Lewy body dementia

Description, Causes and Risk Factors: Alternative Name: Dementia with Lewy bodies, diffuse Lewy body disease, cortical Lewy body disease. Abbreviation: LBD. Dementia is the general term for a gradual progressive decline in a person's memory and other mental abilities. Lewy bodies are neuronal inclusions composed of abnormally phosphorylated, neurofilament proteins aggregated with ubiquitin and -synuclein (alpha-synuclein). In LBD, significant Lewy body formation occurs in paralimbic and neocortical structures, and extensive depletion of acetylcholine neurotransmission in neocortical areas occurs as a result of degeneration in the brain-stem and basal forebrain cholinergic projection neurons. Dementia with Lewy bodies is thought to be the second or third most common cause of dementia, accounting for 15% to 20% of cases of dementia which start after the age of 65. The disease is more common in men than women with a ratio of 2:1. The mean age at onset of symptoms is 68 years. The average time from onset to death is 6.4 years, with the most frequent cause of death being aspiration pneumonia. The cause of Lewy body dementia is unknown. Some speculate that genetics plays a role, and studies are underway to investigate this possibility. There are certain similarities with Alzheimer's disease and Parkinson's disease. Genetic studies are trying to discover which genes may contribute to the development of LBD, but these are still at an early stage. Just as the amyloid protein may play a central role in Alzheimer's disease there may be a protein or proteins which are central to the nerve cell damage in LBD. A distinctive pattern of ubiquitin and -synuclein immunoreactive neuritic degeneration has additionally been identified in LBD. Lewy neurites are seen in the substantia nigra, hippocampal region CA2/3, dorsal vagal nucleus, basal nucleus of Meynert and transentorhinal cortex. These extensive neuritic changes are probably more relevant for neuropsychiatric symptom formation than the relatively sparsely distributed cortical Lewy bodies Symptoms: Signs and symptoms may include:
  • Gradual loss of mental abilities, including orientation and memory, reasoning and intelligence.
  • Difficulty problem solving.
  • Hallucinations.
  • Tremors.
  • Sleep disturbance.
  • Repeated falls.
  • Transient loss of consciousness.
  • Neuroleptic sensitivity.
  • Systematised delusions.
  • Hallucinations in other modalities.
Diagnosis: Differential diagnosis may include:
  • Alzheimer's disease.
  • Parkinson's disease.
  • Progressive supranuclear palsy.
  • Multisystem atrophy or multiple system atrophy.
  • Creutzfeldt-Jakob disease.
  • Late-onset delusional disorder.
  • Depressive psychosis.
  • Mania.
To diagnose LBD, a specialist will take a precise history of the pattern of the person's symptoms. A CT, CAT, or MRI scans may reveal degeneration, or shrinkage, of the brain. A SPECT scan, may be able to show up some of the changes that are happening, but this is still being investigated. Currently, definitive diagnosis of Lewy body dementia can be made only at autopsy. There is considerable overlap between Lewy body dementia and both Alzheimer disease and Parkinson disease. The definitive diagnosis may include progressive cognitive decline that interferes with normal social or occupational functioning. Memory and visuospatial deficits are often, but not necessarily, prominent. In addition, two of the following three features must also be present:
  • Recurrent visual hallucinations.
  • Fluctuating cognition.
  • Spontaneous motor features of parkinsonism.
Treatment: There is no cure yet for LBD. Research continues to search for a specific course of therapy. The present form of treatment usually focuses on treating the symptoms. A group of drugs developed for treating Alzheimer's disease may be helpful. The potential side effects of these drugs vary from person to person.
  • Medications called cholinesterase inhibitors are considered the standard treatment for cognitive symptoms in LBD. The effect of these drugs varies from person to person.
  • Movement symptoms may be treated with a Parkinson's medication. Potential medication side-effects vary from person to person.
  • For hallucinations, your physician may recommend a cautious trial of antipsychotic medication. Potential medication side-effects vary from person to person. Hallucinations must be treated very conservatively, using the lowest doses possible under careful observation for side effects.
Non-Medical Treatments:
  • Physical Therapy: options include cardiovascular, strengthening, and flexibility exercises, as well as gait training. Aerobic or water exercise may be helpful.
  • Speech therapy: Speech therapy may also improve muscular strength and swallowing difficulties.
  • Occupational Therapy: May help maintain skills and promote function and independence. In addition to these forms of therapy and treatment, music and aroma therapy can also reduce anxiety and improve mood.
  • Individual and family psychotherapy can be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
Disclaimer: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.  


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