Lewy Body Disease: Difference between revisions

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== Clinically Relevant Anatomy<br> ==
== Introduction  ==
Lewy body disease or Lewy body [[dementia]] (LBD), is a [[Neurodegenerative Disease|neurodegenerative disease]] (specifically a [[synucleinopathy]]) related to [[Parkinson's|Parkinson disease]].<ref name=":0">Radiopedia [https://radiopaedia.org/articles/dementia-with-lewy-bodies Dementia with Lewy bodies] Available:https://radiopaedia.org/articles/dementia-with-lewy-bodies (accessed 13.9.2022)</ref>[[File:Dementia 3.jpg|thumb|Dementia]]
There are 2 types of LBD generally described in the literature:<ref name="Mckeith">McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, Salmon DP, Lowe J, Mirra SS, Byrne EJ, Lennox G. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB) Report of the consortium on DLB international workshop. Neurology. 1996 Nov 1;47(5):1113-24. [https://www.ncbi.nlm.nih.gov/pubmed/8909416 PMID:8909416]</ref>


add text here relating to '''''clinically relevant''''' anatomy of the condition<br>
# Dementia with Lewy Bodies: dementia occurring first or within one year of movement disorder.
# Parkinson Disease Dementia: dementia occurring in a patient who receives a diagnosed of Parkinson's disease and then develops dementia symptoms after one year or more of the diagnosis.


== Mechanism of Injury / Pathological Process<br>  ==
People with either type generally develop similar symptoms as the disease progresses. Distinct Parkinsonian symptoms such as slowness of movement, rigidity, REM [[Sleep Deprivation and Sleep Disorders|sleep]] behaviour disorder and visual hallucinations can help to distinguish DLB from Alzheimer’s disease.<ref name="National">National Institute on Aging. Lewy Body Dementia: Information for Patients, Families, and Professionals. (Accessed 4 May 2017). https://www.nia.nih.gov/alzheimers/publication/lewy-body-dementia/basics-lewy-body-dementia</ref>
== Epidemiology ==


add text here relating to the mechanism of injury and/or pathology of the condition<br>  
* Occurs in older patients (onset typically in 50-70 years of age), and is sporadic. However a family history of LBD and Parkinson disease will increase a person's risk.<ref name=":2">Haider A, Spurling BC, Sánchez-Manso JC. [https://www.ncbi.nlm.nih.gov/books/NBK482441/ Lewy body dementi]a. InStatPearls [Internet] 2022 Oct 23. StatPearls Publishing.Available:https://www.ncbi.nlm.nih.gov/books/NBK482441/ (accessed 6.10.2023)</ref>
* LBD is one of the most common causes of dementia (accounting for up to  20% to 30% of cases<ref name=":2" />) along with [[Alzheimer's Disease|Alzheimers disease (AD)]]<ref name="National" />.
 
== Etiology ==
The etiology of LBD is unknown. [[Genetics and Health|Genetics]], environmental factors, and changes linked to [[Older People Introduction|aging]], may have a role and research is still ongoing.<ref name=":1">Haider A, Spurling BC, Sánchez-Manso JC. Lewy body dementia. InStatPearls [Internet] 2021 Jul 12. StatPearls Publishing.Available:https://www.ncbi.nlm.nih.gov/books/NBK482441/ (accessed 13.9.2022)</ref>
 
LBD has been found to be strongly linked to a [[Proteins|protein]] called [[Alpha-Synuclein (α-syn)|alpha-synuclein]]. The abnormal accumulation of this [[Proteins|protein]] in certain regions of the [[Brain Anatomy|brain]] causes dramatic [[Cognitive Impairments|cognitive]] and motor deficits affecting behaviour, mood, movement, and thinking.


