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Diagnosis and Management of Dementia

Michael Mistric, PhD, RN, FNP, BC Nurse Practitioner Michael E. DeBakey VA Medical Center. Diagnosis and Management of Dementia. Objectives. Describe the demographics associated with Alzheimer’s dementia Describe the clinical features of Alzheimer’s dementia

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Diagnosis and Management of Dementia

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  1. Michael Mistric, PhD, RN, FNP, BC Nurse Practitioner Michael E. DeBakey VA Medical Center Diagnosis and Management of Dementia

  2. Objectives • Describe the demographics associated with Alzheimer’s dementia • Describe the clinical features of Alzheimer’s dementia • Describe the medical management of Alzheimer’s dementia • Describe caregiver support services for individuals with Alzheimer’s dementia • Describe caregiver’s basic social process of formulating expectations of dementia care

  3. Dementia: What it is • A syndrome that has multiple reversible and irreversible causes and requires systematic evaluation of the patient presenting with a cognitive complaint • An acquired, persistent decline (not secondary to delirium) involving at least three of the following five domains: language, memory, visiospatial skills, executive function, and personality and mood Cummings, Benson, LoVerme (1980) Reversibledementia. JAMA, 243(23)

  4. Why Use Alzheimer’s Disease (AD) as the Exemplar? • Approximately 5 million Americans have Alzheimer’s disease (AD).  Unless a cure or prevention is found, that number will increase to 14 million by 2050. • An estimated 280,000 Texas have Alzheimer’s disease. • One in eight persons over 65 and nearly half of those over 85 have AD.  A small percentage of people as young as their 30s and 40s get the disease. • AD is degenerative disease of the brain from which there is no recovery. • AD is now the seventh leading cause of death in adults. 2010 Alzheimer's Disease Facts and Figures (alz.org)

  5. Why Use Alzheimer’s Disease (AD) as the Exemplar? • Direct and indirect costs of AD and other dementia’s amount to more than $148 billion annually. • Almost 10 million Americans are caring for a person with AD or another dementia; approximately one out of three of these caregivers is 60 years or older. • In 2005, it was estimated that unpaid caregivers of people with AD and other dementias provided 8.5 billion hours of care valued at almost $83 billion dollars.   • More than half the states in the United States provide more than a billion dollars in unpaid care each year – Texas $5.8 billion. 2010 Alzheimer's Disease Facts and Figures (alz.org)

  6. Quick Patho Overview The primary pathologic features of AD are amyloid deposition, neurofibrillary tangle formation, and neuronal loss

  7. AD and the Brain • Plaques and Tangles: The Hallmarks of AD • The brains of people with AD have an abundance of two abnormal structures: • beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells • neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell An actual AD plaque An actual AD tangle

  8. AD and the Brain • Beta-amyloid Plaques • Amyloid precursor protein (APP) is the precursor to amyloid plaque. • 1.APP sticks through the neuron membrane. • 2.Enzymes cut the APP into fragments of protein, including beta-amyloid. • 3.Beta-amyloid fragments come together in clumps to form plaques. 1. 2. In AD, many of these clumps form, disrupting the work of neurons. This affects the hippocampus and other areas of the cerebral cortex. 3.

  9. AD and the Brain • Neurofibrillary Tangles Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles.

  10. The 10 Warning Signs • Trouble with abstract thinking • Misplacing things • Changes in mood or behavior • Changes in personality • Loss of initiative • Memory loss • Difficulty with familiar tasks • Problems with language • Disorientation to time and place • Poor or decreased judgment

  11. DSM-IV Criteria for Dementia • Memory impairment and 1 or more: • Aphasia (language disturbance) • Apraxia (inability to carry out motor activities • Agnosia (failure to recognize objects) • Disturbed executive function (planning, organizing) • Cognitive deficits • Gradual onset, continued decline • Deficits not due to another condition • Deficits not exclusive to delirium

  12. AD and the Brain The Changing Brain in Alzheimer’s Disease No one knows what causes AD to begin, but we do know a lot about what happens in the brain once AD takes hold. Pet Scan of Normal Brain Pet Scan of Alzheimer’s Disease Brain

  13. Importance & Significance of Diagnostic Work-Up • Treat a reversible condition • Treat co-morbid conditions • Avoid exacerbation • Limit complications • Relieve symptoms • AD no longer a diagnosis of exclusion • Drugs & programming depend on staging • Caregivers can be secondary victims: provide for them as well

