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Lewy Body Dementia: The Misdiagnosed Dementia
Closely related to Parkinson’s and Alzheimer’s dementia but pathologically different, Lewy body dementia is characterized by neurons that have been destroyed by miniscule clumps or “bodies” of destructive ubiquitin and alpha-synuclein proteins. Although physicians can analyze symptoms and examine results of laboratory tests to present a diagnosis of LBD, only an autopsy can provide definite evidence of this kind of dementia.
Who Gets LBD?
Doctors are not yet sure why some people develop LBD, although several risk factors are suspected of promoting its emergence. These include:
- Being at least 60 years old
- More males than females get LBD
- Having a close family member with LBD
Because this kind of dementia has little if nothing to do with reduced blood flow to the brain, the health of a person with LBD may not directly influence the growth of atypical protein clumps the way high cholesterol, hypertension and diabetes may promote the progression of Alzheimer’s and vascular dementias. The usual life expectancy of someone diagnosed with LBD is about six to seven years following that diagnose but this amount can be significantly less if that person’s health is suffering one or more disorders.
Similarities with Alzheimer’s Disease
Dementia with Lewy bodies results from the degradation of neurons that release acetylcholine, a neurotransmitter responsible for motor control, muscle contraction and brain cell communication. Cognitive impairment in both Alzheimer’s and Lewy body dementia is caused by substantially reduced levels of acetylcholine in the brain but LBD attacks much of the cortical area while Alzheimer’s plaques and tangles target the hippocampal regions where memory is processed.
Symptoms frequently overlap in the late stages of both diseases when most areas of the brain have experienced atrophy and massive cell death. Visual hallucinations, delusional thinking, severe memory and attention deficits and problems with fine motor tasks can affect people with Alzheimer’s or LBD. In addition, autopsies sometimes reveal the presence of both dementias in patients, with the neurofibrillary tangles found strictly in Alzheimer’s exacerbating the Lewy bodies clustering in cortical regions.
Lewy Body Dementia in Parkinson’s Disease
People suffering from Parkinson’s disease experience abnormal accumulations of the same proteins that distinguish LBD from other dementia types. Damage to inner brain structures called the substantia nigra produces the classic Parkinson’s symptoms of muscle tremors, stiffness, shuffling instead of walking and slowness of movement. Destruction of dopaminergic neurons within the substantia nigra also decreases dopamine levels, another important neurotransmitter involved in hundreds of physiological functions including motor ability, attention and learning.
Symptoms Specific to Lewy Body Dementia
LBD can cause dramatic fluctuations in cognitive abilities and range of motion. Someone with this type of dementia may seem fairly normal and alert one day but appear significantly impaired the next, with unpredictable behavioral changes triggered by schedule changes, environmental stress or physical injuries due to falling. Later stages of LBD produce hallucinations and delusions that often provoke agitation, irritability, and depression, making it difficult for both patient and caregiver to cope with the disease.
Lewy Body Dementia Medication
Unfortunately, when someone with Parkinson’s has LBD, the medication used to treat motor impairment tends to aggravate psychotic symptoms. Alternately, the antipsychotic medication meant to reduce hallucinations and delusional thinking exacerbates the tremors and muscle rigidity associated with Parkinson’s.
A medication sometimes used for Alzheimer’s called donepezil seems to relieve LBD symptoms more than Alzheimer’s symptoms. A cholinesterase inhibitor, donepezil improves attention and memory as well as the overall ability to do some everyday tasks. Although it does not do anything to alleviate psychotic symptoms, it can give people with Lewy Body dementia the ability to process perceptual input more clearly.
Clonazepam, a muscle relaxant, anticonvulsant and anxiolytic medication, is often prescribed for rapid eye movement sleep disorder, a condition associated with LBD. During the rapid eye movement stage of sleep, people experience their most vivid dreaming but usually remain asleep, no matter how active the dreams are. People whose brains are clogged with LBDs cannot stay still while dreaming. Normal motor inhibition is severely lacking which causes them to twitch violently, throw themselves out of bed and suffer injury because of the disorder.
Tips to enhance the well-being of the caregiver include:
- Do not feel guilty if you need a break. Take advantage of respite care and reward yourself with enjoyable activities and reconnecting with friends and family.
- Depression is serious and debilitating. Do not hesitate to get professional help if you start feeling sad, angry or hopeless all the time
- Thoroughly educate yourself about dementia in order to understand what your loved one is experiencing
- Do not neglect your physical and mental health. Exercise regularly, eat health food and take the time to socialize
Numerous dementia resources and support services are available on the Internet to provide caregivers with valuable information concerning Lewy Body dementia treatment plans. Some of these include the Lewy Body Dementia Association, Alzheimer’s Association and the Family Caregiver Alliance.