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SIU5 Neurology > Memory and dementia > Flashcards

Memory and dementia Flashcards

1
Q

what is an engram?

A

a physical representation or location of memory

a hypothetical permanent change in the brain accounting for the existence of memory

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2
Q

how is learning different to memory?

A

learning- the acquisition of knowledge

memory- the storage of knowledge

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3
Q

The engram - Hebb’s law

A

cells that fire together, wire together

  • Synapses strengthened by intense activity
  • memory depends on populations of interacting neurones
  • pattern of strengthened synapses defines memory
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4
Q

how does short term workiing mem form?

A

neurones innervates each other, reverberating activity

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5
Q

how is mem activated?

A

Once network of strengthened synapse formed in engram

Next time we receive a part of the input will trigger the whole network activation (smell, emotions, fear)

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6
Q

what is Long Term Potentiation (LTP)

does it have a voltage threshold

A

Glutamate produces post syn EPSP via AMPA rec, the EPSP resp gets strong and bigger after repeated stimulation gives potentiated AMPAr EPSP
YES, need enough summated AP by frequent repetitive stimulations. cant if once in a while

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7
Q

What are the requirements for inducing an LTP (ie reach the voltage threshold)

A

Need ca influx through NMDAr overcoming mg blockage

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8
Q

NMDA receptor – dual gating?

A
  • Glutamate and Mg++
  • glutamate alone - no current flows via
    NMDAr due to Mg++ blockage.
    need - large amount of glutamate release
  • repetitive activation of AMPAr cause depolarisation
  • relieves Mg++ block
  • Ca and Na influx via NMDAr
  • Ca cause threshold AP cause LTP
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9
Q

what is very important in (control of) synaptic plasticity, learning and memory

A

Mg-dependent gating

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10
Q

How is LTP manifested?

A 
post-syn:
- more AMPAr
- sensitive AMPAr, longer reaching to cell surface 
- more synapses
pre-syn:
- more amount of glutamate re per AP
- more releasing sites
- more glutamate vesicles
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11
Q

explain the MOA of LTP introduction

A

Phosphorylation of AMPAr by intracellular PKC/PKA- AMPAr become hypersensitive
pi of calmodulin- Insertion and synthesis of new AMPAr by CaMKII.
Retrograde messenger - nitric oxide NO from post-syn- increase presynaptic glutamate release, amount in vesicles.

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12
Q

Is NMDAr the only dertermining factor for LTP memory formation?

A

NO, other factors also involved e.g. Ach in AD, amines

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13
Q

LTP is induced/ expressed/ maintained by what factors?

A

Induced by NMDAr activation and Ca++
Expressed by AMPAr
Maintained by changes in no., sensitivity of post-syn AMPAr and no. of synpases. Also changes in amount, no. of Re site and amount in vesicles of glutamate from pre-syn. (NO –retrograde messenger increases the amount of glutamate release)

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14
Q

What are the 3 main types of memory:

A

procedural (action), emotional (love and fear), declarative (words and history)

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15
Q

Which brain areas in cortex are involved in memory formation:

A 
In cortex: 
temporal,  
parietal – sensory, 
cingulate - remembering emotional charged events, 
olfactory- smell, 
prefrontal- risk/planning.
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16
Q

Which brain parts are involved in each of the type of memory?

A

Procedural: cerebellum, striatum, brainstem and SC/ motor output
Emotional: amygdala, hypothalamus (sexual desire, pleasure, aggression and anger)/ hormonal, autonomic output
Declarative: entorhinal (temporal lower cortex)/ parahippocampal cortex
HIPPOCAMPUS is involved in all types of memory

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17
Q

Genetic mutations identified in early onset AD (<65 years)

A

In presenilin genes - excess gamma-secretase activity – make more A-beta42 which is MOST likely to form plaques

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18
Q

Genetic risk factor in late onset

A

ApoE4 mutations - increased aggregation

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19
Q

what happen to henry molaison (HM)’s brain? what effect does it have?

