Week 6 - Changes Across The Lifespan Flashcards

1
Q

Classifying tests of cognition

A
Fluid abilities:
Proficiency in…
-Reasoning 
-memory 
-speed
Designed to assess efficiency or effectiveness of processing at the time of assessment.
Crystallised abilities:
Evaluations of
-General knowledge
-Vocabulary
-Acquired knowledge
Designed to assess cumulative products for processing carried out in the past
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2
Q

Cognitive ability

life outcomes

A

Cognition – mortality relations: decreased risk of early mortality with high early life cognitive ability
Better general health
Lower depression scores
High cognitive ability at age 11, less psychiatric contact up to age 77
At least some of these relations do not appear to be attributable to social class or educational level
Evidence points to this: cognition is associated with acquisition and maintenance of health – conductive behaviours

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3
Q

Age and achievement

A

Earlier peaks and rapid declines (F: novel problem-solving)

  • Pure mathematics
  • Lyric poetry
  • Theoretical physics
  • Mathematicians peak age: 26.5

Later peaks and slower declines (C: accumulation of knowledge)

  • Novel writing
  • History
  • Philosophy
  • Historians peak age: 38.5
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4
Q

Aging: why are things not worse?

A

Rarely need to perform at one’s maximum

Shift with age from novel processing to reliance of accumulated knowledge

Commission is not the only determinant of success in life. Others include personality, attitude, motivation, experience and task specific skills

Accommondations at the individual level (E.G., more older people avoid driving at night)
Accommodations at the societal level (E.G., automation reduces cognitive demand – scanning barcodes at cashier)

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5
Q

Neurotypical / normal cognitive aging

A
Fluid intelligence (down)
Crystallised intelligence (up)
Processing speed (motor responses, fluency) decline form beginning from the 30s & onwards
Attention: selective & divided attention (down)
Attention: working memory (down)
Attention: simple auditory span (only slight decline in later life)
Language ability (largely unchanged)
Visuospatial ability (largely unchanged)
Executive function (mostly decline with age)  
Explicit memory: episodic (lifelong decline)
Explicit memory: semantic (decline only in later life)
Implicit memory: (largely unchanged)
Memory acquisition (down)
Memory retrieval (down)
Memory storage (largely unchanged)
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6
Q

Neurotypical / normal aging in the brain

A
Grey matter (down) after age 20
Reduction in neuron size and reductions in connections to other neurons. Reductions are not explained by cell death 
White matter (down) more than grey matter (down) with increasing age 
Reduced white matter tract integrity
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7
Q

Avoiding cognitive decline

Cognitive reserve

A

Some people have a greater ability to withstand pathological changes to the brain, such as accumulation of amyloid protein, due to greater brain reserve

Higher levels of education, participation in certain activities, higher socioeconomic status, and baseline intelligence protects against the clinical manifestations of brain disease

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8
Q

Avoiding cognitive decline

Cognitive retraining

A

People can be trained to do better on cognitive testing. These improvements can be maintained for years

Cognitive training via home videotape has been shown to be 74% as effective as laboratory-based training, so issue of accessibility is side-stepped.

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9
Q

Atypical aging (neurodegenerative)

Alzheimer’s disease

A

The cortex shrivels up, damaging areas involved in thinking, planning and remembering

Ventricles filled with cerebrospinal fluid grow larger

Hippocampus shrinks severely

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10
Q

Atypical aging (neurodegenerative)

Huntington’s disease

A

Enlargement of the frontal horns of the lateral ventricles

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11
Q

Atypical aging (neurodegenerative)

Braak stages

A

1 & 2
Autonomic and olfactory disturbances

3 & 4
Sleep and motor disturbances

5 & 6
Emotional and cognitive disturbances

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12
Q

Models of lifespan cognitive change

A
  1. Single ‘mirror-image’ view
    Performance rises in childhood, is maintained in middle age & declines in late adulthood
  2. The different lifespan trajectories of crystallised intelligence (cognitive pragmatics) and fluid intelligence (cognitive mechanics). The former is well maintained at older ages whereas the latter declines.
  3. Representations are generally well maintained at older ages, but some knowledge is either lost (especially with lack of practice) or becomes inaccessible. Control processes develop at different ages and also decline differentially, depending in part on the brain areas involved.
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13
Q

Cognitive development and risky behaviour

A

Early adolescence
Puberty heightens emotional arousability, sensation-seeking, reward orientation

Middle adolescence
Period of heightened vulnerability to risk-taking and problems in regulation of affect and behaviour

