The Lewy body dementia It is a degenerative disease, very similar to Alzheimer's dementia, but with specific characteristics that make it a very particular dementia syndrome.
In fact, until a few years ago, it did not "exist." That is, this type of disorder had not been discovered and the people who suffered from it were diagnosed with Alzheimer's disease (AD).
However, in 1980, the psychiatrist Kenji Kosaka coined the concept of "Lewy body disease" when witnessing a type of dementia very similar to Alzheimer-type dementia, but with certain differences..
In fact, this characteristic name (Lewy bodies) refers to the particles that were discovered in the neurons of patients with this type of disorder, which are responsible for producing the degeneration of the brain..
Although Alzheimer's dementia and Lewy body dementia share many characteristics, in Alzheimer's these particles are not present in neurons, so the cause of both types of dementia seems to be different.
However, many Lewy body dementia patients are still “misdiagnosed” with Alzheimer's today. To try to clarify a bit the properties of Lewy body dementia, below we will discuss all its characteristics and which of them make it different from Alzheimer's dementia..
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The main symptom of Lewy body dementia is cognitive impairment, which includes memory problems, problem solving, planning, abstract thinking, ability to concentrate, language, etc..
Likewise, another important characteristic of this disorder is cognitive fluctuations.
This refers to the fact that patients with Lewy body dementia do not always have the same cognitive performance. That is to say: sometimes they seem to have greater mental and intellectual capacities, and sometimes they seem to have a more advanced deterioration.
These variations in their performance are explained by the alterations in the attention and concentration processes that people with this type of dementia present..
In Lewy body dementia, attention and concentration undergo unpredictable changes. There are days or moments of the day when the person can be attentive and concentrated, and there are other days when their concentration can be totally deactivated..
In this way, when the person with Lewy body dementia has greater attention and concentration, their cognitive performance increases, and they perform mental activities more effectively, they have better functioning, they speak more fluently, etc..
However, when attention and concentration are more impaired, their cognitive performance plummets.
Another relevant symptom in Lewy body dementia are motor signs: stiffness, muscle stiffness, tremor and slow movement, which present in a practically identical way as in Parkinson's disease.
Finally, another main symptom of Lewy body dementia is hallucinations, which are usually visual. Older adults with Lewy body dementia often hear and interpret voices that do not exist, and sometimes see items in a hallucinatory way.
However, in Lewy body dementia other symptoms may also appear, such as:
Despite the multiple similarities, there are also divergent aspects between both diseases, therefore, in many cases it is possible to differentiate a Lewy body dementia from an Alzheimer-type dementia.
The main differences are:
Lewy body dementia is the third leading cause of dementia behind Alzheimer's disease and vascular dementia. In fact, Lewy bodies have been witnessed in the neurons of patients with dementia in approximately 20-30% of autopsies performed..
Studies have found that the prevalence of MCI among people over 65 is 0.7%. The onset of the disease varies between 50 and 90 years of age, and the lifetime prevalence of patients with this type of dementia is usually very short.
In people with MCI, between 6 and 10 years usually elapse between the onset of their disease and their death, thus being one of the dementias with the worst prognosis..
Lewy body dementia begins when the famous Lewy bodies appear in a person's neurons. Lewy bodies are cytoplasmic inclusions that are made up of different proteins, especially alpha-synuclein..
That is, the brain of patients with Lewy body dementia suffers an alteration in the synthesis of this protein, therefore, it binds to the nucleus of neurons, and thus constitutes Lewy bodies..
Therefore, in the patient's neurons, these bodies begin to appear, which collaborate in the death of the neuron itself and initiate cognitive deterioration.
Likewise, Lewy bodies are distributed through neurons in different regions of the brain, producing a large number of alterations and causing cognitive deficits in many different areas..
The cause of Lewy body dementia, that is, why Lewy bodies begin to “stick together” in neurons, is currently unknown. However, there seems to be some consensus that there is a genetic component in the development of this disease.
Genes such as the apolipoprotein gene or the cytochrome P450 gene appear to be involved in Lewy body dementia.
Likewise, the first seems to be also related to Alzheimer's and the second to Parkinson's, a fact that could explain the characteristic symptoms of Alzheimer's and Parkinson's disease that also occur in Lewy body dementia.
However, these genetic patterns alone would not explain the development of the disorder..
Regarding the environment, there are no conclusive studies on what the risk factors for Lewy body dementia could be, however the following seem to be related:
Lewy body dementia has a wide range of symptoms, which is why it is important to carry out different therapeutic interventions.
With regard to cognitive impairment, it is important to carry out cognitive stimulation activities to try to slow down the progress of the disease as much as possible..
Working on the patient's deficits such as attention, concentration, memory, language or visual construction, can favor the maintenance of their cognitive abilities.
As regards hallucinations, these should only be treated when they produce anxiety or agitation in the patient. Conventional antipsychotics such as haloperidol are contraindicated due to their strong side effects.
In those cases where it is essential to treat hallucinations, atypical antipsychotics such as risperidone can be administered..
Finally, parkinsonian symptoms are also often difficult to treat since antiparkinsonian drugs tend to be ineffective and produce many side effects in patients with MCI.
When the tremor or rigidity is very high, small doses of L-dopa can be administered..
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