A

temporal lobes removed for epilepsy. short term memory severely affected, cannot form new memory, long-term memroy is ok

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20
Q

Cognition enhancers - smart drugs

A
  1. cholinergic modulators: anticholinesterases- donepezil (aricept), galatamine, rivastigmine [swap if 1 fail]
    agonist- nicotine
  2. stimulants: amphentamine, methylphenidate, modafanil, caffeine
  3. 5HT drugs: 5HT6 antagonists
  4. GABAa blockers: suritozole inverse agonist bc BZ cause mem lost
  5. AMPA kinase- piracetam, IDRA21
  6. mGluR5 positive allosteric modulators
  7. if ChEi fails, non-competitive NMDA blocker: memantine -neuroprotective reduce cytotoxicity
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21
Q

2 causes for amnesia

A

alcohol/drug induced

head trauma : short or long term

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22
Q

symptoms of dementia

A
  • 1st sign mem impairment
  • general cognitive decline: risk taking, impaired judgement, spatial/ visual impairment, paraphasia, psychosis.
  • inability to form new mem
  • mood swing, apathy, lost of self
  • diff completing familiar task - forget rule of game
  • confused w time and place
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23
Q

is it an age dependent disease? above what age dose it likely to happen?

A

yes, >65 1%

>95 53%

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24
Q

where in the brain does alzheimer first manifest/ affect?

A

shrinkage of temporal and frontal cortex

damage of entorhinal cortex- memory and speech

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25
Q

alzheimer’s cellular pathology, what are the diagnostic hallmarks?

A
  1. NP neuritic plaques, extracellular insoluble amyloid- beta- protein
  2. NFT neurofribrillary tangles, intracellular cytoskeletal protein tau
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26
Q

which neurones were the first to be affected/ cell death?

A

ach and glutamate

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27
Q

abnormal Amyloid precursor protein is cleaved into what component, does it exist in nomral brian?

A

amyloid-beta 40/42

not normally produced

28
Q

what enzymes instead what enzyme is presented in abnomral brain in alzheimers
what enzymes are the same in normal and abnormal brain

A

beta- secretase instead of alpha-secretase

gamma-secretase in second step are the same

29
Q

what enzymes helps enhance the aggregation of amyloid- beta protein into neuritic plaque?

A

apoE4- apolipoprotein

30
Q

possible basis of neuronal death in AD

A

A-beta neuritic plaque and metal ions CU/FE = H2O2
peroxidation of mem lipids
disruption of fucntion of rec, trans, ca channels
excess ca accumulation- cytotoxicity
cell death due to activation of enzymes lipases, caspases, proteases and free radical production O-, NO- same in stroke.
ca causes pi of tau cytoskeletal protein, formation of neurofribrillary tangles
disruption of microtubular trans,
disrupt function of transporter due to lack of right proteins- vicious cycle

31
Q

how do we slower the AD progression? what med can we use?

A

beta/ gamma secretase inhibitor
anti-amyloid-beta vaccine, mABs
anti-tau vaccine, mABs
CU and ZN cheltors
antioxidants- vitC
statins- prevent promoting amyloid deposition
diabetes drug pioglitazone (Actos) because it may lessen beta-amyloid and inflammation in the brain
oestrogen based hormone therapy during menapause

32
Q

AD biomarks are most detectable at what stage?

what are the three method used to detect them at different stages of AD?

A

most detectable in EARLY stage! conc of biomarkers decreases over time!
imaging (brain)- lumbar puncture (ICF)- blood drawing

33
Q

what are the criteria required by DSM-IV before a diagnosis of dementia of the Alzheimer type may be assigned. Additionally the term “early onset” is applied to patients who are 65 years old or less and “late onset” to those who are over 65.
A, B, C, D, E- ellusion, F

A

A Development of both 1) memory impairment 2) one (or more)of the following: aphasia, apraxia, agnosia- failure to recognise things despite nomral sensory function, disturbance in executive functions ie planning, solving problems
B Deficts causing significant impairment in social and occupatinal function
C Characterised by gradual onset and continuing decline
D Not cuased by other reasons like vitb12 deficiency, hypotheroidim, other CNS disease or substance misuse
E The deficist do not occur only during the course of delirium
F The disbance is not better accounted for by another disorder eg depression, or schizophrenia

34
Q

risk factors of AD

A
  • Increasing age
  • family history - familial Alzheimer’s disease (FAD) of late onset is associated with the ApoE є4 allele on chromosome 19- NP (NOT a diagnositc tool)
  • People with Down’s syndrome
  • Early onset AD is associated with the following genes: presenilin1 (chromosome 14), presenilin gene 2 (chromosome 1) and the APP gene (chromosome 21).- more gamma secretase- amyloid-beta42- NP
35
Q

other risk factors of AD

what reduces the risk?