Late adolescence
Maturation of frontal lobes facilitates regulatory competence

Running a yellow light
Reward centre
Heightened activity in the ventral striatum (woo-hoo)

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14
Q

Neurodevelopmental disorders

A

Neurological disorders with known prenatal cause (genetic or acquired)
[E.g. Williams syndrome, fetal alcohol syndrome]

Disorders where abnormal neurodevelopment is inferred: actual cause is complex or unknown
[E.g., developmental dyslexia, autistic disorder, specific language impairment (SLI), developmental coordination disorder (DCD), developmental dyscalculia]

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15
Q

Neurodevelopmental disorders

Static views

Dynamic views

Neuroconstructivism

A

Static views
Inspired by models of adult neuropsychological patients

Dynamic views
Dynamic nature of neural & cognitive development over time

Neuroconstructivism
“…Recognising that the infant brain is not only less differentiated and less modular than the adult brain But that, early on, it is highly interconnected. Only through experience and pruning do brain circuits gradually become increasingly specialised And localised (I.E., relatively modularised) over the course of development (3, 7–9). Environmental factors play a key role in ontogenesis (10), affecting both gene expression and progressive neural specialisation. “
“… The application of the static adult neuropsychological model to developmental disorders ignores the ontogenic history of the organism, and the roots of development are often critical for understanding the dynamic Trajectory that leads to the sociocognitive end state. “

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16
Q

Neurodevelopmental disorders

Limitations of applying adult neuropsychological models to understand neurodevelopmental disorders

Focus on Dissociations rather than associations

A

“The problem with developmental disorders is that, although one may see fractionation along the lines of major domains of functioning (e.g. language, spatial perception, motor co-ordination, social cognition, numeracy) within any one domain, the typical observation is one of a complex pattern of associated impairments rather than the highly selective deficits that may be found in acquired disorders. And this should not surprise us, because, in the developing child, an impairment at an early stage of processing would affect all the processes downstream of that stage.”

17
Q

Neurodevelopmental disorders

Limitations of applying adult neuropsychological models to understand neurodevelopmental disorders

Focus on bottom-up processing

A

“Searching only for the earliest stage of processing at which impairment could be seen” (e.g., weak vocabulary in a child’s has its roots in the child’s difficulty in discriminating between speech sounds “…however, this ignores the ample evidence for interaction between levels in language development.”

18
Q

Neurodevelopmental disorders

Limitations of applying adult neuropsychological models to understand neurodevelopmental disorders

Static rather than developmental models

A

“In a developmental disorder, even if dissociations are fond between deficits, these can be misleading, the pattern of impairment may change over time”

“… compensation for developmental disorders”

19
Q

Neurodevelopmental disorders

Limitations of applying adult neuropsychological models to understand neurodevelopmental disorders

Assumption that modality of deficit and nature of errors relate to primary underlying cause

A

Flexibility in conceptualisation is lacking

Example: ”…snowling and nation (1997) found in a longitudinal study that not only did many poor readers show characteristics of both surface and phonological dyslexia, but that they moved from one subtype to another over a two-year period.”

20
Q

Neurodevelopmental disorders

Limitations of applying adult neuropsychological models to understand neurodevelopmental disorders

Modules as hard-wired innate systems

A

“…models of developmental processes suggest a very different story, whereby “modularity”, in the sense of a domain-specific and informationally encapsulated system, emerges with experience”

21
Q

Neurodevelopmental disorders

Problems for the subject in general

  • emphasis on representational rather than processing deficits
  • problems in interpreting differential deficits
A

“…it must be stressed that i am not saying that cognitive neuropsychology has nothing to offer developmental psychology. Case studies of adults with acquired lesions can provide important insights into the stages of processing that are involved in a particular cognitive process, and they can lead to the development of ingenious tasks for pinpointing the underlying cause of impaired language performance. However, it is dangerous to assume that a model of cognitive processing that is derived from the Study of adults can be applied without modification to children: there is ample evidence that the nature of underlying representations may evolve in the course of development, and there may be far more interaction between levels of processing in children than adults. When interpreting dissociations, one needs to be aware that the profile of impairment can change with age and that an impairment affecting one stage of processing may have bottom-up or top-down influences on the development of other stages.”

22
Q

Adams father is a neurologist who has been taking MRI’s of this son’s brain ever since he was 5 years old. Adam is now 25 years old.

What signs of normal cognitive aging would Adam’s brain already display?

A. Decrease in grey matter volume
B. Increase in grey matter volume
C. Decrease in white matter volume
D. Increase in white matter volume

A

A. Decrease in grey matter volume