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Flashcards in Stroke/Dementia Deck (13)
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1
Q

neuroimaging techniques for TBI

A
  • Xray
  • CT scans
  • MRI
  • Intracranical pressure monitoring
2
Q

Long term problems with PBI

A
  • White (axon bodies) + Grey (neuron ends) = degeneration long after injury (Sidaros et al., 2009).
  • Diaschesis
3
Q

Lesions (2)

A

** CAN COME FROM CLOSED OR PENETRATING HEAD INJURY**

Focal:

  • enclosed to one area of brain; they are circumscribed areas of injury to brain tissue following brain injury.
  • often cause SPECIFIC deficits bc they’re not wide spread
    a) focal closed head = assoc. with vasucalr damage. Hemorrhages/tumors/bruising
    b) Focal penetrating injuries = when an object penetrates the skull and directly injures an area of the brain.

Diffuse:

  • spread out; diffuse injury could go unnoticed cos it’s microscopic
    a) Diffuse axonal injury (DAI) – axons get snapped; doesn’t show up v well on brain scans
    b) Diffuse ischemic injury – when an are of the brain is starved of oxygen = cerebral anxoia)
4
Q

STROKE

what?

A

loss of bloody supply -> some loss of function

  • ischemic = blocking of artery by a thrombus
  • haemorrhagic = bursting of an aneurysm
    ^ 2 major consequences: because you’re leaking blood the destination will not get any blood to it & also the blood that you’re leaking out = problematic, pushes on brain tissue + causes damage that way

CAUSED BY

  • heart attack
  • atherosclerosis
  • arterial fibrillation
5
Q

DEMENTIA

what

A

**Can’t be definitively defined until autopsy

  • overall term for a collection of symptoms
  • Damage and neurodegeration to brain cells; inability to connect with each other
  • Alzheimer’s is the most common type of D = neurofib plaques and tangles
  • multi-infarct/vascular dementia = occurs after stroke
  • Lewy body dementia = inclusions in neurones called lewy bodies
6
Q

Alzheimer’s + neurofib plaques

A

The amyloid cascade hypothesis,

PLAQUES = amyloid is normally broken off and disposed of in the brain (i.e. broken down) BUT in alz it isnt + SO β-amyloid (Aβ) accumulates and forms these plaques.

TANGLES = tau protein holds the structure within the signalling neurons. BUT in D tau dislodges from the skeleton and combines together. The skeleton disintegrates and the neuron dies. The high amount of tau creates the NFT + this causes neuronal death.

one does not come without the other; Some say that the plaques cause tangles cos they block the synapse

Wang et al. (2016)//Skaper (2012)//Bloom (2014) = all say its the cause not consequence of dementia

7
Q

Brain regions affected in Alzheimer’s

A

a) STM goes firs: hippocampus + STM (Bn-Yakov & Dudai, 2011)
b) Then spreads to cerebral cortex affecting:
- Language areas: Cappa + Perani, 2003
- Reactive aggression + executive functioning: Herron (2017)
- Dorsal lateral pfc: working memory (Postle, 2006)
- Visual perception: occipital and temporal lobes (Rolls, 2000)
- Eventually starting to target more long term memories ingrained deep in the cerebral cortex (frontal and parietal) (Reed & Squire, 1998).

8
Q

Cognitive decline in dementia

what are the main 6 key symptoms? Says who?

A
  • While symptoms of dementia can vary greatly, at least TWO of the following core mental functions must be significantly impaired to be considered dementia:

a) Memory* (key feature)
b) Communication and language (aphasia)
c) Ability to focus and pay attention (ex functioning)
d) Reasoning and judgment (ex functioning)
e) Visual perception (agnosia)
f) awareness of environment (links with volition in ex functioning)

^ ICD 10 (World Health Organization. (1992).

