Dementia Flashcards
Delirium
- A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment).
- The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day.
- Theres a disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception).
Types of dementia
- Alzheimer’s
- Frontotemporal
- Lewy Body
- Parkinson’s Vascular
- Huntington’s
- HIV
- Traumatic Brain Injury
- Prion Disease
Dementia causes a progressive decline in intellectual functioning severe enough to _______
interfere with person’s normal daily activities and social relationships
Dementia causes progressive declines in
- memory
- visual-spatial relationships
- performance of routine tasks
- language and communication skills
- abstract thinking
- ability to learn and carry out mathematical calculations
2 categories of dementia
Reversible and Irreversible
*Individuals must have intensive medical physical to rule out reversible types of dementia
Reversible causes of dementia
"DEMENTIA" D-drugs, delirium E-emotions (depression) & endocrine disorders M-metabolic problems E-eye & ear problems N-nutritional disorders T-tumors, toxicity, trauma to head I-infections A-alcohol, arteriosclerosis
Irreversible causes of dementia
- Alzheimer’s
- Lewy Body Dementia
- Pick’s Disease (Frontotemperal Dementia)
- Parkinson’s
- Heady Injury
- Huntington’s Disease
- Jacob-Cruzefeldt Disease
Alzheimer’s Dementia
- Insidious onset/gradual progression
- Memory & learning impairment, sometimes executive impairment
- Then perceptual-motor & language impairment
- Social cognition affected late in disease
- Gait disturbance, dysphagia, incontinence, myoclonus, seizures
- 5% Diagnosed between around age 65, prevalence increases steeply, esp in 80s
- Mean survival 10yrs after diagnosis
Alzheimer’s dementia- About 0.1 % autosomal dominant inheritance, which have an onset before age
65
-This form of the disease is known as early onset familial Alzheimer’s disease
Alzheimer’s dementia-
Most of autosomal dominant familial AD can be attributed to mutations in one of three genes:
- those encoding amyloid precursor protein (APP)
- those encoding presenilins 1 and 2
*Most mutations in the APP and presenilin genes increase the production of a small protein called Aβ42, which is the main component of senile plaques.
Most cases of Alzheimer’s disease do not exhibit
autosomal-dominant inheritance
Alzheimer’s dementia- environmental and genetic differences may act as risk factors. The best known genetic risk factor is the
inheritance of the ε4 allele of the apolipoprotein E
know mini mental status exam
in other deck too
Frontotemporal Dementia
- Encompasses Pick’s disease and several related illnesses.
- Insidious onset/gradual progression
- Reflect loss of frontal and temporal lobe function
- FT dementia accounts for 15% cases of dementia
- Higher proportion in individuals younger than 65
- Tau inclusions, pick bodies
Symptoms of Frontotemporal Dementia
-Broad decline in insight
-Social skills, interpersonal conduct
-And executive functioning
-Mental rigidity
-Easily distractibility, labile affect and speech and language impairments
(echolalia and perseveration)
-Disinhibition
-Apathy
-Loss of sympathy/empathy
-Perseverative or compulsive behavior
-Hyperorality and diet changes
Frontotemporal Dementia shows a prominent decline in ______, but a relative sparing of _________
- prominent decline in social cognition or executive abilities
- also decline in language ability, object naming, grammar
- Relative sparing of learning, memory, and perceptual-motor function
Frontotemporal Dementia average age of onset is
53 years followed by fatal progression lasting less than 4 years
Compared to Alzheimer’s disease, FT Dementia does not have impairments in
visual-spatial abilities – a function governed largely by the parietal lobes
- maintain their ability to copy a picture but not to draw one from their memory.
- do not lose their sense of direction, even in new surrounding
- do not manifest constructional apraxia
FT shows prominent personality and behavioral disturbances accompanied by only relatively mild ________
memory impairment
On CT/MRI, FT shows
- Frontal and anterior temporal lobes are atrophic. -Plaques and tangles are uncommon or absent
- Pick’s disease – neurons containing argentophilic (silver staining) inclusions (Pick bodies)
FT has some gene mutations, 10% linked to mutant gene on _______
chromosome 17, which codes for tau (MAPT)
Dementia with Lewy Bodies
- Cognitive decline, ≥1 yr prior to onset of parkinsonism features
- Fluctuating cognition w/ variations in attention/alertness (looks like delirium)
- Recurrent VH
- REM sleep behavior disorder
- Severe neuroleptic sensitivity (50%)
- Lewy bodies have greater distribution than in Parkinson’s
Dementia with Lewy Bodies age
Older than 65
-sometimes initially diagnosed as alzheimer’s
Pathology of Dementia with Lewy Bodies age
- abundance of intracytoplasmic inclusions (lewy bodies) in cerebral cortex neurons that stain with alpha- synuclein antibodies
- Concentration of lewy bodies correlates with dementia
- Similar to Alzheimer’s disease, but older individuals with nonspecific cognitive deficits.
