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Flashcards in Dementia & Memory Deck (18)
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1
Q

Why is memory described as plastic?

A

Able to change and strengthen neuronal connections in order to form new memories

2
Q

How does short-term memory become long-term memory?

A

Consolidation

  • emotion
  • rehearsal
  • association
  • automatic

Long-term potentiation:

  • glutamate (NMDA receptors)
  • hippocampus

Long-term depression: weakening of infrequently used synapses

3
Q

Outline the formation, interpretation, and storage of memory.

A

Senses —> cortical sensory areas

FORMATION:
Cortical sensory areas —> amygdala and hippocampus

INTERPRETATION:
Amygdala and hippocampus —> diencephalon, basal forebrain, and pre-frontal cortex

STORAGE:
- diencephalon, basal forebrain, and pre-frontal cortex —> cortical sensory areas

4
Q

Contrast retrograde and anteretrograde amnesia.

A

Retrograde amnesia e.g. Alzheimer’s disease
= failure to retrieve old memories

Anteretrograde amnesia e.g. lesion in hippocampus
= failure to form new memories

5
Q

Give some examples of causes of amnesia. How does the onset time vary?

A

Alzheimer’s disease

Vascular interruption

Tumours

Trauma

Infection

Wernicke-Korsakoff syndrome —> confabulate to fill gaps in memory

ECT —> lose sense of identity

TIA —> transient global amnesia

6
Q

What is the definition of dementia?

A

Chronic and progressive deterioration of behaviour and executive functions due to organic brain disease

Acquired loss of cognitive ability sufficiently severe to interfere with normal functions and quality of life

7
Q

What are the diagnostic criteria for dementia?

A

Cognitive/behavioural symptoms which:

  • affect ability to function in normal activities
  • represent a decline from a previous level of function
  • cannot be explained by delirium or other major psychiatric disease
  • has been established by history-taking from patient and informant, and formal cognitive assessment

Involves impairment of at least two of:

  • ability to acquire and remember new information
  • judgement
  • ability to reason or handle complex tasks
  • visuospatial ability
  • language functions
  • personality
  • behaviour

Rate of progression depends on primary cause of tissue degeneration

8
Q

Describe the pathophysiology of vascular dementia.

A

e.g. stroke

Stepwise progression of cortical damage

Subcortical damage to connecting neurones

S&S:

  • rigidity of thinking
  • apathy
  • personality changes
9
Q

Describe the epidemiology, pathophysiology, and symptoms of Alzheimer’s disease.

A

EPIDEMIOLOGY:

  • 47% over 85yrs
  • 2:1 female:male
  • prognosis of 5yrs

Insidious onset (affects memory - hippocampus - first)

S&S:

  • unsure of things
  • repeating questions
  • apathy
  • short-term memory problems (hippocampus; can usually remember events from childhood clearly)
  • difficulty recognising objects and faces (temporal lobe)
  • become lost; dressing dyspraxia (parietal lobe)
  • passivity; inability to initiate, carry on, and sequence tasks; loss of social functions, incontinence (frontal lobe)

PATHOPHYSIOLOGY:

  • beta-amyloid deposits in brain
  • global cortical atrophy
10
Q

Describe the epidemiology, pathophysiology, and symptoms of Lewy body dementia.

A

EPIDEMIOLOGY:

  • ~4%-10%
  • 1:1 male:female
  • 8yr prognosis after initial symptoms

S&S:

  • Parkinsonism
  • prominent visual hallucinations
  • delusions
  • paranoia
  • REM sleep behaviour disorder (no muscle atonia —> act out dreams which are freq. frightening/violent)
  • haloperidol sensitivity —> worsening movement difficulties, speech/swallowing problems

note: fluctuates in severity from day to day (differentiates from delirium)

PATHOPHYSIOLOGY: alpha-synuclein deposits

11
Q

Describe the epidemiology, pathophysiology, and symptoms of fronto-temporal dementia.

A

Includes Pick’s disease, primary progressive aphasia)

EPIDEMIOLOGY:

  • 1:1 male:female
  • family history in ~10%-15%
  • may be associated with movement disorders e.g. motor neurone disease, progressive supranuclear palsy
S&S: 
BEHAVIOURAL VARIANT: 
- loss of inhibition 
- inappropriate social behaviour 
- loss of motivation without depression
- loss of empathy/sympathy 
- change in preferences 
- repetitive/compulsive/ritualistic behaviours 
- loss of control over eating/drinking 
- difficulties with planning, organisation, and decision making 
- lack of insight 
- incontinence 
- loss of awareness of personal hygiene 
- perseveration 
- mutism 
- echolalia 
SEMANTIC:
- loss of vocabulary with fluency of speech 
- asking meaning of familiar words 
- loss of recognition of familiar faces/objects 
PROGRESSIVE NON-FLUENT: 
- slow, hesitant, difficult speech 
- grammatical errors in speech 
- impaired understanding of complex sentences 
- loss of literacy skills 

+ memory preserved in early stages
+ crave sweet/fatty food
+ lose table etiquette

PATHOPHYSIOLOGY: tau inclusion bodies

12
Q

Give some examples of causes of dementia.

A
ACUTE e.g viral encephalitis
SUBACUTE e.g. sporadic CJD 
MEDIUM e.g. normal pressure hydrocephalus 
CHRONIC 
- Alzheimer's 
- Lewy body dementia 
- fronto-temporal dementia 
- vascular dementia

INFECTION: CJD, HIV, viral encephalitis, progressive multifocal leucoencephalopathy (JC virus)

METABOLIC: hepatic disease, (para)thyroid disease, Cushing’s

NUTRITIONAL: Wernicke-Korsakoff syndrome (thiamine deficiency), B12/folate deficiency

TUMOUR: e.g. subfrontal meningioma

CHRONIC INFLAMMATION: collagen vascular disease, vasculitis, MS

TRAUMA: heady injury, punch drunk syndrome

DRUGS/POISONS

Normal pressure hydrocephalus

13
Q

What is punch drunk syndrome?

A

Seen in boxers and alcoholics

Caused by repeated cerebral contusions

Characterised by:

  • weakness in lower limbs
  • unsteadiness of gait
  • slowness of muscular movements
  • hand tremors
  • hesitancy of speech
  • mental dullness
  • dementia
14
Q

What is normal pressure hydrocephalus?

A

Abnormal build-up of CSF in ventricles (usually due to global cortical atrophy) causing ventriculomegaly

CSF pressure remains normal (communicating hydrocephalus)

Causes dementia, dyspraxic gait, urinary incontinence

15
Q

What are some important investigations in dementia?

A

FBC

Electrolytes, Ca2+, glucose, renal function, liver function

Thyroid function

Serum vitamin B12 and folate

Midstream urine (?delirium caused by UTI)

CXR or ECG if indicated

MRI/CT to detect subcortical vascular changes and focal atrophy

16
Q

Where is memory stored?

A

Stored throughout cortex e.g. visual memory in visual cortex, auditory memory in auditory cortex

Declarative memory (e.g. name, DOB, address) stored in hippocampus and cortical regions

Procedural memory (e.g. tying shoelaces, riding a bike) stored in cerebellum, pre-motor cortex, and basal ganglia

17
Q

What form of memory appears first in development?

A

Declarative memory - info retrieved from long-term storage into consciousness

18
Q

What structures of the CNS are involved in procedural memory?

A

Procedural memory - expressed as a motor skill

  • cerebellum
  • putamen
  • caudate nucleus
  • motor cortex