A

Head trauma
Gender – female more susceptible
Envrionmental toxin as neurotoxin – alcohol intake, pesticides
High intraneuronal ca level – cytotoxic
Education and ongoing intellectual acitvity reduce the risk

36
Q

DEMENTIA (conditions to be excluded before diagnosis of dementia is made. conditions that can be treated)

A 
D	-	Drugs/medication
E	-	Emotional problems, eyes, ears
M	-	Metabolic
E	-	Endocrine					
N	-	Nutritional deficiency
T	-	Tumour					
I	-	Infection
A	-	Anaemia or alcohol
S	-	Systemic disease
37
Q

How to reduce the risk of having dementia?

A 
Lower cholesterol 
Reduce BP
Control diabetes
Lower homocysteine level (you get it from meats, also means low level of vitb12, low folate, high level of homocysteine is a RF for heart disease)
Exercise regularty throughout life
Engage in intellectual activities
Dancing and learning languages 
reduce alcohol intake 
smoking cessation
38
Q

antipsychotics are contraindicated in which type of dementia?

A

lewy body dementia

39
Q

what are the symtpoms for lewy body dementia?

A

Fluctuating (cognition) periods of confusion with
visual hallucinations
early gait disturbances (falls++) (like parkinsons walk)
extrapyramidal features such as rigidity, bradykinesia, tremor and fixed posture
Visuospatial and frontal deficits
Memory impairment is often less than in the other dementias in the early stages

40
Q

how to distinguish PDDparkinson disease dementia and DLB dementia lewy body?
not clinically sig tho, no diff in trt

A

PD pt who develop a dementia > 12 months after the initial motor symptoms occur should be diagnosed as PDD.
If the dementia before the motor symptoms, or the duration of the motor symptoms is < 12 months before the dementia occurs then the diagnosis is DLB.

41
Q

Disgnostic indicators for DLB

A

Reduction in choline acetyltransferase ChAT (similar to AD)
Loss of DA in NS pathway (similar to PD)
Lewy bodies in automic ganglia- postural hypotension, in cortex- cognitive failure and psychosis
Muscarnic rec preserved due to absence of NFT

42
Q

s/e of ChEi eg. donepezil

A

Parasympathomimetic
ACh bind to muscarinic rec (m1,3,5 stimulstory, 2,4 inhibtiory)
M1 - increase gastric juice GI problems
M2- decrease HR, CO
M3- bronchocontrisction- syncope care in asthma;COPD
muscle cramps

43
Q

like PD medicines, (L-DOPA), ChEi will have no long term efficacy and effect will reduce as AD progresses because

A

there are less ACh neurones eg NicR to receive the ACh

less Ach will be produced

44
Q

What are the other things you can eat that helps with dementia (despite lack of evidence)

A

Gingko biloba – increase BF via vasodilation, decrease blood viscosity, decrease free radicals
Antihypertensives and statin useful in VaD
Thiamine – if deficit
Fish oil – improve congitive function
Aspirin – prevent futher ischeamia/ TIA

45
Q

role of pharm in dementia

A
  1. recog symptoms: forgetfulness
  2. refer to GP
  3. establish link to local Dementia Advisor
46
Q

What is the only trt that is licenced for aggression in AD if all other trt fails? what is the recommanded duration

A

Risperidone, max duration 6w

47
Q

Should antipsychotics be used to treat aggreassion and psychosis in dementia? why?

A

yes, Moderate efficacy if use over 12 w
But increased CVR and stroke, death
Not effective for longer term trt
So non-pharmacological trtr should be used, there is evidence supporting efficacy

48
Q

What are the emerging safer pharm trt for aggression in dementia

A

Memantine, carbamazapine and citalopram

49
Q

what are the clinical presentation for VAD?

A

VAD: sudden onset, step wise progression, due to hx of stroke, TIA, focal neurological deficit, patchy cognitive impairment (can be agnosia, apraxia, dysathria), depression, night confusion
preserved insight!

