Download Dementia memory loss, personality change, impaired intellectual

Dementia
1. memory loss, personality change, impaired intellectual fxns
2. from dz/trauma
3. NOT part of normal aging and impact ADLs and relationships
Definitions:
1. memory: store, retain, recall info and experiences; can be long/short
2. executive fxn: ability to plan, organize, sequence, or abstract info
3. attention: concentrating on one aspect of environment while ignoring other things
Agnosia
1.
2.
3.
4.
inability to recognize sensory input
visual: can’t name common objects (eg: watch, pencil)
auditory: can’t recognize sounds
responsible lesions: occipitotemporal region
Apraxia
1. sensory and motor systems intact, but can’t perform common actions
2. eg: brushing hair, blowing out a match
3. responsible lesions: dominant inferior parietal lobe
Amnesia
1.
2.
3.
4.
anterograde: can’t recall events/form new memories after an injury
retrograde: can’t recall events that occurred before an injury
responsible lesions: hippocampus, temporal lobe, and its connections
major finding in alzheimer’s
Memory in the Brain
1.
2.
3.
4.
memory and recall located in hippocampus
amygdala, striatum, mammillary bodies involved
hippo: spatial & declarative learning
amygdala: emotional memory
Common Memory Disorders
1.
2.
3.
4.
5.
Alzheimers: most common dementia
Vascular & Lewy Body: next most common; often +Alz
Benign Forgetfulness of Aging: normal cognitive changes
Mild Cognitive Impairment: pre-dementia state
Delirium: acute, cognitive disturbance; many causes; coexists with dementia
a. characterized: decline in consciousness, loss of attention
b. related to: medication, metabolic disturbance, infection
Types of Dementia
1.
Cortical
a. Major symptoms: disturbances in memory, language, perception, function
b. regions affected: temporal (medial), parietal, frontal
c. Dz: Alzheimer’s, Lewy Body, Vascular dementia, frontotemporal dementia (Pick’s dz)
2. Subcortical
a. Major symptoms: emotional probs, slowed motor fxn, disturbed executive fxn, less
pronounced memory loss
b. regions affected: thalamus, striatum, midbrain, striatofrontal
c. Dz: Parkinson’s, progressive supranuclear palsy, normal pressure hydrocephalus,
Huntington’s, Creutzfedlt-Jakob, chronic meningitis
3. Neurodegenerative
a. primary degenerative dz process of CNS
b. most common underlying cause of dementing illnesses
c. Dz: Alzheimer’
4. Other
a. origin of degenerative process causing the dementing illness is outside the CNS or it is of
NONorganic etiology
b. eg: structural dz/trauma, vascular dz, hereditary metabolic dz, demyelinating dz,
infectious dz, metabolic/nutritional dz, psychiatric dz
Treatable Dementia
1. Less than 10%
2. In order to rule out reversible/treatable conditions consider: structural processes,
infections, metabolic dz, nutritional def, psychiatric issues
3. Examples:
a. pseudodementia from depression
b. normal-pressure hydrocephalus
c. thyroid hormone deficiency/excess
d. thiamine def. (Wernicke-Korsakaff)
e. tertiary syphilis
f. pernicious anemia
g. alcoholism
Dementia Work-Up
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Serum Chemistries
Urinalysis
CBC w/diff
folate & Vit B12
Liver, renal, thyroid fxn
serologic studies for syphilis (RPR)
LP if +RPR
EEG
MRI <65 old, <2 yr hx, focal neurologic sx, nl pressure hydrocephalus signs, falls, trauma
neuropsychological testing (bedside and formal)
Bedside Neuropsych Testing
1. MMSE- memory and language
2. Clock Drawing- visuospatial
3. “how would you comb your hair”; “how would you blow out a match” apraxia
Alzheimer’s Dz
1.
2.
3.
4.
most common
5.2 million Americans
6th leading COD
Characteristics:
a. gradual memory loss & difficulty learning
b. problems with reasoning and judgement
c. loss language skills
d. disorientation
e. can’t perform routine tasks
5.
6.
7.
8.
9.
10.
11.
12.
f. personality & behavior change later on in dz
Causes:
a. undetermined
b. chromosomes 1, 14, 21 early onset
c. chromosome 19 (ApoE4 gene) late onset
d. amyloid plaques and neurofibrillary tangles
Amyloid plaques: clumps “beta-amyloid” that accumulate b/n abnormal n cell axons and
dendrites dense, insoluble structures
a. neocortex & hippo
Neurofibrillary tangles: twisted paired strands hyper-phosphorylated MT-associated protein
called tau inclusion bodies from damaged neuronal MTs
a. correlation b/n density of NF tangles on post mortem autopsy and measured antemortem cognitive decline
ACh
a. important NT in areas of brain involved in process of memory formation (hippo, cerebral
cortex, amygdala)
b. decreased by ~90% in Alz Dz cognitive impairment & disordered memory
c. pharmacotherapy: inhibit breakdown of ACh
Diagnosing
a. hx
b. direct exam of mental/physical status
c. lab findings
d. neuropsychological testing
e. neuroimaging
f. the only way to confirm ddx of Alz dz is via post-mortem exam (brain autopsy)
Management
a. nonpharmacological behavioral interventions
i. behavioral interventions by care givers
ii. safe/structured environment
iii. active tx
iv. psychotherapeutic interventions
v. pastoral interventions
b. cognitive enhancers
i. cholinesterase-inhibitor
1. Donepezil (Aricept)
2. Rivastigmine (Exelon)
3. Galantamine (Reminyl/Razadyne)
ii. Glu antagonist
1. Memantine (Namenda)
c. meds for behavioral symptomatology
i. antipsychotics- NO
ii. antidepressants
iii. mood stabilizers
iv. anxiolytics
v. hypnotics
vi. pain meds
d. education and support for caregivers
i. caregiver burden counseling
ii. legal services
iii. medical/ancillary services
iv. advocacy groups
Long term Care
a. sometimes the best clinical strategy to provide as much independence and functionality
as possible in least restrictive environement
b. challenging
c. requires preparation
Basic Needs in Alz Dz
a. mental stimulation
b. physical activity
c. social engagement
d. proper nutrition
13. Research on Alz Dz
a. Amyloid cascade hypothesis
b. Amyloid based treatment strategies
c. Tau based treatment strategies
d. Neuroprotective treatment strategies
Benign Forgetfulness of Aging
1.