== Clinical Presentation  ==
== Clinical Presentation  ==
[[File:Frontal lobe.jpeg|right|frameless]]
The clinical features of LBD are the consequence of the blockage of information transfer from the striatum to the [[Cerebral Cortex|cortex]], more notably the [[Frontal Lobe|frontal lobe]].


add text here relating to the clinical presentation of the condition<br>  
Core features:<ref name="Gn">Gnanalingham KK, Byrne EJ, Thornton A, Sambrook MA, Bannister P. Motor and cognitive function in Lewy body dementia: comparison with Alzheimer's and Parkinson'ss. Journal of Neurology, Neurosurgery &amp; Psychiatry. 1997 Mar 1;62(3):243-52. http://jnnp.bmj.com/content/jnnp/62/3/243.full.pdf</ref>


== Diagnostic Procedures  ==
# Fluctuating cognitive impairment especially in executive function, attention and alertness
# Visuospatial impairment, including visual hallucinations (detailed and vivid)
# Concurrent parkinsonian symptoms may be present but are less common, more frequently occurring years after the onset of dementia eg early [[Extrapyramidal and Pyramidal Tracts|extrapyramidal]] features (dystonia, akathisia, muscle rigidity, [[bradykinesia]], tremor, tardive dyskinesia
Watch this 3 minute video showing a personal story "It happened little by little. First he would forget things, then he'd lose track of what he was doing. LBD took over the life of the man you're about to meet."<br>


Lewy Body Disease (LBD) can have two forms of clinical diagnoses which are dementia with Lewy bodies and Parkinson’s disease dementia <ref name="Lewy">Lewy Body Dementia Association. What is LBD? Available from: https://www.lbda.org/category/3437/what-is-lbd.htm [Accessed May 5, 2017]</ref>. There are many different diagnostic tools that can be used to diagnose an individual with Lewy body Disease. For every patient that gets diagnosed with LBD, it varies with different types of symptoms that they experience. Symptoms may change from day to day or hour to hour <ref name="Lewy" />.<br>It is difficult to diagnose Lewy Body Disease with dementia because it shows similar signs and symptoms to those of Alzheimer and Parkinson’s disease. Therefore LBD can sometimes be missed when diagnosing an individual <ref name="Lewy" />. But overall, when individuals progress and develop more symptoms of LBD then it becomes easier to diagnosis.<br>To diagnosis the type of LBD, physical and neurological evaluations are used and a thorough patient interview is done. For example,<br>· Medical history (past and current diseases and disorders)<br>· Medications<br>· Movement evaluation<br>· Current symptoms<br>· Social history<br>· Functional abilities<br>· Cognitive abilities (attention, language, memory, visual)<br>· Brain imaging (CT or MRI)<br>· Blood tests.<br>Ultimately, all these evaluations can’t provide a conclusive diagnosis of LBD. The only way to confirm if an individual has LBD is to have a post mortem autopsy of their brain <ref name="Lewy" />. With clinical imaging, cortical and subcortical atrophy can be noticeable with LBD. Atrophy can also be seen in the grey matter of the temporal, frontal, and parietal lobes and the insular cortex in an individual with LBD <ref name="Morra">Morra LF, Donovick PJ. Clinical presentation and differential diagnosis of dementia with Lewy bodies: a review. International journal of geriatric psychiatry. 2014 Jun 1;29(6):569-76.</ref>. There can also be volume loss in the hippocampus, amygdala, and the basal ganglia specifically the substantia nigra&nbsp;<ref name="Morra" />. In particular with Parkinson disease dementia, there can be atrophy of the nirgrostriatal system and also compromised dopamine transporters <ref name="Morra" />. <br> <br>Clinical Diagnosis of DLB:<br>To make a diagnosis of dementia with lewy bodies, it has to have one of the core features which are fluctuation in cognition, visual hallucinations, and motor parkinsonism <ref name="Mckeith">McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, Salmon DP, Lowe J, Mirra SS, Byrne EJ, Lennox G. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB) Report of the consortium on DLB international workshop. Neurology. 1996 Nov 1;47(5):1113-24</ref> If two are present, a higher case can be made for a patient with DLB.<br> <br>With changes in cognition, a patient can experience variations in attention and alertness. They can also experience confusion from time to time and can have changes in fluctuation in mental abilities and behaviour <ref name="Mckeith" />. The changes can occur from day to day and can vary in amplitude for a patient experiencing these cognitive changes.<br> <br>With motor parkinsonism, it is usually mild with patients with DLB. Some of the features are rigidity, bradykinesia, masked face, stooped posture, and shuffling gait <ref name="Mckeith" />. A patient can have a mix of these features associated with motor parkinsonism. If a patient experiences motor parkinsonism more than a year after a diagnosis of DLB, it is more appropriately to diagnose the patient with Parkinson's with dementia instead <ref name="Mckeith" />.<br> <br>Furthermore, there are suggestive secondary features that can exist with a patient with DLB. If the one of the core features exist with an existing secondary feature, the diagnosis of DLB is very likely <ref name="Mckeith" />.<br> <br>Suggestive Features:<br>- REM sleep behaviour disorder<br>- Severe neuroleptic sensitivity<br>- Low dopamine transporter uptake in basal ganglia<br> <br>Moreover, there are other features that DLB can show but are not diagnostic specificity <ref name="Mckeith" />. <br>- Unexplained loss of consciousness<br>- Falls and syncope<br>- Severe autonomic dysfunction<br>- Systematized delusions<br>- Depression<br> <br>Clinical Diagnosis of PDD:<br>One of the core features of developing Parkinson’s disease dementia is having idiopathic PD before getting dementia and to have a confirmed diagnosis of Parkinson disease <ref name="Poewe">Poewe W, Gauthier S, Aarsland D, Leverenz JB, Barone P, Weintraub D, Tolosa E, Dubois B. Diagnosis and management of Parkinson’s disease dementia. International journal of clinical practice. 2008 Oct 1;62(10):1581-7.</ref>. Also individuals with PDD will have a decreased global cognitive impairment that disrupts daily life. They will present with a impairment of one of the cognitive domains which are attention, executive function, visual abilities, and memory <ref name="Poewe" />. The tests to evaluate the cognitive domains are described in Table 2 in <ref name="Poewe" />. <br><br>
{{#ev:youtube|RSRbR1R4mz0|300}}


