheis now also tended to be overall aggressive towardsothers, which was not her usual manner. Inaddition, her son reported that his mother hadbegun to require supervision in dressing, bathing,and grooming and required reminders to changehis clothes. Frequently, Allie would wear the sameclothes repeatedly. It was also noted that she hadbecome socially withdrawn.
CASE STUDYDuring the doctor’s evaluation, she was veryupset when she was examined, because she didnot comprehend why she was there.Throughout the visit, she had difficulty findingwords. Even without any other medical orneurological evaluations, all these indicationsmade it obvious to the neuropsychologist thatshe had classic Alzheimer’s disease in themoderately severe stages.
ALZHEIMER’S DISEASE Severe type of mental Prognosis for patient is deterioration, or poor. (2007, Lippincot dementia, usually Williams & Wilkins) affects older people. (2007, Seeley et. Al, Essentials of Anatomy Causes gradual memory loss, decline in the ability to perform routine tasks, and Physiology) disorientation, difficulty in learning, loss of language skills, impairment of Progressive, judgement and personality changes. degenerative brain ( 2008, Sabbagh, The Alzheimer’s disease that impairs Answer)memory, thinking, and behaviour. (2007, Lippincot Williams & Wilkins) NO ONE IS IMMUNED
ALZHEIMER’S DISEASE 1906: Dr. Alois Alzheimer first described the disease. 1974:Founding of National Institute on Aging 1980:Alzheimer’s Association founded.Jerome H. Stone is the President.
ALZHEIMER’S DISEASE 1993: Tacrine (Cognex)- First Alzheimer Drug approved by FDA. 2000: Alzheimer’s Disease Association of the Philippines was founded. 2011: President Obama signs NationalAlzheimer’s Project Act (NAPA) into law.
1994: Ronald Reagan’s Alzheimer’s Diseasediagnosis announced.
STAGES OF AD:1. PRE-CLINICAL ALZHEIMER’S DISEASE-Begins near the hippocampus (structureessential to formation of both short & longtermmemories)-Affected region begins to shrink.
STAGES OF AD:2. MILD ALZHEIMER’S DISEASE-Cerebral cortex begins to shrink.-Memory disturbance usually noticed.-Poor judgement and problem-solving skills,careless in work and household.-Irritable, suspicious or indifferent.-Cognitive impairments: Agitation, apathy,dysphoria and aberrant motor behaviour.
STAGES OF AD:3. MODERATE ALZHEIMER’S DISEASE-Client demonstrate Language disturbance,characterized by impaired word-finding andcircumlocution (talking around subject ratherthan about it directly)-Paraphasias (words used in the wrong context)-Apraxia (motor disturbance)-Hyperorality (desire to take everything into themouth to chew, suck or taste)
STAGES OF AD:4. SEVERE ALZHEIMER’S DISEASE-Plaques and tangles are widespread throughoutthe brain.-Clients can’t recognize family and loved ones.-Voluntary movement is minimal, limbs are rigidwith flexor posturing.-Aspiration pneumonia is common.
LOCAL STATISTICS 7,900 patients were hospitalized with initial diagnosis of Alzheimer’sdisease. ( Hospital Episode Statistics, DOH, 2000)
3 HALLMARKS OF AD:1. Beta-amyloid plaques- Composed of degenerating axons and dendrites.- Dense deposits of protein & cellular material that accumulate outside & around nerve cells.
Beta-amyloid PlaquesAmyloid precursor protein (APP) isthe precursor to amyloid plaque. 1.1. APP sticks through the neuronmembrane.2. Enzymes cut the APP intofragments of protein, including beta-amyloid.3. Beta-amyloid fragments come 2.together in clumps to form plaques.In AD, many of these clumps form, disruptingthe work of neurons. This affects thehippocampus and other areas of the cerebralcortex. 3.
3 HALLMARKS OF AD:2. Neurofibrillatory Tangles-Fibrous proteins-Twisted fibers that build up inside the nervecells.
3 HALLMARKS OF AD:3. Neuronal Cell DeathComposed of degenerating axons and dendrites.-Dense deposits of protein & cellular materialthat accumulate outside & around nerve cells.
CLINICAL MANIFESTATIONS Presence of β-amyloid plaques neurofibrillary tangles in and neuronal cell death in: Frontal Lobe Temporal Lobe Parietal Lobe Occipital Lobe (includes the hippocampus)- challenges in - impaired personal - Troubleplanning -memory care skills understanding visual- impairment in disturbance/ images and spatialmental flexibility and impairment relationshipsspontaneity (difficulty in -impairment of visual-socialization is remembering short- memoriesimpaired term memory) ;- low problem - reduced inhibitionsolving skills of talking-agitation -difficulty in recognizing words -difficulty in remembering verbal material
Medscape Medical News reported on the latest publishedresearch in Alzheimer’s disease on November 7, 2012 indicatingindividuals carrying a mutant gene for Alzheimer’s diseasedemonstrate markers 20 years before onset of memory changes.In addition to markers in the cerebral spinal fluid, the individualsshow structural changes in the brain other than the amyloidplaques and tangles commonly found in patients with the disease.Dr. Eric M. Reiman, the first author on this recent study,published his results in Lancet Neurology on November 6, 2012.His research group from the Banner Alzheimer’s Institute inPhoenix, Arizona studied about 5000 people who carry the genemutation that produces Alzheimer’s disease as early as age 45years in Colombia.