2.
3.
4.
5.
6.
7.
mild loss of memory- slow to recall names/ dates
adequate ADL’s and IADL’s
poor performance on delayed recall tasks = most sensitive indicator
verbal fluency intact
vocab can increase
dementia NOT normal end product of aging
“mild cognitive impairment”- pre-dementia state
Lewy Body Dementia
1.
2.
3.
4.
5.
6.
7.
8.
3rd most common form dementia
overlap w/ Alz and PD
visual hallucinations
PD features prominent
sensitive to antipsychotic med SE
rapid evolution of dementing processes
Lewy Bodies (hallmark of PD) found in brainstem, limbic system, and cortex
dementia develops w/in year of PD or when comes first
Parkinson’s Dz
1.
2.
3.
4.
5.
6.
dementia in ½
executive function > language/ visuospatial
brainstem
bradykinesia = hallmark
depression common
drugs used to treat can induce psychosis/delirium; these need to be ruled out before ddx of
dementia can be made
Vascular Dementia (Multi-Infarct Dementia)
1.
2.
3.
4.
5.
2nd most common form dementia
brain damage 2* stroke/ MI
MRI- neuronal damage
hypertension/other vascular dz
overlap with Alz. Dz  mixed dementia
Frontotemporal Dementia
1.
2.
3.
4.
5.
6.
Pick’s Dz Pick’s Bodies
atrophy of frontal and temporal lobes
up to 5% dementia
Frontal Lobe syndrome inappropriate social behavior (disinhibition)
earlier onset than other forms of dementia (~50s)
~1/2 pts have fam hx; link to mutation of tau on chrom 17
Normal Pressure Hydrocephalus
1.
2.
3.
4.
classic triad: dementia, gait disturbance, urinary incontinence
enlarged ventricles
no elevated ICP
clinical treatment: shunt placement; can lead to reversal of dementia in cases of head
trauma/SAH
Creutzfeldt-Jakob Dz
1. prion dz
2. symptoms: dementia, myoclonus, abnormal EEG (diffuse slowing w/ periodic sharp
waves/spikes)
3. spongiform encephalopathy
4. rapidly progressive- death w/in year
5. possible transmission via tissue transplantation sx
Pseudodementia
1.
2.
3.
4.
5.
6.
“Dementia syndrome of depression”
5% pts
may coexist w/other dementias
symptoms: poor concentration, apathy, anhedonia, sleep disturbance, psychomotor retardation
treatable & reversible
responds to antidepressants
Korsakoff’s Syndrome
1.
end result of untreated/partially treated Wernicke’s Encephalopathy caused by thiamine
deficiency resulting in CNS enzyme dsyfxn
2. near total inability to make new memories
3. pts confabulate responses
4. chronic alcoholism
5. treatment: thiamine replacement therapy
AIDS
1.
2.
3.
4.
5.
6.
7.
direct action HIV on brain
subcortical > cortex
bradykinesia
little to no disturbance w/ language
early features: forgetfulness, poor concentration, slowed thinking
late features: executive dysfxn, apathy
treatment: anti-virals
Head Injury
1. retrograde > anterograde
2. doesn’t progress unless further trauma occurs
3. CTE, Dementia Pugilistica, Boxer’s Dementia
Transient Global Amnesia
1.
2.
3.
4.
5.
dramatic memory disturbance
typically only once; more can happen over several years
temporal & spatial disorientation
orientation for person intact
retro/anterograde amnesia for hours
6. anxious/distressed
7. ask same Q over & over
8. vascular insuff to midbrain (including hippo & midline thalamic projections)
Psychogenic Amnesia
1.
2.
3.
4.
inconsistent loss recent & remote memory
relative indifference to deficits
“who am I?” (disoriented to person)
aka “dissociative amnesia”
Huntington’s Dz
1.
2.
3.
4.
5.
AD chromosome 4
excessive CAG repeats
onset: 30-50 years
dementia + chorea
atrophy of cerebral cortex and heads caudate nuclei
Subdural Hematoma
1.
2.
3.
4.
reversible dementia
tearing of bridging veins in subdural space
symptoms: headaches, confusion, inattention, apathy, memory loss, drowsiness, coma
lateralizing signs less prominent (hemiparis, hemianopsia, CN abnormalities)
Delirium
1.
2.
3.
4.
5.
6.
acute, disorganized mental process
shifting attention, awareness, consciousness
disordered thinking
impaired perceptual discrimination
fluctuating cognitive deficits
cause: substance intoxication, substance w/drawal, infection, medical condition