In addition to Alzheimer’s and Parkinson’s, there are different forms of dementia. Because they are less common compared to Alzheimer’s and Parkinson’s, they are also less known. One of these lesser-known forms of dementia is Lewy Body Dementia (LBD). This progressive and degenerative form of dementia is characterized by the presence of accumulations of certain proteins in the brain cells (the so-called Lewy Bodies). LBD has a complex picture and affects the entire functioning of a person. From physical exercise and posture, to behavior and psychological functioning. LBD has a lot of overlap with Parkinson’s and Alzheimer’s diseases, both patho-physiologically and in terms of symptoms, and is therefore difficult to diagnose.
Lewy Bodies
Frederic Lewy (1885 – 1950) was one of the first discoverers of abnormal protein accumulations in brain cells. A Japanese psychiatrist described the condition in 1976, but it was not until the 1990s that the form of dementia was internationally recognized. This had to do with the fact that the proteins could only then be detected in the brains of deceased dementia patients.
The condition is characterized by an accumulation of proteins in the cytoplasm of brain cells. These accumulations are also seen in Parkinson’s disease. In addition, dopamine-producing neurons die, as happens in Parkinson’s disease. Acetylcholine-producing neurons also gradually die, as happens in Alzheimer’s disease. Unlike Alzheimer’s disease, the brain does not show atrophy (or shrinkage). Scientists think the loss of acetylcholine-producing neurons is responsible for cognitive decline, and the loss of dopamine-producing neurons for movement disorders.
Difference with Parkinson’s and Alzheimer’s disease
Some scientists do not yet view Lewy Body Dementia as an independent condition, but that these three conditions are within the same spectrum.
The accumulation of proteins in the brain cells also happens in Parkinson’s disease, where it only happens in the substantia nigra . This part of the brain is responsible for movement, among other things. LBD involves protein accumulation in other parts of the brain, such as the cerebral cortex. This part of the brain has many more functions, which means LBD also has a broader spectrum of symptoms.
The distinction between Parkinson’s disease and LBD is therefore more one of definition. When dementia symptoms occur more than a year after the symptoms of Parkinson’s, it is called Parkinson’s disease. If these symptoms occur immediately or at least within a year of the Parkinson’s symptoms, there will probably be Lewy Body Dementia.
Symptoms
Specific symptoms in a person with LBD will vary from person to person, but there are some symptoms that are very prominent. One of the most recognizable is the fluctuating level of attention and alertness: a patient can have a very good day, only to have a very bad day afterwards.
About 75% of people with LBD experience visual hallucinations. In LBD, these hallucinations are not necessarily disturbing, and a patient may even be amused by what he or she is seeing at that moment. In addition, the hallucinations can usually be described very clearly by the patient himself or herself, and he or she may sometimes realize that what he or she is seeing is not really there. This awareness is often lacking in hallucinations in other syndromes (such as schizophrenia or manic depression).
Another common symptom of Lewy Body Dementia is one the condition shares with Parkinson’s disease. Due to the degeneration of dopamine-producing brain cells, symptoms related to the musculoskeletal system will eventually occur increasingly. Muscle stiffness (rigidity) and lack of movement (akinesia) in particular occur quickly. The typical bent-over posture and taking small steps, as Parkinson’s patients do in various stages of the condition, also occur with LBD.
A high sensitivity to anti-psychotics and anti-emetics (anti-vomiting and anti-nausea drugs) is present in LBD. This is a critical point of LBD because patients cannot be treated with these agents. These groups of medications act on the neurotransmitters that are severely affected in LBD, causing patients to become hypersensitive to their components. If a patient with LBD is administered these drugs, there is a high risk of life-threatening muscle stiffness and catatonia.
Therapy
There is no cure for Lewy Body Dementia, and treatment consists mainly of palliative care where symptoms are mainly controlled. The treatment can be divided into pharmacotherapeutic treatment and nursing care.
Pharmacotherapeutic treatment
Medication treatment focuses on the one hand on resolving motor disorders and on the other hand on improving cognitive processes. Medication that is used for both Alzheimer’s disease and Parkinson’s disease is also used in the treatment of Lewy Body Dementia. Examples include Levodopa and Donepezil.
The contradictory aspect of pharmacotherapeutic treatment for Lewy Body Dementia is the side effects of different drug groups. For example, medications that alleviate motor disorders can increase hallucinations. The medications that reduce hallucinations (such as haloperidol) in turn have an increased risk of motor restlessness. The pharmacotherapeutic treatment will therefore mainly focus on finding the right balance in these drug groups.
A small-scale study found that some LBD patients prescribed a small dose of quetiapine (Seroquel) showed a small decrease in the intensity and amount of hallucinations. It should be noted that some of the patients studied had to discontinue treatment due to side effects of quetiapine, such as daytime sleepiness or faintness when standing up (orthostatic hypotension).
Emergency services and nursing care
Due to the degenerative aspect of LBD, a patient will ultimately have to rely on professional care, where the condition can be managed at home by informal caregivers in the initial period.
Because the hallucinations in LBD are not of a serious nature, the best approach is one of acknowledgment without stimulation or condemnation. Statements such as “Tell me more about…” are more stimulating, and can have a detrimental effect on an LBD patient’s frustration and are not recommended. When the hallucinations become problematic, the care provider or informal caregiver can look for ‘triggers’ in the environment, such as a TV or radio that is turned on loudly.
A daily structure with clear routines provides the lowest levels of frustration, and care for LBD patients can best be based on providing this structure. Changes in this daily structure can, in addition to sleep problems or physical discomfort, cause significant behavioral changes, and the informal caregiver or care provider must be permanently alert to this.
Nevertheless, LBD patients have good days and bad days, as do patients with Parkinson’s disease. The care surrounding LBD patients is therefore very diverse and can vary greatly from day to day.
Cause
The cause of Lewy Body Dementia is still unknown. As with Alzheimer’s disease, Lewy Body can occur sporadically, and there appears to be no genetic predisposition that family members can pass on to each other. In 2007, it was shown that there was a link between developing LBD and the Park11 gene , a gene also associated with Parkinson’s disease.
Epidemiology
In 2015, approximately 60% to 75% of diagnosed dementias are Alzheimer’s disease. About 15% consists of dementia of the Lewy Body type, which also includes Parkinson’s disease. The other forms of dementia consist of vascular disorders and Korsakov’s.
