Lewy Body Dementia

Dementia with Lewy Bodies is the second most common form of dementia in the US, affecting 1.4 million Americans in the last twenty years. It’s a neurodegenerative disease characterized by clumps of a-synuclein protein that form and increase over time within the cerebral cortex and midbrain area, inside of the neuron nuclei. Alpha synuclein begins accumulating in the neurons because of misfolding, though it’s still not understood why the change occurs in the protein. Some estimate that it happens because of genetic mutation, but more research needs to be done before a definite explanation can be given about the change. The disease most commonly effects those over sixty and those who have had previous family members suffer from Lewy Body dementia or Parkinson’s Disease. There is currently no certain risk factor gene used to test for chance of developing the disease, although the APOE4 gene used for Alzheimer’s is estimated to have a possibility as a predictor.

Many discoveries on the progression and causes of Lewy Bodies have been generally recent. Similar to the progression of Alzheimer’s Disease, caused by the increase of plaques and tangles, over time during Lewy Body Dementia the neuron pathways in the brain are interrupted by cell death caused from the protein buildup. It’s not certain whether the lewy bodies form before or after the dementia diagnosis in a patient, or if they are caused by or cause dementia in a person. Some researchers believe it may vary case by case, but studying the development of the bodies in the neuron nuclei is difficult since the clumps are only visible during an autopsy of the brain.

 

Diagnosis and Symptoms

Since observation is the only way to diagnose without autopsy, there are many times the dementia is misdiagnosed for Parkinson’s Disease or Alzheimer’s Disease (AD). Lewy Body’s main symptoms include: hallucinations, movement disorders, autonomic nervous system faults, cognitive issues, apathy, sleep difficulties, and depression. Many of the physical traits of the disease, such as the difficulties with continuous, smooth motion of the body, as well as depression and issues with the brain’s production of dopamine, line up with the symptoms of Parkinson’s Disease. Although patients affected by AD have further brain disintegration at end stages, a slower progression of symptoms, and occur more in women than men, (which is opposite to the Lewy Body’s Dementia patient pool), it can be difficult to judge patient cases correctly at times. Hallucinations may also occur in Parkinson’s disease, but not to the same extent or frequency as people with Lewy Body’s may experience.

 

Comparison to Parkinson’s Disease

​The most common disease Lewy Body’s is misdiagnosed for is Parkinson’s Disease. Both of the two diseases have an early onset, with the average age of Parkinson’s diagnosis also being around sixty years old. The main difference used to tell the two apart is the starting symptoms, which will be mainly physical for those with Parkinsons’ and cognitive for patients with Lewy Body’s disease. Parkinsons’ motor issues will form faster and become more severe gradually over time. In some cases with dementia, a patient’s symptoms may go unnoticed until they reach a greater intensity, making it difficult to figure out which symptoms appeared first, and what may have been regular life habits or side effects of other medications being taken during the time period. Many people brush aside troubles with memory as a common issue with aging or lack of sleep.

Both disorders have formations of lewy bodies that appear in neurons, but the locations for the protein deposits of the two are different. Significantly larger lewy bodies can be found in the brain stem of a Parkinson’s patient, which causes the physical symptoms in the disease such as hand tremors, difficulty with balance and walking, and smooth movement. These are also easier to spot in an autopsy, which is why Parkinson’s was discovered before Lewy Body dementia. Lewy Body dementia may also showcase lewy bodies found in this area, but the main location for this disorder is inside the cerebral cortex, with protein accumulations that are smaller and more difficult to spot than those in Parkinson’s. Dopamine production centers, the cause of Parkinson’s disease development, are impaired in both the diseases. Since the Substantia Niagra contains damaged neuron pathways in both diseases, physicians have to be careful when prescribing medications that affect dopamine production  to avoid further reducing the amount of dopamine in the patients’ bodies. Drugs like Leuodopa (a dopamine analogue) or Sinemet (which supports neurotransmitters influencing dopamine) may be used for both disorders for physical symptoms involving bodily movement. Both diseases also benefit from using physical therapy or recreational activities that boost coordination as treatments continue. It’s important to work on the strength of the patient so that their independency can continue for as long as possible. Neither disease has a cure, but there are options available for both to suppress symptoms that cause the patient discomfort and difficulty with daily living activities.