50
Q

non-pharm trt for behaviour change in dementia patient eg depression, anxiety and agitation

A
  • Reality orientation (put clock and watch by the bed/ open curtain during the day, draw curtain and use small table lamp during night)
  • talking therapies- Behaviour intervention (CBT)
  • Occupational activities:
  • Environmental modifications- may be moved from hospital to care home, try keep similar setting of for the room if that is the trigger, try keep the same staff (new unkown staff might trigger anxiety?)
  • Validation therapy
  • Reminiscence
  • Sensory stimulation- give book to read, watch tv to distract the attention
  • increase Social interaction- esp in care home, have relatives/carers visit
  • join support groups like alzheimers society
  • Sleep hygiene: Re-establish bed time routine by reading a book, drinking hot chocolate, sleeping in a cool room.
51
Q

OTC med that helps w behaviour disorder due to dementia

A 
AChEI or memantine
Try lavender or melisaa oils- lemon balm
aromatherapy
diffuser 
drops on pillow
Nytol has Diphenhydramine, is structurally related to antipsychotics, sedative antihistamines(allergy) help with sleep
52
Q

How do we support medicine takers with poor memory?

A
  • set alarm clock on phone to remind them take medication
  • write diary as a memory aid
  • calendar on fridge, doors with chart for medications
  • telephone call from family
  • carers
  • keep an eye on medicine usage (collection, returns) be proactive
53
Q

what is delirium? what is it also called?

A

an ‘acute congitive impairment syndrome’
‘acute confusional state’, ‘ intensive care psychosis’ and ‘organic brain syndrome’
it is a cognitive impairment WITH lost of conciousness developed over short time (hr to days)

54
Q

how does delirium differ from dementia?

A

dementia is an acquired generalised impairment of cognitive functions: memory, intellect and personality. withOUT loss of conciousness. ALERT

55
Q

which medical unit has the highest rate of delirium occurance?

A

intensive care unit `

56
Q

what factors precipitate delirium?

A 
MediCapU
Medicines CNS acting -anticholinergic, BZ, TCA, TT, morphine
Electrolytes imbalance (low na)
Dehydration
Infection
Constipation/impaction
Alcohol, anti-D, anxiolytic w/d
Pain
Urinary retention
57
Q

Confusional states (delirium) often present with

A

disturbed

disinhibited: restlessness, oversensitive to stimuli
frightening: lethargic, quiet

58
Q 
What are the current prevention strategies for delirium?
SOFTES
s- stimuli (tv, book)
o- orientation
f- family support, fall risk ass
t- trigger
e- envrionemtn
s- sleep hygiene
A

Maintain competenece by encourging physical activity, using stimulatant eg radio, tv
provide orientation by having clocks, calendars around
Provide support by family visit
Remove potenital delirium triggers eg pain, dehydration, infections, one nurse per shift, reduce med, avoid anti-cho drugs
Provide an unambiguous environment by mangeing light brightness, noise level, temperature during day and night
Train good sleeping hygiene, sleep around the same time after hot chocolate in a cool dark room

59
Q

describe what is a emotional lability

A

rapid and unpredictable shift from one emotional state to another

60
Q

what are the clinical presentation of delirium?

A

Disorientated in time, place, person (reversed ‘sleep-wake cycle’)
Emotion liability - rapid MOOD change (restlessness to lethargic)
Level of consciousness (fluctuated throughout day)
Integration (impaired perceptions, visual hallucinations, slowed thought process)
Rapid onset (hr to days)
Irrelevent stimuli (change of nurses, wards, poor concentration, easily distractable w books etc)
Utterance (incoherent speech)
Memory loss (short-term)

61
Q

assessment for delirium

A
  • Hx of delirium, what was the trigger
  • physical exam: infection, dehydration?
  • AMTS- abbreviated mental test score
  • Confusion Assessment Model (CAM)
62
Q

how is delirium different from psychotic disorder?

A
  • lost of memory
  • disorientation
  • fluctuated
63
Q

describe the Confusion Assessment Model (CAM)

A
  • acute onset and flucuating course of confusion AND
  • inattention AND/OR EITHER
  • unorganised thinking
  • altered level of consciousness
64
Q

Treatment of Delirium

A
  • 1st line: non-pharm options
  • treat underlying cause eg infections
  • review/ stop any med that exacerbates symp
  • prevent harming behaviour to self and others
  • prescribe non-cholingeric antipsychotics
65
Q

If a person is a risk to themselves or others…what trt to use
is elderly pt good with antipsyc?
what conditions are contraindicated

A

short-term (usually for 1 week or less) haloperidol/ olanzapine
start low go slow
elderly sensitive to antipsychotics adverse effects especially sedation- falls
contraindicated in PD, LBD

66
Q

why long term antipsychotics are not recommended in delirium?

A

stroke increased by over 3-fold with risperidone or olanzapine
more than doubled with any other atypical antipsychotic agent.

SIU5 Neurology (13 decks)

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