Differential Diagnosis Of The Lewy Body Dementias
Few clinically useful biomarkers differentiate DLB and PD from MSA and the parkinsonian tauopathies PSP and CBD, and careful history and examination remain the method of choice. Although unusual, cognitive impairment and dementia have recently been described in MSA37,38 and can no longer be used as strong evidence against the diagnosis. The early and profound development of dysautonomia, in association with parkinsonism and/or cerebellar ataxia characterizes MSA39 and can help in its differentiation from DLB and PDD. When present, ataxia is a strong distinguishing feature of MSA. Conversely, the presence of visual hallucinations and fluctuations would argue in favor of DLB or PDD. Late in the course of MSA, cerebellar atrophy and the hot cross bun pons sign may be appreciated on MRI.
In addition, hallucinations are uncommon in MSA, PSP, and CBS, as are fluctuations of attention and arousal. The presence of these problems should direct the clinician toward DLB and PDD. REM sleep behavior disorder has been described in both PSP and CBD but is more common in the synucleinopathies . In contrast to PD, motor impairments in MSA, PSP, and CBD are rarely responsive to dopamine replacement .
Fluctuations Of Attention And Arousal
Attention and alertness may fluctuate, leading to episodes of staring and perturbed flow of ideas, or to frequent daytime drowsiness and naps during the day. These episodes can be hard to quantify and need to be disentangled from toxic metabolic processes such as medication side effects or infections. A recent fluctuations scale vetted for this purpose is the Dementia Cognitive Fluctuation Scale,13 which aggregates prior scales. The fluctuations screen requires a positive response to at least three of the following: Does the patients inability to organize thoughts in a coherent way vary significantly over the course of the day? Does the patient spend more than 1 hour sleeping during the waking day? Is the patient drowsy and lethargic for more than 1 hour during the day, despite getting the usual amount of sleep the night before? Is the patient difficult to arouse on a usual day? This approach had a sensitivity of 80% and a specificity of 76% in differentiating clinical syndromes of DLB and PDD from AD and vascular dementia, but has yet to be neuropathologically validated.
Slowing The Progression Of Symptoms
The same healthy lifestyle changes that are used to prevent dementia can also be useful in slowing the advancement of LBD symptoms.
To learn more about putting these strategies into action, see Preventing Alzheimers Disease.
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Resources For People Newly Diagnosed With Parkinson’s
You have Parkinsons disease. Four words that come with a diagnosis full of questions and uncertainty. However you choose to start processing, youre not alone. The Michael J. Fox Foundation has developed resources to help individuals and families move through the earliest days with Parkinsons disease and beyond.
Wondering where to start? , “Navigating Parkinson’s: Your Guide to the Early Years,” for insights, wisdom and practical perspectives on everything from finding acceptance to navigating doctors appointments.
A Golden Opportunity to Speed a Cure
Understandably, few people think about participating in research following a Parkinsons diagnosis. But people at this early stage of disease are in a unique position to help speed new treatments. The Parkinsons Progression Markers Initiative is our landmark study on a mission to stop the disease. If youre recently diagnosed and not yet taking medication, call 877-525-PPMI or email to get started.
Your First Year with Parkinson’s: Practical Tips for the Road Ahead
A Parkinsons diagnosis can bring many questions and emotions. But the good news is that you dont have to figure out everything at once. Movement disorder specialist Rachel Dolhun, MD, shares tips for making your way forward.
Different Types Of Dementia
The term âdementiaâ is really an umbrella term for several diseases, including:
Now letâs dive deeper in to these two forms of dementia: Alzheimerâs Disease and Lewy Body Dementia.
Mechanisms For Dementia And Disease
Multiple pathologic processes have been linked to cognitive impairment and psychosis in DLB and PDD, including -synuclein deposition with secondary synapse impairment,7,52,53 amyloid burden,10,54 and dopamine55 and acetycholine9 cell loss .5260 The difference in the timing of cognitive and motor impairments in DLB and PDD likely reflects a difference in the temporal sequence of these pathologies. One possibility is that in DLB, cortical lesions, mostly -amyloid, arise early, driving cognitive impairment. Then, -synuclein pathology ascends from brainstem to cortex. In contrast, in PDD, cortical lesions arise late, and ascending -synuclein pathology drives the clinical syndrome. Amyloid PET imaging in DLB and PDD supports this model, showing high amyloid burden in most cases of DLB, with more modest accumulation in PDD.54 Antibodies targeting -amyloid have entered clinical trials in AD and MCI.61 Although the outcomes are uncertain, the strategy is applicable to DLB and possibly to PDD, where amyloid accumulation appears to contribute to certain clinical features, including the timing and rate of cognitive decline.54 A similar immune targeting approach is under development for -synuclein. If successful, this strategy would be applicable to both DLB and PD, irrespective of cognitive impairment.