== Outcome Measures ==
== Pathophysiology ==  


add links to outcome measures here (see [[Outcome Measures|Outcome Measures Database]])
The characteristic feature of dementia with Lewy bodies is the accumulation of Lewy bodies throughout the brain. These intracellular inclusions result from the aggregation of misfolded α-synuclein. Neurofibrillary tangles are also present, however they lack an amyloid core, as seen in AD<ref name=":0" />.[[Image:Lewybody.png|alt=|center|thumb|620x620px|Regions of the [[Brain Anatomy|brain]] affected by LBD include: cerebral cortex, [[Limbic System|limbic]] cortex, [[hippocampus]], [[midbrain]], [[brainstem]].]]


== Management / Interventions<br>  ==


add text here relating to management approaches to the condition<br>
Source (http://labiotech.eu/major-cns-disease-milestones-in-biotech-2015/)


== Differential Diagnosis<br> ==
== Diagnostic Procedures ==


There are many similar diseases and disorders similar to Lewy body dementia. LBD is a form of dementia but there many different forms of dementia. For example, Alzheimer’s disease is another form of dementia. Those symptoms include progressive loss of memory, regression of cognitive dysfunction (thinking and judgement), depression, personality changes and disorientation of time and place <ref name="Lewy" />. An individual can develop Alzheimer’s disease and then progress to express core features of dementia with Lewy bodies. The difference between Lewy body Disease with dementia and Alzheimer’s is unpredictable cognitive abilities and attention, changes in movement patterns, visual hallunications, and REM sleep behaviour disorder <ref name="Lewy" />.
It is important to realise that there is a significant overlap between many neurodegenerative diseases, and that a clear-cut distinction between entities is not always possible. No precise test can accurately diagnose LBD. A thorough assessment is useful to reach an alternative working diagnosis (or rules out similar conditions):


With Parkinson with dementia, it often starts with a movement disorder that leads to the diagnose of Parkinson disease then the core the features of Parkinson with dementia start to appear.
* Detailed history and examination
* Assessment of [[Cognitive Impairments|cognitive]] function
* [[Blood Tests|Blood tests]] (e.g., [[Vitamin B12 Deficiency|vitamin B12]] levels, chemistry panel, [[Thyroid Gland|thyroid]] profile, [[syphilis]], [[Human Immunodeficiency Virus (HIV)|HIV]]) to rule out other causes of dementia