Non-cognitive features of Dementia with Lewy Bodies (aka-S/S)
- characterized by mild extrapyramidal features, masked face, bradykinesia, and gait impairment.
- sudden unexpected changes in cognition, attentiveness and alertness; mimics episodes of delirium or toxic-metabolic encephalopathy
- Visual Hallucinations: detailed visions of people and animals, associated with lewy bodies in the temporal lobes
- Visual hallucinations also frequently develop in pts with advanced Alzheimer’s and Parkinson’s disease – but not at the onset of these illnesses
About 50% of patients with Dementia with Lewy Bodies have REM sleep behavior disorder, which consists of
running, punching, and similar motions while asleep
DLB is similar to extrapyramidal symptoms you see in Parkinson’s however DLB does not __________
repond to Parkinson’s treatment with L-dopa
-also pt will have visual hallucinations
DLB pt with visual hallucination can be treated with
- antipsychotic agents
- dopamine blockers, readily produce pronounced extrapyramidal signs
- small amounts of antipsychotic agents can cause EPS (extrapyramidal symptoms)
DLB treatment- what to give for cognitive function and visual hallucinations
Cholinesterase inhibitors stabilize or improve cognitive function and reduce visual hallucinations for several months
DLB treatment- what will help REM sleep behavior disturbance
Long acting benzodiazepines, such as clonazepam, suppresses the REM sleep behavior disturbance
Neurocognitive disorder due to Parkinson’s
- Established Parkinson’s Disease prior to cognitive decline
- Many diagnosed in their 60s, mild neurocognitive disorder occurs early but does not progress to major neurocognitive d/o until late
- Apathy, depressed/anxious mood, hallucinations/delusions, change of personality
- Lewy bodies present
Vascular Dementia
- Clinically consistent with vascular etiology:
1. Onset of cognitive deficits is temporally related to cerebrovascular event
2. Evidence for decline is prominent in complex attention and frontal-executive tasks
3. Evidence of the presence of cerebrovascular disease
4. History, physical exam, and/or neuroimaging
5. Classically is acute stepwise decline in cognition
Vascular Dementia risk factors
- HTN, DM, obesity, smoking, high cholesterol, high homocysteine levels
- Diagnosis: MRI/CT
Med to give for Vascular Dementia
Because of frequent comorbidity of Alzheimer’s Disease, cholinesterase inhibitors provide symptomatic benefit in vascular dementia
see comparative chart
slide 30, screen shot in folder
Traumatic Brain Injury
- LOC, post-traumatic amnesia, disorientation, neurological signs
- Emotional and personality changes, physical sx (tinnitus, dizziness, fatigue)
- CT/MRI– not always, but may reveal petechial hemorrhages or evidence of contusion
HIV
- Need documented infection with HIV
- 25% of pts with HIV have mild neurocognitive D/O
- Risk: poor control of HIV
- CSF – high viral load; MRI- cortical thinning, ↓ brain volume, ↓ white matter
Prion Disease
- Rapid progression; most common is Creutzfeldt-Jakob
- triad of dementia, myoclonus, and distinctive EEG patterns
- CSF: 14-3-3 protein and tau protein
- MRI: multifocal gray matter hyperintensities
Huntington’s
- CAG repeats on chromosome 4
- 50% will develop dementia
- MRI- volume loss in basal ganglia
Treatment for vascular dementia
KNOW!
- preventative measures: diet and exercise, control of HTN/DM, statins may slow progression
- Cholinesterase inhibitors (donepezil, rivastigmine, galantamine, tacrine); Increase Ach, modest improvement in memory and goal-directed thought
- NMDA antagonist - (Memantine); Protects neurons from excessive glutamate activity, which may be neurotoxic
Psychosocial intervention:
Reduce stressors, education of caregivers, safety (assess driving, prevent wandering, reduce risk of falls)
How to manage agitation
- All antipsychotics have a black box warning: Risk of increased mortality when used for dementia- related psychosis – deaths due to cardiac or infectious events*
- Antidepressants, cholinesterase inhibitors, non-pharmacologic (redirection, recreational therapy) antipsychotics, mood stabilizers, benzodiazepines
Treatment for Lewy body dementia
use quetiapine or clozaril if need to use an antipsychotic
Pseudodementia
-“Depression in old age”
-Depression occurs first, then neurocognitive deficits
Relatively abrupt onset
-Evaluation : MSE, neuropsychological testing - Lack of effort on part of the patient – “I don’t know”
Treatment for psuedodementia
Improvement with antidepressant treatment
