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NEURO 210 > Lecture 16: Dementia and Memory > Flashcards

Lecture 16: Dementia and Memory Flashcards

1
Q

What is dementia?

A

global deterioration of intellectual function in the face of unimpaired consciousness

impossible to tell if they have dementia if they re unconscious

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2
Q

How do we approach and evaluate someone with dementia?

A

general medical history

general neurological history

neurobehavioral history

psychiatric history

toxic, nutritional and drug history

family history

objective examination: physical, neurological, neuropsychological

family members bring them in for treatment, not the patients

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3
Q

What are bedside tests for the assessment of mental state?

A

administer at clinic, objective measure of decline over time

mini-mental status examination (MMSE) and Montreal objective cognitive assessment (MOCA)

MOCA: score of 30 is max, lower the score the greater the impairment

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4
Q

What are the domains of cognition that are tested when assessed a patients mental state?

A

level of consciousness: i.e. alert, drowsy, stuporous, etc.

orientation: time, place, person

memory: remote, recent, immediate (3 object recall), same thing they do at bedside

attention and concentration: (serial 7’s, digit span), ability to concentrate on the task at hand

knowledge, insight

language: fluency, comprehension, repetition, object naming, tests for apraxia, reading, writing

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5
Q

What are some general characteristics of the symptoms of dementia?

A

symptoms of dementia reflect the part of the brain that is affected

patients with dementia frequently exhibit visual-spatial difficulties indicating involvement of the parietal cortex

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6
Q

How do reflexes indicate dementia symptoms?

A

neurological examination frequently reveals abnormal reflexes related to dysfunction of the frontal lobes

primitive reflexes found in infants return in dementia

frontal lobe dysfunction

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7
Q

What is the pout reflex?

A

tap lips with tendon and hammer, a pout response is observed

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8
Q

What is the glabellar reflex?

A

patient cannot inhibit blinking in response to stimulation (tapping between eyes)

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9
Q

What is the grasp reflex?

A

stroking palm of hand induces “grasp”

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10
Q

What is the plamo-mental reflex?

A

quick scratch on palm of hand induces sudden contraction of mentalis muscle in face

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11
Q

What are two ways to think of causes and types of dementia?

A

the part of the brain that is mostly affected, e.g. frontal (anterior) versus parietal (posterior) lobes/cortex

that rapidity of progression of the dementias

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12
Q

What does damage to the anterior (frontal) lobe cause in terms of dementia?

A

frontal pre-motor cortex

behavioral changes/loss of inhibition, antisocial behavior, facile and irresponsible (less executive function)

other dementias, frontotemporal dementia (Pick’s), Huntington’s disease (areas deep in the brain are affected)

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13
Q

What does damage to the posterior (parietal) lobe cause in terms of dementia?

A

parietal and temporal lobes

disturbance of cognitive function (memory and language) without marked changes in behavior

Alzheimer’s disease (in the end if affects the whole brain)

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14
Q

What is the intellectual decline pattern of encephalitis?

A

acute (weeks)

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15
Q

What is the intellectual decline pattern of Creutzfeldt-Jackob (mad cow disease)?

A

subacute (months)

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16
Q

What is the intellectual decline pattern of normal pressure hydrocephalus?

A

chronic (years)

difficulty controlling bladder and walking affects ventricles and CSF

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17
Q

What is the intellectual decline pattern of Alzheimer’s disease?

A

chronic (years)

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18
Q

What are examples of degenerative dementias?

A

Alzheimer’s disease

Lewy body dementia

Tauopathies, frontotemporal dementia (Pick’s disease, progressive supranuclear palsy)

Huntington’s disease

Parkinson’s disease

Wilson’s disease (problem with copper binding proteins)

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19
Q

What are examples of cerebrovascular dementias?

A

vascular dementia (multi-infarct dementia)

CNS vasculitis

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20
Q

What are examples of structural dementias?

A

normal pressure hydrocephalus

brain tumor

head injury

subdural hematoma

21
Q

What are examples of infection caused dementias?

A

Creutzfeldt-Jacob disease

neurosyphilis, others

HIV

sequelae of viral encephalitis

22
Q

What are examples of toxic/metabolic dementias?

A

drug induced, treatable

alcoholism

toxins, heavy metals, CO

vitamin deficiencies (B12, thiamine, folate)

hypothyroidism

uremia and dialysis-related

hepatic encepgalopathy

23
Q

What are examples of immune disorder and cancer caused dementias?

A

lupus, paraneoplastic disease

24
Q

What is the relationship between dementia and depression?

A

frequently accompanies and clouds assessment of dementia

25
Q

What are the laboratory investigations for dementia?

A

complete blood count, thyroid function tests, B12 level, folate, serum electrolytes, glucose, urea, creatinine, calcium, liver function tests, toxicity screen for drugs (prescription and otherwise)

test for syphilis and HIV

optional: neuroimaging (CT/MRI), EEG, cerebrospinal fluid exam

26
Q

What are common themes that run in neurodegenerative dementias?

A

there is usually an age-dependent progression and worsening of dementia reflecting loss of neurons and their connections in the CNS

some parts of the brain and neurons within these regions are more vulnerable to the insult (whatever it happens to be)

proteins, that are misfolded and abnormally deposited in specific brain areas seem to play a key role in these diseases

for most part, precise cause(s) unknown and hence no definitive treatment available to stop progression of disease

27
Q

What is Alzheimer’s disease?

