Alzheimer’s disease and Lewy body dementia: Discerning the differences

CNE 1.75 contact Assessment hours LEARNING O BJECTIVES is key for 1. Compare Alzheimer’s disease and Lewy body dementia as to pathophysiology, signs, optimal symptoms, and management. 2. Describe how to screen for memory loss.

management. The authors and planners of this CNE activity have dis- closed no relevant financial relationships with any com- By Lisa Kirk Wiese, PhD, RN, PHNA-BC, mercial companies pertaining to this activity. See the last page of the article to learn how to earn CNE credit. CNE; Jennifer Lingler, PhD, MA, CRNP, FAAN; and Allison Lindauer, PhD, NP Expiration: 1/1/24

10 American Nurse Journal Volume 16, Number 1 MyAmericanNurse.com AS the U.S. population ages, the risk for age-re- tant dates or events, misplacing items, word- lated illnesses such as Alzheimer’s disease and finding difficulty, impaired judgment and deci- other types of dementia increases. According to sion making, and needing more help from Lang and colleagues, about 50% of individuals family members to perform daily tasks. with dementia are undiagnosed. When demen- As the disease progresses throughout the tia is diagnosed early, opportunities to address brain, symptoms become more severe and it increase. These opportunities include pursu- eventually encompass all major aspects of ing health behaviors that reduce progression, cognition and function. In addition, patients initiating medications earlier to help moderate may exhibit significant behavioral changes, symptoms and to potentially slow progression, including wandering, irritability, agitation, ag- as well as participating in research and ad- gression, paranoid delusions, and depression. vanced care planning. Nurses in all settings must increase their knowledge and under- Pathophysiology standing of dementia to ensure early detection. Alois Alzheimer is credited with the 1906 discovery of the neuropathological changes What is dementia? associated with AD. Specifically, abnormali- Dementia is any syndrome that manifests in ties in two proteins, beta amyloid and tau, three main sets of symptoms: debilitating cogni- represent the neuropathological hallmarks of tive decline, decreased independence in activi- AD. Excess beta-amyloid proteins form ties of daily living, and behavioral changes. plaques in the extracellular space and are Alzheimer’s disease (AD) is the most common thought to impair neuron-to-neuron commu- More than type of dementia and is sometimes used incor- nication. Tau neurofibrillary protein tangles 5 million rectly to include all forms of dementia. Another cluster within neurons, which affects neuron common type of neurodegenerative dementia is health and causes cell death. The beta amy- Americans Lewy body dementia (LBD), which consists of loid and tau changes lead to inflammation are living two diseases: dementia with Lewy bodies and and brain atrophy. Recent evidence highlight- Parkinson’s disease dementia. Other causes of ed by the Alzheimer’s Association points to with AD, and dementia include cerebrovascular disease and amyloid plaques and tau tangles depositing that number frontotemporal degeneration. In many cases, 20 years or more before the first AD symp- the presentation of dementia is characterized as toms appear and formal diagnosis. is projected “mixed,” meaning that more than one patholog- Together, these cellular alterations lead to to reach ical process is at play. Frequently, mixed de- cognitive changes that manifest as memory mentias involve both vascular dementia and a loss, functional impairment, and behavioral 7 million neurodegenerative disease. In this article, we symptoms. Previously, amyloid and tau accu- by 2025. review the core features and current manage- mulations were detectable only at autopsy, ment approaches for AD and LBD. but they’re now detectable in positron emis- sion tomography (PET) scans and their pres- Alzheimer’s disease ence can be inferred from abnormal findings According to the Alzheimer’s Association’s 2020 in cerebrospinal fluid (CSF). Alzheimer’s Disease Facts and Figures Report, The first recognizable symptomatic stage of more than 5 million Americans are living with dementia is called mild cognitive impairment AD, and that number is projected to reach 7 (MCI), which is characterized by subjective million by 2025. Traditionally viewed as a mem- complaints of cognitive changes and objective ory plus syndrome, AD dementia typically deficits that are detectable during cognitive presents as a progressive episodic memory de- testing; everyday functioning remains mostly cline and impairment in a second cognitive normal. MCI was operationalized in sentinel ar- domain such as executive function or lan- ticles by Petersen and is now widely regarded guage. Such decline may involve the inability as a risk state for AD. In recently published to recall recently learned information, create practice guidelines, Peterson and colleagues new memories, or recognize familiar faces or note that people over age 65 with a diagnosis objects. For example, someone with AD may of MCI are three times more likely to develop repeat a question within minutes, or tell the AD. Up to 55% of those with MCI may revert to same story they told earlier the same day. Oth- normal cognitive function over time. MCI also er common features include forgetting impor- can be a precursor to other forms of dementia.