  14. AD Research: Diagnosing AD Providers today use a number of tools to diagnose AD: • a detailed patient history • information from family • and friends • physical and neurological exams and lab tests • neuropsychological tests (MMSE, GDS, Global Deterioration Scale, Affect Balance, BEHAVE-D • imaging tools such as CT scan, or magnetic resonance imaging (MRI), PET scans

  15. Assessment Protocols • Complete PE & History • Mini-Mental State Exam (MMSE) or Physical Self-Maintenance Scale (PSMS) to establish baseline cognition and functional ability • Global Deterioration Scale – useful for staging • Affect Balance or Geriatric Depression Scale • Katz ADLs – IADLs • BEHAVE-AD

  16. Cultural Considerations • Members of various ethnic groups, cultures, and races manifest and cope differently with the disease, care-giving, and related stresses • Some Asian/Pacific Islanders view AD as a normal part of aging • Some Hispanics view AD as a spiritual test or punishment for a past deed. • Some African Americans rely on their spiritual faith to deal with the illness and care-giving.

  17. Research Findings: African Americans • 1st degree African American relatives have higher risk than Caucasians. • African Americans are 4 times more likely to develop AD by age 90 • African Americans and Hispanics may be at higher genetic risk based on APOE-4 allele aberration • Hypertension and hypercholesterolemia each place African American at a 4 times risk for AD http://www.ethniceldercare.net

  18. Socio-Cultural-Behavioral: African Americans • African American family members & caregivers may not consider dementia an illness, but rather an expected consequence of aging • Some believe it is a form of mental illness • May be believed to be the result of “worriation” and behaviors may be interpreted as “spells” • First cue may be in the failure to carry out role and social functions (later than desired recognition per professional assessment) http://www.ethniceldercare.net

  19. Research Findings: Hispanics • Hispanics may be 2 times more likely than Caucasians to develop AD by age 90 • Vascular dementia has higher prevalence than AD http://www.ethniceldercare.net

  20. Socio-Cultural-Behavioral: Hispanics • Female family members are the designated caregivers • Dementia may be viewed as some form of mental illness • Dementia is a source of shame, embarrassment, stigma; and, therefore may be a barrier to getting help • Problem not typically shared in the cultural network http://www.ethniceldercare.net

  21. Socio-Cultural-Behavioral: Asians/Pacific Islanders • Dementia is a form of normal aging • Dementia is a form of mental illness • Dementia is a source of shame • Dementia is a family secret that should not be shared • Dementia is a result of fate http://www.ethniceldercare.net

  22. Stages of Dementia • Early Dementia “All dressed up and no where to go” • Middle Dementia “I want to go with you” • Late Dementia “In his own little world”

  23. Characteristics:Early Stage Dementia • Physical Appearance • May still dress self appropriately • Awareness • “Lost in Time” • Behaviors • Wandering • Anxious • Resistance to ADLs • Sleep disturbance

  24. AD and the Brain Preclinical AD • Signs of AD are first noticed in the entorhinal cortex, then proceed to the hippocampus. • Affected regions begin to shrink as nerve cells die. • Changes can begin 10-20 years before symptoms appear. • Memory loss is the first sign of AD. Slide 20

  25. Caregiving Challenges:Early Stage Dementia • Eating • Eats independently • May need cueing • Remove stimulants from diet • Toileting • Needs supervision locating bathroom and reminders to go • Usually continent • Hydration • Needs supervision • Provide favorite beverages frequently

  26. Caregiving Challenges:Early Stage Dementia • Dressing • Needs help locating and choosing clothing • Coaxing--resistance • Personal Hygiene • Needs supervision-is relatively independent • Bathing • Needs supervision • Awareness of need to bathe is variable

  27. Characteristics:Middle Stage Dementia • Physical Appearance • Looks unfinished; does not want to change clothes • Change in posture • Awareness • May be awareness of past versus present • Unable to think in the abstract • Behaviors • Wanders, is suspicious, resistant to caregivers, social butterfly

  28. AD and the Brain • AD spreads through the brain. The cerebral cortex begins to shrink as more and more neurons stop working and die. • Mild AD signs can include memory loss, confusion, trouble handling money, poor judgment, mood changes, and increased anxiety. • Moderate AD signs can include increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements. Mild to Moderate AD Slide 21