Other forms of dementia that are similar to LBD are vascular dementia and frontotemporal dementia. Vascular dementia is when a stroke occurs within the brain which causes decrease in oxygen in the brain and symptoms of disorientation, walking difficulties, shuffling gait, and inappropriate behaviour <ref name="Lewy" />. With frontotemporal dementia, the common symptoms are changes in personality and behaviour, language and speech impairments and movement changes <ref name="Lewy" />. <br><br>
* [[Medical Imaging|Imaging]] studies (e.g., CT scan, MRI scan, SPECT scan, PET scan)
* [[CSF Cerebrospinal Fluid|Cerebrospinal fluid]] examinations have no significant role when conducted in these patients
* [[Sleep Deprivation and Sleep Disorders|Sleep evaluation]] for REM sleep behavior disorder<ref name=":1" />


== Key Evidence  ==
== Management    ==


add text here relating to key evidence with regards to any of the above headings<br>  
There is no effective treatment for LBD and the condition is progressive. Pharmacological Management includes cholinesterase inhibitors. They treat the cognitive symptoms of LBD and are central to treatment. eg rivastigmine, galantamine, and donepezil.  Acetylcholine is an important neurotransmitter for memory. People with eg LBD have reduced levels present in their brains. Cholinesterase inhibitors inhibit this enzyme , improving brain network communication.<ref name=":2" />.


== Resources <br>  ==
The other pharmacological agents are used to treat behavioural symptoms.


add appropriate resources here
* Home care nurses play a crucial role in regularly assessing the patient and providing support services.
* Education of the caregiver is essential, the loved ones needing to be aware of the behavior changes, hallucinations, and fluctuations in cognition. Caregivers have to monitor the patient closely as they have a love level of functioning, with most unable to perform ADLs and are prone to falls and aspiration pneumonia.
* The pharmacist  needs to educate caregivers that no medical therapy will cure the cognitive changes and the drugs simply manage behaviour and motor deficits ( and many have adverse effects).
* A mental health nurse is often needed as depression is common. Close communication between members of the interprofessional team is vital to improve outcomes.<ref name=":1" />


== Case Studies  ==
== Prognosis ==
LBD has a poor prognosis, with an average life expectancy from initial diagnosis to death 5-8 years. Death usually occurs from one of the many complications eg falls, immobility, cardiac complications, medication side effects, pneumonia, swallowing problems, suicide.<ref name=":2" />


add links to case studies here (case studies should be added on new pages using the [[Template:Case Study|case study template]])<br>  
=== Physiotherapy Management ===
[[File:Elderly-people-doing-balance-exercise.jpg|thumb|Balance training]]
Physiotherapy for Lewy Body Disease is similar to that of Parkinson’s Disease. It can help manage parkinsonism that is prevalent in LBD by providing intervention such as [[Strength Training|strengthening]] and [[flexibility]] exercises and [[gait]] training. [[Aerobic Exercise|Aerobic]] exercise should be included to optimise [[Cardiovascular System|cardiovascular]] fitness.<ref name="Lewy">Lewy Body Dementia Association. What is LBD? Available from: https://www.lbda.org/category/3437/what-is-lbd.htm [Accessed May 5, 2017]</ref> Physiotherapy is especially helpful in improving [[balance]] and [[Postural Control|postural]] stability to minimize the risk of [[falls]]. With the addition of exercise, non-motor symptoms such as cognition, sleep and fatigue will improve. As the disease progresses and the dementia increases, exercise can be hard to do. Therefore, it is important to incorporate exercise in the early and middle stages of Lewy Body Disease. A study<ref>Sondell A, Littbrand H, Holmberg H, Lindelöf N, Rosendahl E. [https://www.ncbi.nlm.nih.gov/pubmed/31781732 Is the Effect of a High-Intensity Functional Exercise Program on Functional Balance Influenced by Applicability and Motivation among Older People with Dementia in Nursing Homes?.] The journal of nutrition, health & aging. 2019 Dec 1;23(10):1011-20.</ref> suggests that a high-intensity functional exercise program has positive outcomes on balance in these patients.<br> <br>Tips to help make exercise easier to maintain:<ref name="Lewy" />  


== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
*Provide visual cues by demonstrating exercises
<div class="researchbox">
*Play upbeat music or music the person enjoys
<rss>Feed goes here!!|charset=UTF-8|short|max=10</rss>
*Arrange exercise classes or include the support/care-person
</div>
*Do exercises in sitting
== References  ==
*Make exercise fun and enjoyable


References will automatically be added here, see [[Adding References|adding references tutorial]].
== References ==


<references />.
<references />
[[Category:Queen's University Neuromotor Function Project]]
[[Category:Neurological - Conditions]]
[[Category:Older People/Geriatrics]]
[[Category:Dementia]]
[[Category:Older People/Geriatrics - Conditions]]
[[Category:Head]]
[[Category:Head - Conditions]]
[[Category:Conditions]]

Latest revision as of 07:52, 6 October 2023

Introduction[edit | edit source]

Lewy body disease or Lewy body dementia (LBD), is a neurodegenerative disease (specifically a synucleinopathy) related to Parkinson disease.[1]

Dementia

There are 2 types of LBD generally described in the literature:[2]

  1. Dementia with Lewy Bodies: dementia occurring first or within one year of movement disorder.
  2. Parkinson Disease Dementia: dementia occurring in a patient who receives a diagnosed of Parkinson's disease and then develops dementia symptoms after one year or more of the diagnosis.

People with either type generally develop similar symptoms as the disease progresses. Distinct Parkinsonian symptoms such as slowness of movement, rigidity, REM sleep behaviour disorder and visual hallucinations can help to distinguish DLB from Alzheimer’s disease.[3]

Epidemiology[edit | edit source]

  • Occurs in older patients (onset typically in 50-70 years of age), and is sporadic. However a family history of LBD and Parkinson disease will increase a person's risk.[4]
  • LBD is one of the most common causes of dementia (accounting for up to 20% to 30% of cases[4]) along with Alzheimers disease (AD)[3].

Etiology[edit | edit source]

The etiology of LBD is unknown. Genetics, environmental factors, and changes linked to aging, may have a role and research is still ongoing.[5]

LBD has been found to be strongly linked to a protein called alpha-synuclein. The abnormal accumulation of this protein in certain regions of the brain causes dramatic cognitive and motor deficits affecting behaviour, mood, movement, and thinking.

Clinical Presentation[edit | edit source]

Frontal lobe.jpeg

The clinical features of LBD are the consequence of the blockage of information transfer from the striatum to the cortex, more notably the frontal lobe.

Core features:[6]

  1. Fluctuating cognitive impairment especially in executive function, attention and alertness
  2. Visuospatial impairment, including visual hallucinations (detailed and vivid)
  3. Concurrent parkinsonian symptoms may be present but are less common, more frequently occurring years after the onset of dementia eg early extrapyramidal features (dystonia, akathisia, muscle rigidity, bradykinesia, tremor, tardive dyskinesia

Watch this 3 minute video showing a personal story "It happened little by little. First he would forget things, then he'd lose track of what he was doing. LBD took over the life of the man you're about to meet."

Pathophysiology[edit | edit source]

The characteristic feature of dementia with Lewy bodies is the accumulation of Lewy bodies throughout the brain. These intracellular inclusions result from the aggregation of misfolded α-synuclein. Neurofibrillary tangles are also present, however they lack an amyloid core, as seen in AD[1].

Regions of the brain affected by LBD include: cerebral cortex, limbic cortex, hippocampus, midbrain, brainstem.


Source (http://labiotech.eu/major-cns-disease-milestones-in-biotech-2015/)

Diagnostic Procedures[edit | edit source]

It is important to realise that there is a significant overlap between many neurodegenerative diseases, and that a clear-cut distinction between entities is not always possible. No precise test can accurately diagnose LBD. A thorough assessment is useful to reach an alternative working diagnosis (or rules out similar conditions):

Management[edit | edit source]

There is no effective treatment for LBD and the condition is progressive. Pharmacological Management includes cholinesterase inhibitors. They treat the cognitive symptoms of LBD and are central to treatment. eg rivastigmine, galantamine, and donepezil. Acetylcholine is an important neurotransmitter for memory. People with eg LBD have reduced levels present in their brains. Cholinesterase inhibitors inhibit this enzyme , improving brain network communication.[4].

The other pharmacological agents are used to treat behavioural symptoms.