MyAmericanNurse.com January 2021 American Nurse Journal 11 LBD vs. AD symptoms

The table compares selected Lewy body dementia (LBD) symptoms and common features of Alzheimer’s disease (AD) in four domains. and apathy may begin in the mild stage. Domain LBD AD* In the moderate stage, cognitive and func-

tional symptoms progress and individuals Cognitive • Episodic memory deficits • Episodic memory deficits that improve with cued that don’t improve with struggle to complete instrumental and basic recall cued recall activities of daily living (such as dressing, • Difficulty retrieving infor - • Difficulty learning and bathing, and sleeping) on their own. Behav- mation encoding information ioral symptoms may be more pronounced and • Early alteration in visuospa- • Visuospatial perception can include delusions, agitation, hallucinations, tial perception changes not as prevalent and disinhibition. Ornstein and Gaugler found • Early poor performance in • Attention impairment that these behavioral symptoms are associated sustained and divided early is possible with family caregiver depression and burden. attention tasks • In the severe stage, people with AD may lose Fluctuating cognition, at- • Fluctuating cognition, tention, and alertness the ability to communicate, become unable to attention, and alertness uncommon attend to activities of daily living (such as eating

• • and bathing), and experience loss of awareness Behavioral Vivid visual hallucinations Hallucinations less of their current surroundings. These individuals (e.g., little people, furry common, not as well- animals) occur early formed; tend to occur frequently require 24-hour care until death. late in disease course • Misidentification delusions • Paranoid delusions AD medications (e.g., Capgras) Although current medications won’t slow or

• Sleep difficulty • Fragmented sleep prevent AD onset and progression, two cate- • • REM sleep behavior disorder Naps during the day and gories of medications have received Food and awake periods at night Drug Administration approval for treating • Depression • Depression symptoms. Information about management is • Anxiety • Anxiety possible presented by Austrom and other experts in • Apathy • Apathy possible the Dementia Care Practice Recommendations

Movement • Bradykinesia • Uncommon from the Alzheimer’s Association. • Rigidity • Uncommon Cholinesterase inhibitors. Donepezil, • Unsteady gait • Uncommon rivastigmine, and galantamine are cholines terase • Rest, postural, or action • Uncommon inhibitors approved to treat mild-to-moderate

tremor AD symptoms. Donepezil also is approved to

• Postural instability with falls • Slow imbalance pro- treat severe AD symptoms. Cholinesterase in- gression hibitors interfere with the breakdown of the neurotransmitter acetylcholine (which plays a Autonomic • Orthostatic hypotension • Not as common • Loss of smell • Not as common key role in attention and memory) and help in- • Constipation • Not as common crease the brain’s circulating supply. • Sialorrhea/rhinorrhea • Not as common These medications are available as pills and

• Sexual dysfunction • Not as common liquids; donepezil is available as an orally dis- • • solving tablet, and rivastigmine can be admin- Urinary incontinence Can occur early in disease • Hyperhidrosis • Can occur early in disease istered via a transdermal patch. • Seborrheic dermatitis • Can occur early in disease The most common side effects of cholin es- terase inhibitors—diarrhea, nausea, vomiting, *Without influence of medication effects or other underlying illness fatigue, loss of appetite and weight, and in- somnia—are transient and subside within the first month of treatment. However, bradycar- AD stages dia and syncope may develop later in the AD stages are classified as mild (early stage), course of treatment, and decisions about ben- moderate (middle stage), and severe (late efit vs. harm must be made in collaboration stage). The mild stage is characterized by with the patient’s care team. readily detectable cognitive ability impair- N-methyl-D-aspartate (NMDA) receptor ment with some impairment in daily function. antagonists. Memantine is the only drug in this Affected individuals may or may not be aware class indicated for moderate or severe AD, either of the cognitive and functional deficits. Be- alone or in combination with a cholinesterase havioral symptoms such as mood changes inhibitor. Memantine is neuroprotective but also