  29. Caregiving Challenges:Middle Stage Dementia • Eating • Trouble using utensils, positioning, and swallowing--precut food, use prompting/cueing • Toileting • Needs assistance with mechanics--wiping, flushing, pulling down underwear, reminders • Hydration • Hydration is dependent on caregiver attention

  30. Caregiving Challenges:Middle Stage Dementia • Dressing • Assistance in dressing due to agnosia, apraxia • Personal Hygiene • Assistance due to agnosia, apraxia, Parkinsonian symptoms • Needs tasks broken down • Bathing • Needs supervision • Awareness of need to bathe is dependent on caregiver

  31. Characteristics:Late Stage Dementia • Physical Appearance • Looks abnormal, undresses, looks lost, posture/balance deficits, loses weight, loss of 3D vision • Awareness • Limited to field of vision, seeks sensory stimulation • Behaviors • Hyper/hypo activity, cannot communicate needs, does not recognize self or loved ones

  32. AD and the Brain Severe AD • In severe AD, extreme shrinkage occurs in the brain. Patients are completely dependent on others for care. • Symptoms can include weight loss, seizures, skin infections, groaning, moaning, or grunting, increased sleeping, loss of bladder and bowel control. • Death usually occurs from aspiration pneumonia or other infections. Caregivers can turn to a hospice for help and palliative care. Slide 22

  33. Caregiving Challenges:Late Stage Dementia • Eating • Total loss in eating skills: using utensils, position, swallowing difficulty • Toileting • Total Care • May resist • Hydration • Unable to pour water or understand need or mechanics of drinking water

  34. Caregiving Challenges:Late Stage Dementia • Dressing • Needs total assistance • May disrobe or fiddle with clothes • Personal Hygiene • Needs total assistance. • Able to do one step tasks – e.g. washing face • Bathing • Unable to comprehend bathing • May resist sponge or bed bath

  35. Treatment Goals • All are focused on maximizing the potential of the patient and managing symptoms • Support cognitive functioning • Reduce and prevent functional disabilities • Ameliorate and mediate behavioral disturbances

  36. AD Research: Managing Symptoms Between 70 to 90% of people with AD eventually develop behavioral symptoms, including sleeplessness, wandering and pacing, aggression, agitation, anger, depression, and hallucinations and delusions. Experts suggest these general coping strategies for managing difficult behaviors: • Stay calm and be understanding. • Be patient and flexible. Don’t argue or try to convince. • Acknowledge requests and respond to them. • Try not to take behaviors personally. Remember: it’s the disease talking, not your loved one. Experts encourage caregivers to try non-medical coping strategies first. However, medical treatment is often available if the behavior has become too difficult to handle. Researchers continue to look at both non-medical and medical ways to help caregivers.

  37. Barriers to Overcome • Still are people that accept memory loss & confusion as a natural part of aging • Cognitive impairments of any kind are not easy to admit, recognize, or discuss • Patients hide or compensate for early signs • Families deny what is being seen

  38. Diagnosis and Evaluation • Requires comparison of cognitive and physical functioning relative to a previous level of performance • Eliminate or reverse any other (vascular, metabolic, etc.) causes • Proceed by clinical criteria and protocols for radiologic & laboratory studies • Refer to neurologist and Alzheimer’s Disease Research Center

  39. Interview and Care for the Caregiver • What Alzheimer symptoms are most prevalent? • What significant changes have you noticed? • Memory • Behavior • Personality • Skills • Other • How have you successfully accommodated for these changes? • What caregiving challenges are you facing? • What activities does your loved one still enjoy? • Describe a special moment you shared with your loved one recently.

  40. Treatment Realities • Current treatments for Alzheimer’s are not designed to reverse the disease process totally, yet they can produce some improvements in cognition. • Existing medications can be effective in slowing the progression of the disease and helping patients remain independent for longer periods of time. • Treating symptoms effectively is valuable not only to patients but also to their caregivers and families.