A

is an irreversible, progressive brain disease that slowly destroys memory and thinking skills

although the risk of developing AD increases with age (in most people with AD, symptoms first appear after age 60), AD is not a part of normal aging

it is caused by a fatal disease that affects the brain

28
Q

How does Alzheimer’s affect neurons?

A

the brain has billions of neurons, each with an axon and many dendrites

to stay healthy, neurons must communicate with each other, carry out metabolism, and repair themselves

AD disrupts all three of these essential jobs

affects neurons processes and ability to metabolize

29
Q

What is the prevalence of Alzheimer’s disease?

A

most common cause (70-80%)

7-9% of Canadian population over 65 have AD, 35.5% of population over 85 have AD

4.5 million people in US and Canada have AD

40% of total health care cost associated with neurological diseases (billions of $)

30
Q

What are the symptoms of Alzheimer’s?

A

impairment of memory and attention

language and communication

abstract thinking

judgement

personality changes

depression

visuo-spatial disorientation (difficulty orienting in space)

31
Q

What are the signs of Alzheimer’s?

A

motor and gait disturbance

poverty of movement and slowness

falls

problems with bladder and bowel control

seizures

32
Q

What is the age of occurrence of Alzheimer’s?

A

most cases occur usually late 60’s or later

33
Q

What is the etiology of Alzheimer’s?

A

familial forms: less than 10% of cases

sporadic (cause unknown): majority of cases >90%

early onset (40s and 50s): usually familial and associated with susceptibility genes that include mutations of amyloid precursor protein (APP), Presenilin 1 & 2 mutations

late onset (60s or later): mostly sporadic; Apolipoprotein E4 gene is the main susceptibility gene, some other genes identified recently

34
Q

What is the neuropathology of Alzheimer’s?

A

cortical atrophy

synaptic and neuronal loss

neurofibrillary tangles (NFTs) with paired helical filaments, abnormally hyperphosphorylated forms of microtubule-associated protein, tau

neuritic plaques with amyloid core

amyloid angiopathy

tau and amyloid are key features

35
Q

What is cortical atrophy?

A

shrinkage of the brain

not specific to AD

36
Q

What are the two abnormal structures that people with Alzheimer’s disease?

A

beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells

neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell

37
Q

How are amyloid depositions formed?

A

membrane protein that sits in the membrane and extends outward, it is thought to be important for neural growth, survival and repair

enzymes referred to as secretases (think of them as scissors) cut the APP into fragments, the most important of which for AD is called beta-amyloid

beta-amyloid is “sticky” so fragments cling to together along with other materials outside of the cell, forming plaques seen in the AD brain and is toxic to neurons

38
Q

What are neurotransmitter abnormalities in Alzheimer’s disease?

A

decrease in chemical messengers in the brain especially acetylcholine (cortex, hippocampus)

39
Q

How to cholinergic drugs treat Alzheimer’s?

A

increase release of Ach

if AchE is inhibited then Ach will be broken down slower

40
Q

What are examples of cholinergic agents?

A

cholinesterase inhibitors

donepezil (Aricept)
rivastigmine (Exelon)
galantamine (Reminyl)

41
Q

What are examples of non-cholinergic agents?

A

memantine (Namenda, Ebixa), a glutamate receptor (NMDA) blocker

42
Q

What are other possible treatments for Alzheimer’s?

A

amyloid vaccine

secretase inhibitors

anti-amyloid agents

drugs that lower cholesterol

43
Q

What are unproven treatments for Alzheimer’s?

A

estrogens, NSAIDs, vasodilators, propentofylline

44
Q

What are some non-drug approaches to treating Alzheimer’s?

A

higher education

intellectual stimulation

exercise and diet (improves cardiovascular)

red wine ?

45
Q

What is dementia with Lewy bodies?

A

fluctuating cognition with pronounced variation in attention and alertness

recurrent visual hallucinations

Parkinsonian features (rigidity or stiffness in muscles, slowness and poverty of movement, tremor)

treatment with cholinesterase inhibitors, antipsychotic drugs (to control behavioral problems and agitation)

loss of pigmented (dopamine-containing) neurons in the substantia nigra in PD and DLB

46
Q

What are Lewy bodies?

A

contain abnormal alpha-synuclein protein

47
Q

What is frontotemporal dementia (Pick’s disease)?

A

female preponderance and at a younger age than AD

focal frontal and temporal lobe atrophy

disinhibition, apathy, perseveration, mental rigidity and affective symptoms

Tau pathology most frequently observed

familial forms: gene on chromosome 7

some forms associated with another neurodegenerative condition: ALS or Lou Gehrig’s disease

no curative treatment

atrophy (shrinkage) of frontal and temporal lobes

high number of Pick bodies (containing tau protein)

48
Q

What is vascular dementia?

A

accounts for 10-15% of dementias

dementia occurs “stroke by stroke” with progressive focal loss of function (“step-wise” function)

risk factors that cause stroke are present: hypertension, diabetes, high cholesterol, smoking

may occur concurrently with neurodegenerative dementia

CT scan may show multiple areas of cerebral infarction

treatment of hypertension and other vascular risk factors

multiple small strokes

NEURO 210 (23 decks)

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