12 American Nurse Journal Volume 16, Number 1 MyAmericanNurse.com LBD pharmacologic treatment options

No pharmacologic treatments have been approved to treat Lewy body dementia (LBD) in the United States. However, the following medica - may help diminish symptoms of agitation, ag- tions are used off-label to treat LBD symptoms. gression, and delusion. It works by blocking the Domain Possible treatment options binding of glutamate (a neurotransmitter that’s harmful when present in excess) to its receptor. Cognitive symptoms • Cholinesterase inhibitors* A fixed combination of donepezil and meman- • N-methyl-D-aspartate receptor antagonists tine also is available but is used less frequently due to its high cost and inability to adjust the Motor symptoms • Carbidopa/levodopa doses of its individual components. Memantine is available in pill as both im- Behavioral symptoms • Antidepressants mediate and extended-release forms. It’s also • Atypical antipsychotics available as a liquid. Sleep symptoms • Melatonin The most common side effects of meman- • tine—headache, confusion, dizziness, and con - Clonazepam stipation—are transient and occur during the Orthostatic hypotension • Fludrocortisone initial titration. • Midodrine

Lewy body dementia *Donepezil has been approved to treat LBD in Japan and the Philippines, and ri- LBD affects over 1.4 million Americans. It’s vastigmine has been approved to treat Parkinson’s disease dementia in the Unit- more common in men than women and pro- ed States and Europe. gresses more quickly than AD. LBD typically begins at age 50 and older. LBD is an umbrella term that encompasses Lewy body composed of abnormal intraneu- two related conditions: Parkinson’s disease de- ronal aggregations of the presynaptic protein mentia (which occurs when cognitive decline alpha-synuclein. Friederich Lewy first described develops after the motor symptoms of Parkin- Lewy bodies in 1912, but alpha synuclein wasn’t son’s disease are established) and dementia described until the late 1990s. with Lewy bodies (which occurs when cogni- tive symptoms begin before or concurrently Symptoms with motor symptoms). According to Galvin, How Lewy bodies accumulate in the brain no unique sign or symptom distinguishes de- may predict its clinical presentation. If they mentia with Lewy body from Parkinson’s de- begin accumulating in the brain stem, the re- mentia; however, time of onset frequently is sult may be autonomic and motor symptoms; used to determine which LBD subtype is pres- Lewy bodies beginning in the neocortex may ent. If dementia occurs before or with the onset lead to cognitive or behavioral symptoms. of motor symptoms associated with Parkin- Symptom presentation is classified into four son’s disease, then dementia with Lewy body domains: cognition, behavior, movement, and is suspected. If the dementia occurs 12 or autonomic function. (See LBD vs. AD symp- more months after Parkinsonism, then Parkin- toms.) A consortium of experts led by McKeith son’s disease dementia is diagnosed. Although established that the diagnosis of LBD is made this 1-year rule continues to be debated, dis- in the presence of dementia combined with at cerning if AD or LBD is present will help direct least two core criteria: parkinsonism, cognitive treatment. Additional neurologic testing can fluctuations, visual hallucinations, and rapid help to determine if dementia with Lewy body eye movement sleep behavior disorder (RBD). or Parkinson’s disease dementia is responsible Cognitive symptoms. Fluctuating cogni- for most of the symptoms. For example, the tion includes seemingly spontaneous changes Lewy Body composite risk score can help de- in attention and alertness, staring spells, on/ tect LBD by focusing the clinical interview on off periods of lethargy, and incoherent common LBD symptoms (psychomotor slow- thought that can change from minute to ing, hallucinations, rigidity). minute, hour to hour, or day to day. Cognition fluctuations can be assessed using tools such Pathophysiology as the Mayo Fluctuations Questionnaire, the About 80% of patients with LBD will have co-ex- Clinical Assessment of Fluctuation, and the isting AD pathology (amyloid plaques and tau One-day Fluctuation Assessment Scale. tangles). However, the signature pathology is a Similar to people with AD, those with LBD