9
Q

stage ONE: screening

  • MMSE
  • mini cog
A

1) Mini mental state examination (memory/language/attention)
- help diagnose dementia and to help assess its progression and severity.
- Series of Qs and tests

ADVANTAGES:

  • quick + easy
  • provide method of monitoring deterioration over time

DISADVANTAGES

  • biased to those with poor education (language and math elements)
  • not v good @ detecting those with a mild cognitive impairment (Arevalo-Rodriguez et al. 2015)

SO
mini cog
1. Remember and a few minutes later repeat the names of three common objects
2. Draw a face of a clock showing all 12 numbers in the right places and a time specified by the examiner

ADVANTAGES

  1. little potential for bias in terms of education or language (Borson 2005).
  2. Less affected by subject ethnicity, language, and education, and can detect a variety of different dementias.
  3. ALSO, detects many people with mild cognitive impairment (cognitive impairment too mild to meet diagnostic criteria for dementia) (Tsoi et al. 2015)
10
Q

stage TWO: one battery for assessing for dementia

A

CERAD – morris et al. 1989

  • Memory and verbal fluency mainly: delayed recall of words, verbal fluency tests EG boston naming test.
  • Generally: performance is affected by age + education. To a lesser degree, sex (Berres et al. 2000)
  • Id Alz subtypes (Fisher, 1999)
  • Translated into many languages (Cho et al. 2008)
  • Widely used in studies of the neuroanatomical findings of Alzheimer’s (Dos Santos et al. 2011)

**Doesn’t directly include tests of planning tho…

11
Q

Further testing of dementia - memory + fluency

A

Verbal fluency tests (language + executive functioning skills “PRIMARILY FLEXIBILITY”) – ability to switch from one demand to another (Lezak, 2012)

  • **Fuld object-memory evaluation (Fuld, 1980)
    a. Name and describe each 10 objects that they are feeling in a bag (tactile naming)
    b. After each response, the object is removed from the bag and the patient is asked to name the object if tactile naming failed
    c. NEXT is the verbal fluency test = Say as many names as they can think of in one min (same sex as patient) (serves as a distractor) (rapid semantic retrieval)
    d. Then required to recall items from the bag previously

fluency trials: food, what makes people happy/sad, vegetables

12
Q

EVAL FOME

A
  • memory components are relatively immune to confounding effects of education and cultural differences = few significant educational, cultural, SES effects have been reported (E.G. Avila et al. 2009)
  • BUT there is relationship between semantic fluency performance and and education + cultural background (Fuld et al. 1988)
  • Need to be at least 70yrs old or will get ceiling effects
  • Can be used across languages and w children (Chung, 2009)
  • Had good predictive abilities – 85% of healthy subjects could be identified as having 85% probability of developing dementia after 4 years.
  • The overlap in scores made my elderly depressed patients and those with dementia was considerable i.e. cant discriminate between elderly depressed and multi infarct dementia (La rue, 1989)

HOWEVER
- Others have found that the scores between elderly participants: depressed patients scores were closer to those of normal controls on FOME measures compared with dementia patients scores (La Rue, 1986)

13
Q

The battery doesn’t look @ Decision making & planning

A

A. TOWER OF LONDON/HANOI
frontal lobe dementia - slower solution times + made more moves/trial and error strategy (Carlin, 2000) –> due to the central executive’s role (DLpfc) in organising wM (Postle, 2006)

  • *ANOTHER REASON WHY THEY MIGHT BE BAD AT HANOI
  • also measures disinhibition = dementia have problem w this - presenting as impulsive and impetuous behaviours that are often difficult to manage
  • And some have suggested that tower of Hanoi is more about inhibiting a prepotent response. This has been supported (Miyake et al. 2000) who showed that response inhibition contributes to success

BUT
- Tower of london cant discriminate Alz dementia from frontal temporal dementia (Valverde et al. 2009)

SO

  • Porteus maze
  • Sensitive to Alz patients but some overlap did occur between Alz and controls (Mack & Patterson 1995)