What Is The Difference Between Lewy Body Dementia And Parkinsons Disease
On a yearly basis, a great many American seniors are told they have Parkinsons disease, but they dont. For a number of these patients, the actual diagnosis is a very similar but lesser-known disease: Lewy body dementia, sometimes referred to as dementia with Lewy bodies or DLB. If youre taking care of elderly parents, understanding DLB is crucial.
Dementia with Lewy bodies affects up to 1.3 million Americans, as reported by the Lewy Body Dementia Association . That approximation might be too low since some individuals whove been incorrectly diagnosed with Parkinsons still have not been given the correct diagnosis.
Symptoms for Lewy body dementia and Parkinsons disease can be quite similar, particularly when they progress, given that they exhibit similar root changes in the brain.
Here are the signs and symptoms you should know about, as reported by the LBDA:
- Worsening dementia Increasing confusion and reduced attention and executive function are typical. Memory impairment may not be evident in the early stages.
- Recurrent visual hallucinations These are commonly complicated and elaborate.
- Hallucinations of other senses Touch or hearing are usually the most frequent.
- REM sleep behavior disorder This may appear years ahead of the onset of dementia and Parkinsons.
- Recurring falls and fainting Includes undetermined loss in consciousness.
- Other psychiatric disruptions These differ from patient to patient.
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Whats The Difference Between Lewy Body Dementia Parkinsons Disease And Alzheimers Disease
Lewy body dementia is an umbrella term for two related clinical diagnoses: dementia with Lewy bodies and Parkinsons disease dementia. These disorders share the same underlying changes in the brain and very similar symptoms, but the symptoms appear in a different order depending on where the Lewy bodies first form.
Dementia with Lewy bodies is a type of dementia that causes problems with memory and thinking abilities that are severe enough to interfere with everyday activities. It specifically affects a persons ability to plan and solve problems, called executive function, and their ability to understand visual information. Dementia always appears first in DLB. The motor symptoms of Parkinsons such as tremor, slowness, stiffness and walking/balance/gait problems usually become more evident as the disease progresses. Visual hallucinations, REM sleep behavior disorder, fluctuating levels of alertness and attention, mood changes and autonomic dysfunction are also characteristic of DLB.
Finally, Alzheimers is characterized by different abnormal clumps called amyloid plaques, and jumbled fiber bundles called tau tangles. These microscopic structural changes in the brain were discovered by Dr. Alois Alzheimer in 1906. These plaques and tangles, together with loss of connections between nerve cells, contribute to loss of coherence and memory, as well as a progressive impairment in conducting normal activities of daily living.
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Diagnostic Criteria For Dementia With Lewy Bodies
The consensus criteria for a clinical diagnosis of DLB reflect the clinical features described previously in this article . Progressive cognitive decline to dementia is required, often involving attention, executive function, and visual-spatial skills. The core features of these criteria include the following: recurrent visual hallucinations that are well formed and detailed fluctuations in attention and alertness and parkinsonian motor signs. Supportive features, also common in PD, include the presence of REM sleep behavior disorder, severe neuroleptic sensitivity, or low DAT uptake in the basal ganglia on SPECT or PET. A diagnosis of clinically probable DLB requires at least two out of three of the core features to be present or one core feature and one supportive feature. A diagnosis of clinically possible DLB requires only one of the three core features to be present.
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Diagnostic Criteria For Parkinson Disease Dementia
Consensus criteria for PDD were developed in 2007 .6,29 These criteria require cognitive impairments across multiple domains but emphasize that noncognitive features such as hallucinations are common. As described previously in the article, the clinical and neuropsychological features of DLB and PDD are similar. Indeed, it is the relative timing of dementia and parkinsonism that defines the clinical distinction between DLB and PDD. Controversy exists over how or whether to distinguish these syndromes.30
Lewy Bodies And Parkinsons Disease
A person with Parkinsons disease may develop dementia and have problems with reasoning and thinking. Lewy bodies are a feature of several brain disorders, including Parkinsons disease and Alzheimers disease, and they may cause rigid muscles and problems with movement and posture.
Research suggests that the similarity of the symptoms of Parkinsons disease and Lewy body dementia may be indicative of a shared link to how the brain processes alpha-synuclein.
It is not possible to test for the presence of Lewy bodies, so researchers must try to determine their effects by carrying out postmortem studies.
There is currently no cure for dementia. However, medication can alleviate the symptoms, while a team of medical professionals and therapists may help a person develop strategies to manage their daily activities.
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Pathophysiology Of Cognitive Impairment
The neurobiological basis for cognitive impairment in DLB and PDD is multifocal, related to a synergistic effect of both Syn/LB and AD pathologies and dysfunction of dopaminergic, noradrenalinergic, serotonergic, and cholinergic systems . The emergence of PDD and DLB occurs on the background of severe dopamine deficits and correlates with a marked loss of limbic and cortically projecting dopamine, noradreanaline, serotonin, and ACh neurons. The relationship between these lesions is not yet fully understood.