MyAmericanNurse.com January 2021 American Nurse Journal 13 may have memory impairment. However, ac- (festination). Unstable posture (such as stoop- cording to Galvin, one difference is that pa- ing over) and balance problems that lead to tients with LBD sometimes benefit from cued increased falls also frequently are associated recall (using cues to jog memory when free with LBD. Other common symptoms include recall fails). In addition to memory, prominent diminished facial expressions, difficulty swal- symptoms in attention, executive function, lowing, and tremor or shaking at rest. and visual perception occur early in the Autonomic/constitutional changes. Lewy course of LBD. Although no single clinical in- body deposits affecting the autonomic nerv- dicator of LBD exists, careful early assessment ous system produce autonomic or constitu- for visuospatial impairment can help differen- tional symptoms—changes in bodily opera- tiate LBD from other dementias. tions that patients have no intentional control Behavioral symptoms. Prominent visual over. Consequently, those with LBD may have hallucinations are a key distinguishing hall- orthostatic hypotension, anosmia (loss of mark of LBD. When present, they typically oc- smell), and frequent constipation. Other com- cur early in the course of the disease. The hal- monly observed symptoms include hyper- lucinations are well formed and typically of hidrosis (excessive sweating), sialorrhea (ex- Because small or dysmorphic people, children, or ani- cessive salivation), seborrheic dermatitis (itchy mals. Auditory or olfactory hallucinations also rash with flaky skin), rhinorrhea (runny nose), of the may occur but are less common. Delusions sexual dysfunction, urinary incontinence, and importance frequently occur in LBD. These delusions in- heat and cold insensitivity. Consistent nursing clude Capgras syndrome, where the person support is essential to effectively manage of early believes that a family member or friend has these complex symptoms. detection, been replaced by an identical imposter. One of the most overlooked but earliest LBD medications cognitive symptoms of LBD is sleep difficulty and RBD, If a patient with LBD is misdiagnosed as hav- screening which is characterized by acting out dreams ing a psychiatric illness because of symptoms during sleep through violent movements, talk- such as hallucinations and illogical think- is now a ing, and falling out of bed. Other common ing, providers may prescribe medications that required symptoms are excessive daytime sleepiness (2 are detrimental. For example, carbidopa/lev- or more hours of sleepiness daily), restless leg odopa, although helpful for patients with component syndrome (walking or movement is needed to Parkinson’s disease, may exacerbate hallucina- of the help relieve uncomfortable leg sensations), tions in those with LBD. Antipsychotic medica- and increased discomfort at rest. tions may relieve hallucinations but also could Medicare/ People with LBD, similar to those with AD, exacerbate rigidity and motor slowness. Medicaid frequently experience depression, exhibited No medications have been approved in the by feelings of worthlessness, sadness, and United States to specifically treat LBD, but ri- annual trouble eating or sleeping. Other behavior vastigmine does have approval to treat symp- wellness visit. and mood changes include apathy or lack of toms of mild-to-moderate Parkinson’s disease desire to participate in previously enjoyed ac- dementia. Treatment should be based on the tivities, agitation (which manifests as restless- four LBD domains; however, all treatment is ness and unexplained irritation), intense lev- off-label. (See LBD pharmacologic treatment els of anxiety (which manifests as anger or options.) To treat cognitive symptoms, cholin - fear when a loved one isn’t present), and fear esterase inhibitors and NDMA receptor antag- about a future event. onists used in AD frequently are prescribed Movement disorder. Many patients with for LBD. Cholinesterase inhibitors may show a LBD experience Parkinsonism symptoms; by more robust initial response in LBD compared definition, all patients with the Parkinson’s with AD. For motor symptoms, carbidopa/lev- disease dementia form of LBD experience odopa may help reduce Parkinsonian symp- them. Early signs may include changes in fa- toms such as slow gait and muscle rigidity. cial expression, hand posture, walking, bal- Unfortunately, these medications may in- ance, and handwriting. LBD motor symptoms crease confusion and hallucinations so titra- include bradykinesia (slowness in initiating or tion should be performed slowly. carrying out a movement), rigidity (stiffness), No medications have been approved to and noticeable gait change such as shuffling manage LBD behavioral symptoms, and many

14 American Nurse Journal Volume 16, Number 1 MyAmericanNurse.com Lewy body composite risk score assessment

The Lewy body composite risk score is an accurate, valid, and reliable tool for differentiating between Lewy body dementia and Alzheimer’s disease.

