Parkinson’s disease is a progressive neurological disorder of the central nervous system that affects an individual’s mobility and ability to perform regular activities. It typically occurs in older adults over the age of 65. The disease impacts physical movements, but the patients can also exhibit impairment of mental functions, thought processes, and memory. This condition is known as Parkinson’s disease dementia and can develop in people living with Parkinson’s at least one year after diagnosis.
Parkinson’s disease initiates in a part of the brain involved in movement. Therefore, its early symptoms include muscle stiffness, tremors, stooped posture, a shuffling step, lack of facial expression, and problem initiating movement. As the disease advances, in the brain changes gradually spread and often start affecting cognitive functions such as memory, judgment, attention span and ability to plan steps for completing a task.
What causes Parkinson’s disease dementia?
The chief brain changes responsible for Parkinson’s disease and Parkinson’s disease dementia are the formation and abnormal deposition of Lewy bodies, the neuronal inclusions chiefly composed of alpha-synuclein protein. Alpha-synuclein protein is abundantly present in the brain, but its function is not fully understood.
Lewy Bodies are also the hallmark of Lewy body dementia (LBD) and may be present in other brain disorders, including Alzheimer’s disease. Research shows that LBD, Parkinson’s disease, and Parkinson’s disease dementia may be due to similar underlying abnormalities in alpha-synuclein processing in the brain. Researchers have also discovered the presence of plaques and tangles, the hallmarks of Alzheimer’s disease, in the brains of people with LBD and Parkinson’s disease dementia.
A recent study1 suggests that the problematic nature of Lewy bodies is because they pull out alpha-synuclein protein from the nucleus of brain cells. According to the study (which was performed on a mice model), these proteins carry out DNA repair in the cells, which may be pivotal in preventing cell death. The possible loss of this function in brain disorders like LBD and Parkinson’s disease dementia might be responsible for the widespread death of neurons.
What are the risk factors?
About 50 to 80% of Parkinson’s patients eventually develop dementia with disease progression. According to some studies, the patients develop dementia approximately 10 years2 after Parkinson’s disease onset.
Certain factors present at the time of Parkinson’s diagnosis may increase the risk of acquiring dementia in the coming years. These risk factors include aging, severe motor symptoms, and mild cognitive impairment (MCI). Experiencing hallucinations before manifesting other dementia symptoms and excessive daytime sleepiness may also indicate an increased dementia risk.
Another risk factor is a Parkinson’s symptom pattern called PIGD (postural instability and gait disturbance), which includes freezing mid-step, balancing problems, difficulty initiating movement, shuffling, and falling.
Symptoms of Parkinson’s disease dementia
Following are the most common symptoms of Parkinson’s disease dementia:
- Changes in appetite and energy levels
- Hallucinations, delusions, and paranoid ideas
- Changes in memory, judgment, and concentration
- Muffled speech
- Depression, anxiety, and mood swings
- Difficulty interpreting visual information
- Loss of interest
- Sleep disturbances such as rapid eye movement (REM) sleep disorder and excessive daytime drowsiness
How is Parkinson’s disease dementia diagnosed?
There is no single precise test or combination of tests for diagnosing Parkinson’s disease dementia. Following are the guidelines for making a diagnosis:
- The diagnosis is Parkinson’s disease dementia if an individual is initially diagnosed with Parkinson’s disease due to the manifestation of movement-related symptoms, and dementia symptoms do not appear until a year or more.
- If the dementia symptoms consistent with LBD develop first or present with movement-related symptoms or occur within a year after movement symptoms, the diagnosis is LBD.
What is the treatment?
Currently, no treatment is available to slow or stop the neuronal damage due to Parkinson’s disease dementia. However, improving the symptoms may help provide temporary relief to the patient. In the case of medications, remember to have a thorough conversation with a doctor to know which drugs will be most effective.
Doctors may prescribe drugs for treating the symptoms:
- Cholinesterase inhibitors drugs (used for treating cognitive changes in Alzheimer’s disease) may alleviate the symptoms of Parkinson’s disease dementia, such as sleep disturbances, hallucinations, and behavioral and cognitive changes.
- Carbidopa-levodopa may treat movement symptoms. However, it may cause complications such as aggravation of confusion and hallucinations in Parkinson’s dementia or LBD patients.
- Clonazepam and melatonin may be prescribed for the treatment of REM disorder.
- Selective serotonin reuptake inhibitors (SSRIs) can help treat depression.
Doctors usually avoid prescribing antipsychotic drugs. Approximately 60% of LBD patients exhibit worsening Parkinson’s symptoms, impaired swallowing, sedation, or neuroleptic malignant syndrome (NMS). NMS is a severe condition that may occur after exposure to traditional antipsychotics and is characterized by fever, rigidity, and muscle breakdown.
References
- Schaser, A.J., Osterberg, V.R., Dent, S.E., Stackhouse, T.L., Wakeham, C.M., Boutros, S.W., Weston, L.J., Owen, N., Weissman, T.A., Luna, E. and Raber, J., 2019. Alpha-synuclein is a DNA binding protein that modulates DNA repair with implications for Lewy body disorders. Scientific reports, 9(1), pp.1-19.
https://www.nature.com/articles/s41598-019-47227-z - Parkinson’s disease dementia. https://memory.ucsf.edu/dementia/parkinsons/parkinson-disease-dementia