Severe pathology also involves the noradrenergic locus ceruleus and the serotonergic dorsal raphe nucleus as well as the ventral tegmental area not always associated with coincidental AD lesions . LC neuronal loss and the accompanying norepinephrinergic deficiency are an important cause and pharmacological target for the treatment of PD/PDD/DLB . The prominent role of serotonergic degeneration also involving the anterior caudate nucleus, the orbitofrontal and cingulate cortex for neuropsychiatric symptoms in PD , emphasizes its important role in both PDD and DLB, and stimulates new insight into novel treatments by modulating 5-HT receptors .
Acknowledgments And Conflict Of Interest Disclosure
Data in this manuscript are original and were generated for the purpose of this study. Photomicrographs were taken from tissue provided by the Newcastle Brain Tissue Resource, which is funded in part by a grant from the UK Medical Research Council , by Brains for Dementia research, a joint venture between Alzheimer’s Society and Alzheimer’s Research UK and by the NIHR Newcastle Biomedical Research Centre awarded to the Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University. DLB research is supported by NIHR Newcastle Biomedical Research Centre in Ageing and Long-Term Conditions. LW is funded by the Alzheimer’s Society. The authors have no conflicts of interest to declare.
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Other Types Of Treatments
- Lifestyle interventions include eating a healthy diet, exercising, and remaining socially active.
- Physical therapy includes cardiovascular, strengthening and flexibility exercises, as well as gait training.
- Speech therapy may improve low voice volume, poor enunciation, muscular strength, and swallowing difficulties.
- Occupational therapy helps maintain skills and promotes functional ability and independence.
- Music and aromatherapy may reduce anxiety and improve mood.
- Individual and family psychotherapy may be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
- Support groups may be helpful for caregivers and persons with LBD to identify practical solutions to day-to-day frustrations and to obtain emotional support from others.
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Dementia With Lewy Bodies Without Parkinsonism
I agree with the proposal of new criteria for the diagnosis and management of dementia with Lewy bodies . Previous criteria did not adequately differentiate DLB from Parkinson disease with dementia as outlined in the articles accompanying editorial.
Lewy body disease includes PD and DLB, thus there should be DLB without parkinsonism as well as PDD. The new criteria outlined four core clinical features: fluctuating cognition with pronounced variations in attention and alertness detailed, recurrent visual hallucinations REM sleep behavior disorder, which may precede cognitive decline and one or more spontaneous cardinal features of parkinsonism including bradykinesia, rest tremor, or rigidity. According to this criteria, a patient who has the first three clinical features but does not have parkinsonism may be diagnosed as DLB.
Braak et al. proposed that brainstem synucleinopathy progresses rostrally to affect the substantia nigra, which may cause parkinsonism. . However, these described patterns of synucleinopathy are not often observed in DLB, especially when synucleinopathy occurs in the absence of parkinsonism. Braak et al.s hypothesis would indicate that visual hallucinations are a result of occipital dysfunction. Meanwhile, attention and alertness are due to frontal dysfunction, which does not necessarily follow Braaks hypothesis. In addition, DLB patients with predominantly frontal dysfunction may not have parkinsonism.
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What Happens In Dlb
People with DLB may have trouble focusing, remembering things, staying awake during the day, or staying asleep at night. They may become more frustrated or confused because of the lack of sleep. They may also hallucinate and see people, objects, or animals that are not there.
Some people with DLB will need help with walking, while others may have hunched posture or trouble using their hands and feet because of stiff muscles. People with DLB may appear to be better and need less help on some days, only to become worse and more confused again and need more help the next day or in a few days. This is because their energy level and focus will vary.
DLB is a disease that changes with time. A person with DLB can live for many years with the disease. Research suggests that a person with DLB may live an average of 57 years with the disease, although this can vary from person to person.
What Is Vascular Dementia
Vascular dementia is the second most common type of dementia in the UK after Alzheimers disease. It occurs when the brain is damaged due to a lack of blood flow.
Sometimes people have both vascular dementia and Alzheimers, giving them a diagnosis of mixed dementia.
If the vascular system within the brain becomes damaged so that the blood vessels leak or become blocked then blood cannot reach the brain cells and they will eventually die.
This death of brain cells can cause problems with memory, thinking or reasoning, and when these cognitive problems are bad enough to impact on daily life, it is known as vascular dementia.
Dementia symptoms specific to vascular dementia include stroke-like symptoms, suchas as muscle weakness, movement and thinking problems and mood changes, such as depression.
There are several different types of vascular dementia, due to the varying levels of damage on the affected part of the brain.
They include stroke-related dementia, single-infarct and multi-infarct dementia and subcortical vascular dementia.
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Demographic And Clinical Characteristics
Table reports full details of subject demographic and clinical characteristics. No significant differences were found for age, gender, and disease duration among groups. As expected, MoCA median scores were lower in DLB and AD patients compared to HC .
Table 2 Demographic and clinical characteristics
What Are The Volunteer Requirements
Volunteers must be a minimum of 18 years of age or have parental knowledge and consent. Some volunteer positions require at least a one-year commitment to LBDA to assure continuity and stability of our services. If the volunteer position requires a time commitment, this will be discussed during the application process.
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