Please rate the following as being present or absent at least three times over the past 6 months. Does the patient have: Yes No

Slowness in initiating and maintaining movement, or frequent hesitations or pauses during movement?

Rigidity (with or without cogwheeling) on passive range of motion in any of the four extremities?

Loss of postural stability (balance) with or without frequent falls?

Tremor at rest in any of the four extremities or the head?

Excessive daytime sleepiness and/or seem drowsy and lethargic when awake?

Episodes of illogical thinking or random, incoherent thoughts?

Frequent staring spells or periods of blank looks?

Visual hallucinations (see things not really there)?

Appear to act out his/her dreams (kick, punch, thrash, shout, or scream)?

Orthostatic hypotension or other signs of autonomic insufficiency?

Reprinted with Permission from Dr. James E. Galvin. Galvin JE. Improving the clinical detection of Lewy body dementia with the Lewy body composite risk score. Alzheimers Dement (Amst). 2015;1(3):316-24. common psychotropic medications can have Screening for memory loss deleterious side effects in patients with LBD. Because of the importance of early detection, In general, all classic neuroleptic medications, cognitive screening is now a required compo- such as haloperidol, should be avoided. When nent of the Medicare/Medicaid annual well- possible, nonpharmacologic approaches should ness visit. Several measures are available that be attempted to alleviate these symptoms. (To nurses can use to briefly assess for risk of cog- learn more about nonpharmacologic strate- nitive decline. For example, the Quick De- gies, visit myamericannurse.com/?p=69690.) If mentia Rating Scale (QDRS) is a 5-minute in- necessary, careful use of atypical antipsychot- formant interview that addresses ten cognitive ic medications (such as quetiapine or pima- domains: memory and recall, orientation, de- vanserin) can be tried but require close mon- cision-making and problem-solving abilities, itoring. Attention to physical ailments such as activities outside the home, function at home constipation and pain should be the first pri- and hobbies, toileting and personal hygiene, ority because they can trigger behavioral behavior and personality changes, language changes. Mood symptoms are common in and communication abilities, mood, and at- patients with LBD. Selective serotonin reup- tention and concentration. The QDRS format take inhibitors, which help increase the helps to avoid problems such as patient anxi- amount of serotonin in the brain, appear to ety with cognitive testing, which can lead to reduce irritability, agitation, and depression. refusing to be tested. The scale also can be RBD frequently is treated with melatonin or completed by family members. Scores of the clonazepam. 30-item scale range from 0 (no impairment in Treating autonomic symptoms is challeng- any domain) to 30 (indicating severe cognitive ing and requires a holistic nursing approach, impairment). The QDRS has strong reliability including identifying therapies targeted to and validity when correlated with other com- each symptom. For example, constipation and mon cognitive assessment tools, such as the diaphoresis in the context of orthostatic hy- Clinical Dementia Rating scale (r=0.80, P <.001) potension require comfort measures com- and the Mini-Mental State Exam (r=-.599, P bined with safety strategies. Effective nursing <.001); the Mini-Mental State Exam requires care will make a critical difference in prevent- payment for use. In addition, the QDRS pro- ing or mitigating the physical health chal- vides enough information to stage dementia lenges associated with dementia syndromes. severity, and it can be used by clinicians to

MyAmericanNurse.com January 2021 American Nurse Journal 15 Modifying behaviors to decrease dementia risk

