Loss of memory - due to brain pathology

2 types:

• Retrograde - loss before triggering incident
• Anterograde - loss of ability to make new memories after triggering incident

Acute, rapidly developing, fluctuating state of reduced awareness (ALL of the following are true):

• trouble shifting/focusing attention
• at least one defect of memory, orientation, perception, or language
• Not better explained by demention

Causes: GMC, Multiple Etiologies, Substance-Induced, and NOS

- most causes in CNS, more likely from toxicity

Dementia

- Memory loss AND other cognitive deficits (apraxia, agnosia, exec. fucntiong ,etc.)

- No prominent impairment in ability to shift/focus attention

- Cause w/in CNS, not somewhere else in body

- Relatively fixed/unchanging

- Recovery uncommon

- Different types of demenia

- Significant tissue loss & behavior functioning

MMSE cutoff <21

Something beyond normal aging:

- Primarily memory complaints, should be corroborated

- Middle ground b/w DAT, but not everyone progresses

- Objective memory impairment

- Normal general cognitive function

- Intact activities of daily living (not yet demented)

Amnestic --> Alzheimer's

Multiple Domains--> Alzheimers/Vascular/

Mild Impairment        Normal Aging

Single, non-memory domain -->

Frontotemporal dementia/ Lewy Body/ Primary progressive aphaisa/Vascular Dementia

• Progressive Cognitive Decline
• Can begin in any cognitive domain, but usually spreads to include others
• Not secondary to stress/mood/static conditions (single stroke/ecephalitis/ head injury)
• Diagnosis made post-mortem via histopathology

• Mostly through clinical cog. exam
• Supported by evidence of a persistent decline - scores more than 2SD from age norms, change in scores (1SD) over a 6-12 mo. period
• Formal DX made post-mortem

- Costs over $100 Billion annually

- Average dx at age 80

- Most common dementia

- Decline over time

- Heritability is 40% in those with early dementia in sibs/parents

• Similar to Alzheimers/Parkinsons
• Prominent memory loss, aphasia, apraxia, exective deficits
• Cog. symptoms vary on a day-to-day basis
• Up to 80% have unexplained periods of increased confusion that mimics delirium
• visual hallucinations (animals/people)

• Protein deposits on nerve cells in cortex throughout brain
• Fluctuations in cognition and confusion, hallucinations at early stages
• Can have lewy bodies in cortex without tangles in DAT
• worse visuospatial, better memory compared to DAT

PD - midbrain lewy bodies

LBD - cortical lewy bodies

AD - cortical neuritic plaques/ neurofibrillary tangles

PD - Autonomic dys. sometimes seen

LBD - often seen

AD - rare

PD- Bradykinesia, falls, resting tremor

LBD - Brady., falls, NO resting tremor

AD- Usually none of the above

PD - relatively stable

LBD - prominent day-to-day variability

AD - relatively stability of impairment

PD - robust response levodopa/carbidopa

LBD - marginal repsonse to Levodopa/carbidopa

AD - medications typically anticholinesterase inhibitors

PD - sometimes in late onset

LBD - executive/memory/language and visual disturbances

AD - prominent memory and language disturbances

Creutzfeld-Jakob Disease

Symptoms

- Extremely rapid progression 

- physical signs - myoclonus, jerks

- visual/cerebellar dysfunction

- muscle incoordination, gait, speech

- bx changes - agitation/depression/confusion

- akinetic mutism during terminal stages

- Rare

- Prion disease (protein particle that binds with cells)

- transmissable b/w people

- widening of sulci, atrophy of gyri

- 3 major categories:

• hereditary
• sporadic
• acquired/variant - linked to mad cow

Cognitive Profile - not demented, intact learning/memory, problem solving abilities,

- rapid retrieval compromised, and fluctuations in processing speed and attention

Emotional Profile - depressive symptoms may appear, report apathetic symptoms or appear that way

- typically over 70

- cardiovascular risk factors

- pronounced intellectual decline compared to premorbid

- impairment in one other domain: learning/memory, language difficulty, abstract reasoning

Difficult to differentiate from Parkinson's or pure autonomic failure.

- Early onset (age 40 or later)

- Fast progression, shorter life expectancy than PD

- First, autonomic or urinary dys.

- Usually, no dementia

• agitation/aggression - most common psychiatric referral, low cortical serotonin, mid-late stages, responds to pharmacological intervention
• Sundowning - late day confusion, maybe due to fatiguability, increase cog. cues and late day structure, nap after lunch, psychotropics around 3pm. Nocturnal sundowning - phototherapy/increase daylight, no naps/caffeine, hypnotics, nightlight
• ADL decrements - activities of daily living
• Combativeness - assoc. with exec. dys., limit goals and negotiate, pre-med. with lorazepam, visual agnosia may lead to fearfulness, able to read prosody more than word comprehension
• psychosis - 50% prevalance, usually not a big problem, but may predict more rapid progression, tx = neuroleptics and reality therapy
• disinhibition - No goal oriented bheavior, so susceptible to impulses. Ex. wandering for stimulation seekers (decrease neuroleptics) or screaming (in late stages, rule out pain, increase stimulation), 
• Incontinence - common in strokes and late stage DAT. Use depends.  Often the most difficult symptom for caregivers

- usually early stages - 20/30%

- important bc of diminished quality of life

- predictors include past history/family history

- responsive to anti-depressants

- Also in client and caregivers

- Driving abilities

- Power of Attorney

- Competency to make decisions

- Re-evaluations

- no req. for ability to shift attention or focus

- memory most affected (more than any other function)

- In early phases, confabulation is common.  Make up stories to fill-in gaps in memory.

- Types - GMC, NOS, Substance-induced