In detail

Dementia with Lewy Bodies

Dementia with Lewy Bodies

Dementia with Lewy bodies is considered the second most common type of degenerative dementia after Alzheimer's disease. Although his name is not widely known, his discovery was more than 100 years ago. Heinrich Lewy discovered in 1912 some rounded and anomalous structures that extended extensively through cortical and subcortical structures of the brain. He called them Lewy bodies.

Patients with this type of dementia develop parkinsonism, visual hallucinations and changes in mood. There may also be a decrease in the speed of cognitive processing, diurnal hypersomnia and neurodegenerative dysfunctions. Tröster (2008), describes that the most representative of this dementia are the visuoconstructive alterations and executive alterations, as well as anxiety and apathy. The author emphasizes that this dementia, unlike Alzheimer's, does not usually begin with episodic memory deficits.


  • 1 Diagnostic criteria: dementia with Lewy bodies
  • 2 What is behind dementia with Lewy bodies?
  • 3 Treatment

Diagnostic criteria: dementia with Lewy bodies

In 2005, the Cosistorium on Dementia with Lewy Bodies International, updated the diagnostic criteria that were originally developed in 1996. In this way, it is intended to facilitate diagnosis and to treat this dementia in the most accurate way.

Essential features

For the diagnosis to occur, the essential characteristics are indispensable. First, you should appreciate a dementia with a progressive cognitive decline that is so pronounced that it interferes with social and work life. There are usually attention deficits, as well as visuospatial ability and executive function. The most prominent memory alterations may not manifest in the initial stages.

Core features

There must be at least two of the following characteristics:

  • Fluctuations in cognitive ability that include variations in attention and alertness.
  • Parkinsonism spontaneous motor signs.
  • Recurring presence of complex visual hallucinations formed and detailed.

Suggestive features

A central feature plus another suggestive, define the diagnosis probable dementia with Lewy bodies. No central feature but one or more suggestive features define a possible dementia with Lewy bodies.

  • There is a low uptake of the dopamine transporter in the basal ganglia of the brain, appreciated by SPECT or PET (positron emission tomography).
  • Manifestation of a serious sensitivity to neuroleptics. Sensitivity present in up to 50% of patients.
  • Presence of REM sleep disorders. They may even appear years before dementia or parkinsonism begins.

Features that support the diagnosis

  • Depression.
  • Presence of systematized delusions.
  • Olfactory, tactile and auditory hallucinations (not visual).
  • Nervous system dysfunction.
  • Temporary loss of consciousness that cannot be explained by other causes.
  • Sudden falls and syncopes.
  • A high slow wave activity is seen in the electroencephalogram, with transient acute waves in the temporal lobe.
  • Low uptake in the SPECT (single photon emission tomography) diffusion, with reduced occipital activity.
  • The structures of the middle temporal lobe are relatively conserved by structural neuroimaging.
  • Low uptake in myocardial scintigraphy with metaiodobenzylguanidine.

Features that make diagnosis less likely

  • Parkinsonism only appears for the first time in a state of severe dementia.
  • Evidence of another systemic or neuronal disease that can totally or partially justify the clinical picture.
  • Cerebral vascular disease with focal neurological signs or vascular lesions in neuroimaging techniques.

What is behind dementia with Lewy bodies?

Lewy bodies are round cytoplasmic structures and their main component is the alpha-synuclein protein. When its functioning is normal, the protein is involved in the regulation of neuronal communication. However, when an alteration occurs as in this type of dementia, it accumulates forming aggregates that are inside the neurons.

Schulz-Schaeffer (2010), also has identified Lewy bodies around presynaptic endings. In this way, there are anomalies in the receivers and decrease in the level of the transmitters. They are also observed Amyloid plaques and neurofribular clews. Gradually, Lewy bodies and alpha-synuclein aggregates spread throughout the brain as the disease progresses.

In the case of dementia with Lewy bodies cortical atrophy is seen with significant expansion of the ventricles. Through functional neuroimaging, hypometabolism can be seen, to a greater extent in the parietal, frontal and occipital lobes. As well as in subcorical structures such as the thalamus, basal ganglia, areas of the brainstem and the nigrostriated trunk.

The Occipital lobe is also a protagonist in this dementia due to hallucinations and visuospatial and visuoconstructive alterations. Changes are observed in the secondary visual areas and in their connections with the parietal regions through the dorsal pathway (pathway from where), and with the temporal lobe through the ventral pathway (pathway of the what). This alteration is especially important since it distinguishes with a specificity greater than 80% between dementia with Lewy bodies and Parkinson's disease (Arnedo, Bebimbre and Triviño, 2013).


According to Martín Calle (2006), "The cholinergic neurotransmitter system together with dopamine is one of the most affected neurotransmitters in dementia with Lewy bodies, so the main therapeutic strategies are aimed at restoring cholinergic function". Thus, the authors affirm that"Only acetylcholinesterase (ACE) inhibitors in short-term studies (3-6 months) have proven effective in symptomatic improvement of these patients".

From a psychological point of view, the Arnedo team (2013), highlights the psychological rehabilitation. Among the different functions to work are attention, perception, reasoning and memory. At the same time, spatial and temporal orientation is also enhanced in order to preserve them as long as possible.


Arnedo, M., Bembibre, J. and Triviño, M. (2013). Neuropsychology Through clinical cases. Madrid: Pan American Medical Editorial.

Schulz-Schaeffer, M. (2010). The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia. Neuropathological Act, 120, 131-143.

Tröster, A. (2008). Neuropsychological chracteristics of dementia Lewy body and Parkinson's disease with dementia: differentiation, early detection and implications for mild cognitive impairment and biomarkers. Neuropsycholgy Review, 18, 103-119.