In the past, it was believed that nothing could be done to delay the on- set of dementia or slow its progress. However, research on lifestyle mod- in the brain or CSF. These tests are expensive. ifications that may diminish risk factors for dementia is growing. Recom- Dopamine transporter imaging using single mended strategies that may reduce Lewy body dementia risk include PET scans can be used to diagnose Parkinson’s • refraining from smoking disease. Blood tests aren’t yet available for these • maintaining a healthy diet dementias, but advances are being made. For • getting adequate sleep example, Thijssen and colleagues tested for the • participating in cognitively stimulating activities presence of pTau181 protein in the blood plasma • interacting with others socially of 400 individuals and were successful in distin- • exercising. guishing those who were healthy from those Edwards and colleagues identified several medical (obesity, diabetes, with AD pathology. These findings were cor- hypertension, elevated cholesterol, depression) and lifestyle (dietary roborated with two established biomarkers (pres- fat and cholesterol consumption, smoking, lack of physical activity) ence of pTau181 in spinal fluid and amyloid Alzheimer’s disease (AD) risk factors that may be modifiable with protein in PET scans) being used in AD research. health-promoting interventions. In August 2020, Livingston and col- leagues added other risk factors to this list—traumatic brain injury, After screening pollution, and excessive alcohol consumption. They reported that all If screening indicates that a patient is at risk of the modifiable risk factors account for about 40% of worldwide de- for cognitive decline, they should be referred mentias that could be theoretically prevented or delayed. Recent evidence from Haslam and colleagues’ work with the Fram- to a board-certified advanced gerontological ingham Heart Study about the impact of sugary drink consumption in- nurse practitioner, advanced practice regis- dicates that even a small but consistent change in diet, such as elimi- tered nurse gerontological specialist, neurolo- nating sugar-sweetened soft drinks, may help reduce dementia risk. gist, or other provider comfortable with diag- Improving nutritional habits to include more fruits and vegetables, nosing and treating cognitive impairment. beans, nuts, whole grains, olive oil, and fish (the MIND [Mediterranean- These providers will consider other causes DASH Intervention for Neurodegenerative Delay] diet) should be en- of cognitive decline, such as negative medica- couraged to promote brain health. Also, promising new biomarkers tion effects; trauma; depression; or vitamin B- may aid in early dementia detection. 12, folate, or thyroid deficiency. Symptom-di- rected treatment is more effective the earlier it’s initiated in the disease process. Education determine the need for more formal testing. to adapt healthy behaviors may potentially de- The Montreal Cognitive Assessment (MoCA), lay a patient’s decline, and participation in re- developed by Nasreddine and colleagues, is a search studies is an option for those in the performance-based assessment that addresses early stages of dementia. (See Modifying be- attention, memory, concentration, orientation, haviors to decrease dementia risk.) visuoconstruction skills, and language. Ju- layanont and colleagues’ MoCA-B is geared to- Ease the burden ward individuals with health literacy and educa- As the population ages, nurses need to learn tion levels below 8th grade. The MoCA is more about AD and LBD. Distinguishing be- available in multiple languages, including Span- tween these two conditions is critical to en- ish, Chinese, and Hindi and also as a telephone sure proper treatment and symptom manage- Mini-MoCA, which was designed for use during ment. Regular screening and early dementia periods of quarantine. These assessments are detection offer opportunities for nurses and available at MoCAtest.org. Galvin’s Lewy Body families to partner in research and symptom Composite Risk Score assesses LBD risk and management and ease illness burden. AN can differentiate LBD from AD with high accu- racy, validity, and reliability. (See Lewy body Lisa Kirk Wiese is an associate professor of nursing at the Florida composite risk score assessment.) Atlantic University C. E. Lynn College of Nursing in Boca Raton. Jen- The science behind dementia detection nifer Lingler is professor and vice chair for research at the Health continues to change rapidly. Patients identi- and Community Systems University of Pittsburgh School of Nursing fied with dementia ideally should receive in Pittsburgh, Pennsylvania. Allison Lindauer is an assistant profes- brain imaging (non-contrast computed tomog- sor of neurology at the School of Medicine Oregon Health and Sci- raphy or magnetic resonance imaging) to rule ence University and the Layton Aging and Alzheimer's Disease Cen- ter director of outreach, recruitment, and education in Portland. out other causes. PET and CSF biomarkers can

be used to diagnose AD by testing for the To view a list of references, visit myamericannurse.com/ presence of amyloid plaque and tau proteins ?p=69690.