  41. Primary Treatment • Cholinesterase inhibitors • Receptor agonists • Estrogen • Anti-inflammatory drugs • Antioxidants • Various experimental agents • Behavioral controls

  42. Medications used to treat Dementia • Cholinesterase Inhibitors • Donepezil (Aricept): Mild/Moderate Dementia • Start with 5 mg/day; increase to 10 mg/day in 4 weeks • Nausea; Diarrhea; Poor Appetite • Rivastigmine (Exelon): Mild/Moderate Dementia • Start with 4.6 mg/24 hour patch daily; increase to 9.5 mg/24 hour patch daily in 4 weeks • Nausea; Diarrhea; Poor Appetite • Galantamine (Reminyl): Mild/Moderate Dementia • Start with 8 mg a day; increase by 8 mg every four weeks up to 24 mg a day • Nausea; Diarrhea; Poor Appetite

  43. Medications used to treat Dementia • N-methyl-D-aspartate (NMDA) • Memantine (Namenda): Moderate/Severe Dementia • Start with 5 mg a day; increase by 5 mg a week up to 10 mg twice a day • Headache; Dizziness; Confusion • Tacrine (Cognex): • Not used anymore • Prototypical cholinesterase inhibitor for the treatment of Alzheimer's disease

  44. Cholinergic Receptor Agonists • Muscarinic receptor agonists • M1-type muscarinic acetylcholine receptors play a role in cognitive processing. • In Alzheimer disease (AD) amyloid formation may decrease the ability of these receptors to transmit their signals leading to decrease cholinergic activity. • A number of muscarinic agonists have been developed and are under investigation to treat AD. • These agents show promise as they are neurotrophic, decrease amyloid depositions, and improve damage due to oxidative stress.

  45. Cholinergic Receptor Agonists • Nicotinic receptor agonists • Nicotine has long been known to improve cognitive function, but its adverse effects make it problematic as a treatment for diseases of cognitive dysfunction • Recent research has revealed that certain subtypes of nicotinic acetylcholinesterase receptors (nAChRs) in the brain are involved in cognitive function • Agents that target these nAChRs have shown promise in Alzheimer’s disease • Research also suggests that these agents may not only improve cognition but also be neuroprotective

  46. Estrogen • Early studies of estrogen suggested that it might help prevent AD in older women. • However, a clinical study of several thousand postmenopausal women aged 65 or older found that combination therapy with estrogen and progestin substantially increased the risk of AD. • Estrogen alone also appeared to slightly increase the risk of dementia in this study. • Therefore, based on epidemiological correlations, the use of estrogen to prevent or treat dementia has not been supported by follow-up studies and is not recommended. http://www.medicinenet.com

  47. Anti-inflammatory Agents • Several studies have found evidence of brain inflammation in AD and researchers have proposed that drugs that control inflammation, such as NSAIDs, might prevent the disease or slow its progression and early studies of these drugs in humans have shown promising results. • However, a large NIH-funded clinical trial of two NSAIDS (naproxen and celecoxib) to prevent AD was stopped in late 2004 because of an increase in stroke and heart attack in people taking naproxen, and an unrelated study that linked celecoxib to an increased risk of heart attack. • Therefore, based on epidemiological correlations, the use of NSAIDs to prevent or treat dementia has not been supported by follow-up studies and is not recommended. http://www.medicinenet.com

  48. Antioxidants: Vitamin E • A recent double-blind, placebo-controlled study of Vitamin E and donepezil for the treatment of mild cognitive impairment was unable to demonstrate benefit form Vitamin E and showed only modest and short-term benefit from donepezil. • This result suggested there was no role for the use of Vitamin E in the prevention or early treatment of Alzheimer’s Dementia. Petersen et al. (2005). New England Journal of Medicine (352)

  49. Investigative Vaccines • Many researchers believe a vaccine that reduces the number of amyloid plaques in the brain might ultimately prove to be the most effective treatment for AD. • In 2001, researchers began one clinical trial of a vaccine called AN-1792. • The study was halted after a number of people developed inflammation of the brain and spinal cord. • Despite these problems, one patient appeared to have reduced numbers of amyloid plaques in the brain. • Other patients showed little or no cognitive decline during the course of the study, suggesting that the vaccine may slow or halt the disease. • Researchers are now trying to find safer and more effective vaccines for AD. http://www.medicinenet.com

  50. General Management Guidelines • Look for concurrent illness/problems • Look at medications • Try non-pharmocologic alternatives • Target the dominant symptom • Start drugs low and go slow • Look at drug with best side effect profile • Review compliance • Simplify • Give clear and written instructions

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