  • Home care nurses play a crucial role in regularly assessing the patient and providing support services.
  • Education of the caregiver is essential, the loved ones needing to be aware of the behavior changes, hallucinations, and fluctuations in cognition. Caregivers have to monitor the patient closely as they have a love level of functioning, with most unable to perform ADLs and are prone to falls and aspiration pneumonia.
  • The pharmacist needs to educate caregivers that no medical therapy will cure the cognitive changes and the drugs simply manage behaviour and motor deficits ( and many have adverse effects).
  • A mental health nurse is often needed as depression is common. Close communication between members of the interprofessional team is vital to improve outcomes.[5]

Prognosis[edit | edit source]

LBD has a poor prognosis, with an average life expectancy from initial diagnosis to death 5-8 years. Death usually occurs from one of the many complications eg falls, immobility, cardiac complications, medication side effects, pneumonia, swallowing problems, suicide.[4]

Physiotherapy Management[edit | edit source]

Balance training

Physiotherapy for Lewy Body Disease is similar to that of Parkinson’s Disease. It can help manage parkinsonism that is prevalent in LBD by providing intervention such as strengthening and flexibility exercises and gait training. Aerobic exercise should be included to optimise cardiovascular fitness.[7] Physiotherapy is especially helpful in improving balance and postural stability to minimize the risk of falls. With the addition of exercise, non-motor symptoms such as cognition, sleep and fatigue will improve. As the disease progresses and the dementia increases, exercise can be hard to do. Therefore, it is important to incorporate exercise in the early and middle stages of Lewy Body Disease. A study[8] suggests that a high-intensity functional exercise program has positive outcomes on balance in these patients.

Tips to help make exercise easier to maintain:[7]

  • Provide visual cues by demonstrating exercises
  • Play upbeat music or music the person enjoys
  • Arrange exercise classes or include the support/care-person
  • Do exercises in sitting
  • Make exercise fun and enjoyable

References[edit | edit source]

  1. 1.0 1.1 Radiopedia Dementia with Lewy bodies Available:https://radiopaedia.org/articles/dementia-with-lewy-bodies (accessed 13.9.2022)
  2. McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, Salmon DP, Lowe J, Mirra SS, Byrne EJ, Lennox G. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB) Report of the consortium on DLB international workshop. Neurology. 1996 Nov 1;47(5):1113-24. PMID:8909416
  3. 3.0 3.1 National Institute on Aging. Lewy Body Dementia: Information for Patients, Families, and Professionals. (Accessed 4 May 2017). https://www.nia.nih.gov/alzheimers/publication/lewy-body-dementia/basics-lewy-body-dementia
  4. 4.0 4.1 4.2 4.3 Haider A, Spurling BC, Sánchez-Manso JC. Lewy body dementia. InStatPearls [Internet] 2022 Oct 23. StatPearls Publishing.Available:https://www.ncbi.nlm.nih.gov/books/NBK482441/ (accessed 6.10.2023)
  5. 5.0 5.1 5.2 Haider A, Spurling BC, Sánchez-Manso JC. Lewy body dementia. InStatPearls [Internet] 2021 Jul 12. StatPearls Publishing.Available:https://www.ncbi.nlm.nih.gov/books/NBK482441/ (accessed 13.9.2022)
  6. Gnanalingham KK, Byrne EJ, Thornton A, Sambrook MA, Bannister P. Motor and cognitive function in Lewy body dementia: comparison with Alzheimer's and Parkinson'ss. Journal of Neurology, Neurosurgery & Psychiatry. 1997 Mar 1;62(3):243-52. http://jnnp.bmj.com/content/jnnp/62/3/243.full.pdf
  7. 7.0 7.1 Lewy Body Dementia Association. What is LBD? Available from: https://www.lbda.org/category/3437/what-is-lbd.htm [Accessed May 5, 2017]
  8. Sondell A, Littbrand H, Holmberg H, Lindelöf N, Rosendahl E. Is the Effect of a High-Intensity Functional Exercise Program on Functional Balance Influenced by Applicability and Motivation among Older People with Dementia in Nursing Homes?. The journal of nutrition, health & aging. 2019 Dec 1;23(10):1011-20.