16 American Nurse Journal Volume 16, Number 1 MyAmericanNurse.com

POST-TEST • Alzheimer’s disease and Lewy body dementia: Discerning the differences CNE: 1.75 contact hours CNE Earn contact hour credit online at myamerciannurse.com/alzheimers-disease-and-lewy-body-dementia

Provider accreditation Contact hours: 1.75 The American Nurses Association is accredited as a provider ANA is approved by the California Board of Registered Nurs- of nursing continuing professional development by the ing, Provider Number CEP17219. American Nurses Credentialing Center’s Commission on Post-test passing score is 80%. Accreditation. Expiration: 1/1/24

Please mark the correct answer 7. The signature pathology of LBD is a 12. A drug used to treat orthostatic online. Lewy body composed of abnormal hypo tension in patients with LBD is 1. The neuropathological hallmarks of a. intraneuronal aggregations of the a. Clonazepam Alzheimer’s disease (AD) are abnormali- presynaptic protein alpha-synu- b. Carbidopa/levodopa ties in clein. c. Melatonin a. alpha amyloid and tau proteins. b. intraneuronal aggregations of the d. Midodrine postsynaptic protein gamma- b. alpha amyloid and gamma proteins. synuclein. c. beta amyloid and gamma proteins. 13. Which statement about the man- c. interneuronal aggregations of the agement of behavioral symptoms relat- d. beta amyloid and tau proteins. presynaptic protein beta-synuclein. ed to LBD is correct? 2. The first recognizable symptomatic d. interneuronal aggregations of the a. Nonpharmacologic approaches stage of dementia is referred to as postsynaptic protein alpha-synu- should be used to ease these clein. symptoms. a. initial cognitive impairment. b. Neuroleptic medications, such as b. mild cognitive impairment. 8. A key behavioral symptom of LBD haloperidol, are effective for treat- c. neurofibrillary protein tangle. that usually occurs early in the course ment. of disease is d. neurofibrillary protein strand. c. Pimavanserin is an effective drug a. occasional sensory delusions. that doesn’t require close moni- 3. In which stage of AD do patients b. prominent olfactory hallucinations. toring. begin to experience more pronounced c. occasional auditory delusions. delusions and hallucinations? d. Medications should be tried be- d. prominent visual hallucinations. fore nonpharmacologic approach- a. Mild es are used. b. Moderate 9. A frequently overlooked but early c. Severe symptom of LBD is 14. Which statement about the Quick d. Advanced a. hyperkinesia. Dementia Rating Scale (QDRS), which b. reduced salivation. is used to screen for memory loss, is correct? 4. Which type of drugs used to treat c. sleep difficulties. AD interfere with the breakdown of the a. It addresses five cognitive domains. d. postural hypertension. neurotransmitter acetylcholine? b. It has strong reliability compared a. Anticholinergic agents 10. Which of the following statements to other common cognitive as- b. N-methyl-D-aspartate (NMDA) comparing AD and LBD symptoms is sessment tools. receptor antagonists correct? c. It provides insufficient information c. Cholinesterase inhibitors a. Misidentification delusions are to stage dementia severity. d. Monoamine oxidase inhibitors common in LBD. d. It can’t be used to determine the b. Loss of smell occurs less often in need for more formal testing. 5. Which NMDA drug used to treat AD LBD. 15. Which screening assessment tool is blocks the binding of glutamate to its c. Visuospatial perception changes receptor? geared toward individuals with health are more prevalent in AD. literacy and education levels below 8th a. Donepezil d. Hallucinations are more common grade? b. Rivastigmine in AD. a. Mini-Mental State Exam c. Galantamine b. Lewy Body Composite Risk Score d. Memantine 11. Which drug is used to treat motor symptoms of LBD? c. Montreal Cognitive Assessment-B 6. Lewy body dementia (LBD) encom- a. Clonazepam d. The Quick Dementia Rating Scale passes two related conditions: demen- b. Carbidopa/levodopa tia with Lewy bodies and c. Melatonin a. Parkinson’s disease dementia. d. Midodrine b. mild cognitive impairment. c. moderate-stage AD. d. generalized dementia.

MyAmericanNurse.com January 2021 American Nurse Journal 17