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LBD biobases

kristin's part

Kristin Orr

on 29 April 2010

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Transcript of LBD biobases

Lewy Body
Dementia Introduction to: neurodegenerative
disease one of the most common forms of dementia progressive cognitive decline
visual hallucinations
parkinsonian motor symptoms LEWY BODIES where: how it happens Pathological diagnosis: round inclusions with pale halo cortex -- irregularly shaped with less prominant halo midbrain -- round with prominent halo "alpha-synuclein postive inclusions in the brain" difficulties in diagnosing 76 components of 10 different protein classes PRIMARY LOCATION: brainstem in LBD: throughout the brain autopsy - to confirm diagnosis
Brainstem prominent: nuclei for cranial nerves IX, X,
locus coeruleus, substantia nigra
Limbic (transitional): amygdala, transentorhinal cortex,
cingulated gyrus
Diffuse neocortical: frontal, parietal,
& temporal neocortical Not a lot of information on how & why alpha-synuclein in our brain genetic abnormalities why? misbehaves underlying process is not known abnormal chemical reaction in the cell garbage
deposits build up and cell breaks up Lewy bodies attack the mitocondria
affects the ATP & damages dendrites progressive neuronal death deplete dopamine neurotransmitter deficit drives illness
rather than the neuronal death Symptoms: cognitive impairment: reduced cholinergic activity OR
dopamine dysfunction fluctulations: is it neurochemical or sleep disorder ??
(no clinical measure) visual hallucinations: not fully understood,
may be from dopamine dysfunction Parkinsonism: reduced dopaminergic activity RBD: brainstem neuronal network dysfunction central feature: Dementia slight to extreme
memory problems
changes in speaking (forgetting words)
attention/executive functioning/learning new skills core: fluctuating cognition acute episodes of confusion
hours - days - minutes core: visual hallucinations vivid & well formed
patients reconize not real core: spontaneous features of Parkinsonism changes in gait -shuffle
body stiffness
tremors suggestive: REM sleep behavior disorder [RBD] move, gesture, or speak
confusion between dream/reality
*risk factor in developing LBD* suggestive: sensitivity to neuroleptics repeated falls
unexplained loss of consciousness
visualspatial abnormalities
psychiatric disturbances Supportive: Probable:
dementia plus 2 core
dementia plus 1 core,
1 or more suggestive Possible:
dementia plus 1 core
& 1 or more suggestive
Essential: Associated but not Essential: lewy bodies lewy related neuritis
neurofibrillary tangles
regional neuronal loss
esp. brainstem & nuceus basalis of meyhert
spongiform change & synapses loss
neurochemical abnormalities
neurotransmitter deficits DLB vs. AD cousin of Parkinson's -- biologically identical NOT on spectrum with AD
pathology is overlapping but not identical affects same part of brain: parietal/temporal/occipital neurotransmitter changes:
cholinergic deficit -AD -- HUGE loss in LBD
no serotin deficit in LBD neuropsych testing: impairment: attention
visual perceptual org.
letter fluency
preservation: confontation naming
verbal memory differential diagnosis: diagnosis confirmed after death
most commonly looks like Alzheimer's cognitive decline memory impairment
poor judgement
confusion Fluctuation in ability to function Can also look like: other forms of dementia
Parkinson's: rigid, shuffling gait, mask like face
Frontotemporal: behavioral/personality changes
Vascular (in midbrain): can progress gradually other types of mental illness
psychotic depression
late onset delusional disorder
psychosocial issues develops after age 60 effects independence
driving ability
geographical memory social isolation depression long term
incapable of being
left alone Progression NO CURE or TREATMENT duration: 5-7 years/ 2-20 years severity stages difficult to define symptoms/medicine mangament/duration vary progression regression downward fluctuation due to
medication Treatment current drug therapy can not alter disease pathophysiology current drug therapy aims to treat symptoms: cognition: slowing cognition, ambivalence, psychomotor slowing cholinesterase inhibitor: requires lab monitoring clinicians typically choose to use medications that affect the
frontosubcortical neural networks that mediate attention &
executive functioning like:
dopamine agonists difficulty treating flucuations &
visualspatial impairment drug treatment for hallucinations not always necessary cholinesterase inhibitor
melatonin therapies Insomnia -- is it a primary sleep disorder ? trazodone
chloral hydrate
atypical neuroleptics treatment cont'd Behavioral Treatments routines
psychoeducation for the caregiver effective communication
understand rather than correct
speak slowly & calmly
reassuring rather than orienting preventing, defusing, & managing
sleep disturbances
transitions HOPE !!!!!! progressive neuronal death is less severe
in LBD than with AD or FTD medical therapy more effective HUGE research in AD main task is to understand the basic mechanism breakthrough in 1 better treatments for all 3 pronged attack: symptomatic treatment
neurorestorative Why:
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