 

Comparison to Alzheimer’s Disease

​Lewy Body dementia and Alzheimer’s disease (AD) share cognitive symptoms like: hallucinations, difficulty with memory, confusion, behavioral differences, sudden personality changes, and difficulty remembering or recognizing friends and family members. The two diseases have a gradual loss of neuron connection over time, but Lewy Body’s has a faster progression rate with less brain atrophy. People with Lewy Body dementia may only live up to five years after the start of the disease’s main dementia symptoms, as opposed to the eight to ten years a patient with AD may live up to after diagnosis. AD also has a specific following of recognizable stages Lewy Bodies does not have. Patient’s with Lewy Bodies may have more difficulty with everyday living activities earlier on than patients with AD. Those with Alzheimer’s will need assistance with activities like feeding, dressing, and other mobile acts in later stages, but may be fine and fully functioning in everyday life in the earliest stage for a generally long period of time. In both diseases, exercise, healthier eating habits, and proper sleep are important reducers of risk factors. It is recommended to keep a healthy amount of physical activity to not only prevent the two disorders, but also to assist in overall health and ability to move with ease after diagnosis.

 

Drugs and Treatments

Just like with Parkinson’s Disease, the diseases have some drugs in common to treat symptoms, but there is no cure any of the dementias. Acetyl-cholinesterase inhibitors, like the drugs Donepezil, Galantamine, or Rivastigmine, can be used for both diseases. Acetylcholine is a brain chemical, or neurotransmitter, that is estimated to support memory and cognition, and will disappear with neuron death in the brain. Acetyl-cholinesterase inhibitors work to prevent the natural breakdown of the chemical in order to preserve a lucid state in the patient. The idea of the drug is to prevent the body from discarding the neurotransmitter as it naturally would with age to avoid overcrowding, so that when the disease progresses and makes it so the brain is unable to produce more, there will still be extra remaining for use.

Unfortunately, during an episode where a patient with Lewy Body’s dementia may be experiencing intense confusion or paranoia, anti-psychotics cannot be used as it will make symptoms worse. In contrast, Alzheimer’s Disease patients will be able to receive anti-psychotics normally. Many primary physicians for Lewy Body’s patients will list anti-psychotics as an allergy to prevent them from being used in emergency visits to the hospitals in the case that the doctor or nurse may not have time to fully go through a patient’s chart to see the diagnosis before administering medication. Instead of these medications, dopamine blockers may be used for combative patients. However, because these patients already have reduced dopamine, reducing it further may cause worsening of symptoms, and other negative effects.

 

Want to read more?

​Listed below are some good sources for continued reading and further information to get you started. More can be found with a quick search through google scholar for credible sources. Hopefully you found this article helpful. For more information, please email Ahhcare@gmail.com or check out our website at homenursingtampa.com.

https://www.frontiersin.org/articles/10.3389/fnagi.2021.690293/full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6341685/
https://www.americanbrainfoundation.org/diseases/lewy-body-dementia/

References

  • Loeb, N., Says, D., & Says, N. (2020, October 24). The Differences Between Parkinson’s Disease Dementia and Dementia with Lewy Bodies. Retrieved December 01, 2020, from https://lewybodyresourcecenter.org/lewy-body-dementia-differences-parkisons-disease/.
  • Meng, Y., Wang, P., Song, Y., & Wang, J. (2019). Cholinesterase inhibitors and memantine for Parkinson’s disease dementia and Lewy body dementia: A meta‑analysis. Experimental and Therapeutic Medicine, 17, 1611-1624. https://doi.org/10.3892/etm.2018.7129
  • ​SciShow “The Science of Lewy Body Dementia” [Video file]. Green, H. (2015, November 13). Retrieved from https://www.youtube.com/watch?v=cIHTiY_68JI.
  • ​UCSF Memory and Aging Center. “What is Lewy Body Dementia and How is it Treated?” [Video file]. Mantyh, W. (2020, March 13). Retrieved From https://www.youtube.com/watch?v=Db5H0A_XiQw.