Reiman and colleagues compared carriers of the gene with non-carriersand found structural differences in area of the brain called thehippocampus as well as less grey matter in some parietal lobes inindividuals with the Alzheimer’s gene mutation. The parietal loberesides at the top of the head after the frontal lobe and before theoccipital lobe at the back of the head. The researchers used magneticresonance imaging to uncover the changes in the parietal lobe. Thesechanges occurred 20 years before the onset of memory loss. Byknowing these alterations exist early, researchers can study treatmentsand measure for differences at these sites.According to the Center for Disease Control and Prevention,Alzheimer’s disease causes the most common form of dementia thatproduces loss of thought control, memory and language. The diseaseusually affects men and women over the age of 60 years. The cause ofAlzheimer’s disease remains presently unknown. Most scientists thinkseveral factors such as genetic, environmental and lifestyle contributeto the development of the disease. The discovery of changes in theparietal lobe and hippocampus add significantly to progress in theresearch.
The National Institute on Aging describes theimportance of clinical research for uncovering causes,treatment modalities and disease prevention inAlzheimer’s disease. Patients or families interested inbecoming involved in research trials can go the ClinicalTrials.gov website for more information. The researchtrial website lists trials available in all 50 states and 181countries.Source: http://www.examiner.com/article/remarkable-recent-discoveries-alzheimer-s-disease
Research Topic • Alzheimer’s disease: Abstainers or bingedrinkers. Who are the most at risk population?
Treatment1. Patient & Family education regarding memoryaids, diet, and safety issues may slow theprogression of symptoms.2. Medications:•Namenda•Razadyne•Exelon•Aricept
Treatment3. Cholinesterase inhibitors-Donezepil-Rivastigmine-Galantamine4. Vitamin E- may slow progression of death,institutionalization and severe AD
Ethical Considerations Ethical Issues in the Early Diagnosis of Alzheimer Disease Matthew E. Growdon Mattsson N, Brax D, Zetterberg H. To know or not to know: ethical issues related to early diagnosis of Alzheimer’s disease. Int J Alzheimers Dis. 2010. While a disease-modifying treatment for Alzheimer disease (AD) remains elusive, recent advances have shed light on its pathophysiology, giving patients and researchers alike hope that a viable treatment will emerge. Research efforts have identified promising drug targets for clinical trials and uncovered cerebrospinal fluid (CSF) biomarkers and imaging studies that allow for preclinical detection of AD pathology. The recognition that the hallmark plaques and tangles of AD are detectable in the brains of individuals more then 10 years before they present with any cognitive changes underscored the need to validate biomarkers that could reliably detect AD and chart its progression. In April 2011, the Alzheimer’s Association  updated the criteria for the diagnosis of Alzheimer’s disease dementia for the first time in 27 years. Their report emphasizes biomarker data and lays out research guidelines for the preclinical diagnosis of AD meant to facilitate ongoing clinical research and drug discovery efforts . Implicit in these new guidelines is the hope that effective therapies are around the corner and the belief that interventions should be designed for individuals before their brains are irreversibly damaged. The well-placed optimism of scientific progress can obscure the humanistic dimensions of early diagnosis. In “To Know or Not to Know: Ethical Issues Related to Early Diagnosis of Alzheimer’s Disease,” Niklas Mattsson, David Brax, and Henrik Zetterberg examine the ethical issues surrounding the early diagnosis of AD. They emphasize the potentially harmful consequences of early diagnosis to the patient and raise important questions about personal identity and decision-making competence that are central to the diagnosis and management of AD. Their article is a timely reminder about the powerful, life-altering effects of diagnosis and, above all, the enduring need to place the patient’s desires and preferences at the center of the clinical encounter. As a point of departure, Mattsson et al. consider the potential for misdiagnosis of AD, even in the era of sophisticated biomarker studies. Several studies underscore the high diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers, with sensitivity and specificity around 85-90 percent in identifying incipient AD in patients diagnosed with mild cognitive impairment, an intermediate stage between the expected cognitive decline of normal aging and the pronounced decline of dementia . However, the authors acknowledge the enduring possibility of misdiagnosis in populations or samples in which there is a low prevalence of disease because of false positive screening results. Furthermore, while severe complications are rare, lumbar punctures to obtain CSF are associated with post-LP headaches in 2-4 percent of patients . Colloquially referred to as “spinal taps,” lumbar punctures are feared by many patients, to the point that there have been calls within professional circles to rename the procedure and move it into the mainstream of clinical practice in dementia care .
Nursing Care PlanNursing diagnosis/problem: Altered cognitive and perceptual abilities related to loss of nerve cellsGoal: Provide safe, structured environment
Nursing Interventions Rationale Outcome Criteria 1. Place patient in location 1. The patient with AD is easily 1. Patient will remain safe and where observation is easy confused by new relatively stable. (near nurses’ station, with surroundings. reliable roommate, or where family can stay) 2. Establish and maintain 2. The ability to adjust to a new consistent environment, environment and learn new including staff personnel. material is severely limited. 3. Remove all potentially 3. . dangerous objects (e.g., razor, scissors, matches 4. Approach patient in calm, 4. The behavior of others is unhurried, firm but tolerant mirrored in the patient’s manner. behavior.
References:• Black, J. (2008). Medical-Surgical Nursing 8th Edition. Singapore: Elsevier Pte. Ltd• Morrison A., Lykestos C. (2005). The Pathophysiology of Alzheimer’s Disease and Directions in Treatment. Galen Publishing LLC.• http://www.buzzle.com/articles/lobes-of-the-brain-and-their-function.html• Black, J (2008). Medical-Surgical Nursing 8th Edition. pp. 1746-1747• Sabbagh, M.D., M (2008). The Alzheimer’s Answer• http://www.examiner.com/article/remarkable-recent-discoveries-alzheimer-s-disease