Textbook Notes (380,875)
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PSYC31H3 (106)
Chapter 8

Chapter 8 notes

10 Pages
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Department
Psychology
Course Code
PSYC31H3
Professor
Konstantine Zakzanis

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PSYC31 – Chapter 8
Diffuse brain diseases
do not affect all brain structures equally
usually results from a widespread condition such as infections, anoxia, hypertension,
intoxication, and occurs in most closed head injuries
Behavioural expression: memory, attention, concentration disabilities, impaired higher
level and complex reasoning, and general response slowing
Symptoms tend to be most severe immediately after an injury or they start off subtle
and transient then increase as the progressive condition worsens
Focal lesions
trauma, space-displacing lesions, localized infections, cerebrovascular accidents
symptoms of diffuse damage almost always accompany focal lesions of sudden onset
Clear cut evidence of focal lesions may not appear until later
Focal lesions involve only or mostly one hemisphere
Brain regions are not isolated – they work together as interconnected, distributed
neural networks
Lesions of prefrontal cortex have been associated with face recognition memory
impairment
Lesion site is more likely to predict the nature of the accompanying
neuropsychological deficits than its size stroke
For TBIs, the size of the lesion may be an important determinant of residual functional
capacity
The depth and extent to which a cortical lesion involves subcortical tissue will alter
the behavioural correlates of similar cortical lesions depth of lesion has been
clearly related to the severity of impairment of verbal skills
Anosognosia
Anosognosia with neglect of the paralyzed side lesions of the right optic region of
the thalamus
Anosognosia with amnesia for or lack of recognition of the affected limbs occurs
with lesions penetrating only to the transmission fibres from the thalamus to the
parietal cortex
Anosognosia with “positive symptoms such as confabulations or delusions lesions
limited to the parietal cortex
Diachisis
Diaschisis depression of activity that takes place in areas of the brain outside the
immediate site of damage; usually associated with frontal lesions
Applies more appropriately to the depression of relatively discrete or circumscribed
clusters of related functions than to global dampening
Typically viewed as transient
Similar to disconnection syndromes as they both involve disrupted neural transmission
through subcortical white matter
www.notesolution.com
Cortical lesions that may or may not extend to white matter give rise to diaschisis,
which disconnection syndrome result from damage to white matter that cuts cortical
pathways, disconnecting one or another cortical area from the communication network
of the brain
“an intact hemisphere in a damaged brain cannot operate as it does in an intact brain”
Tissue removal with little or no diseased tissue remaining, repercussions on other
anatomically unrelated functions tend to be minimal and the potential for rehabilitation
runs high
Presence of diseased or dead brain tissue can affect the circulation and metabolism of
surrounding tissue
Severity of damage plays an important role in determining the behavioural correlates
Duration of coma is a good index of the severity of a stroke or TBI but less useful for
assessing severity of a toxic or hypoxic episode
The more rapid the onset of the condition, the more severe and widespread the effects
will be
Non-Progressive Brain Injury
TBI, ruptured aneurysms, anoxia, nutritional deficiencies
In some instances, cerebrovascular diseases act like a progressive disease
Recency of the insult may be the most critical factor determining the patients cognitive
status
Make most rapid gains in the first few weeks and month
Confusion after TBI/stroke is often accompanied by deterioration, difficulty in
concentration, poor memory and recall, irritability, fatigability
Most common behavioural characteristics of an acute brain lesion in conscious
patients are impaired retention, concentration and attention, emotional lability, and
fatigability
After acute stages have passed and a brain lesion has become static, the condition
rarely staysstatic cognitive functions and specific disabilities continue to improve
during the first 6mon to a year
Full recovery is rare improvement proceeds by inclines and plateaus
Rate and nature of improvement are almost always uneven
Old memories and well-learned skills generally return most quickly Ribot’s Law:
recent memory, ability for abstract thinking, mental flexibility, and adaptability are
more likely to return more slowly
Predicting a patients ultimate ability to perform specific functions can be chancy for at
least 1 year after, due to fluctuations
Care must be taken to distinguish true memory defects from attention or concentration
problems
A common chrinc problem is an abiding sense of unsureness about mental experiences
Perplexity
Another difficulty is poor self-awareness, which can limit vocational options and
interfere with rehab efforts
www.notesolution.com
Depression troubles most adults who are not rendered grossly defective by their
injuries usually first experienced in the first year
Heightened irritability is another common complaint
Etiology plays a role in improvement traumatically injured patients to have more
return of impaired functions than do stroke patients
Thrombotic and emolic stroke longer survival time than hemorrhagic
Age may affect outcome at the age extremes but has little influence within young to
middle-aged adults
Premorbid competence may contribute to outcome and may be related to cognitive
reserve
General physical status may be associated with outcome for stroke patients
Early stroke rehabilitation has also been associated with higher levels of improvement,
but healthier patients are more likely to enter early
Poor family support is the more important predictor fo poor outcome
Side of lesion may be important for outcome right hemisphere patients have poor
outcomes but this is not a universal finding
Cerebral blood flow tends to show a progressive decline through the early adult years
greatest decrease involving prefrontal and temporal lobe regions
Age doesn’t appear to play a role in cerebral acetylcholinesterase activity
Older individuals show fewer waves in the alpha frequency than younger persons
Longitudinal studies show less age-related decline in cognition than cross-sectional
studies
Concepts of crystallized and fluid intelligence used to distinguish those abilities that
hold up with age from the ones that decline
Crystallized: over-learning, well-oractice, and familiar skills, knowledge and ability
Fluid: involves reason and problem solving declines after 50-60
Least age effects on vocab, information, comprehension and arithmetic
Greatest age effects on picture arrangements, matrix reasoning, digit symbol and
object assembly
oMost are time taskes possible confounding variable
oMajor change was slower processing speed
Streopsis: binocular vision
Disequilibrium (presbyastasis) occurs as a result of degeneration of vestibular
system structures in normally aging persons
Aging
Verbal fluency tends to decline more with age than confrontation naming
Perceptual integration and reasoning show age related declines
Arithmetic problem solving changes little with age
But when reasoning is required, there is little decline with age
Concept formation and abstraction decrease with age older = concrete thinking
poorly on category test, WCST, tower of Hanoi, trail making B, matrix
www.notesolution.com

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Description
PSYC31 Chapter 8 Diffuse brain diseases do not affect all brain structures equally usually results from a widespread condition such as infections, anoxia, hypertension, intoxication, and occurs in most closed head injuries Behavioural expression: memory, attention, concentration disabilities, impaired higher level and complex reasoning, and general response slowing Symptoms tend to be most severe immediately after an injury or they start off subtle and transient then increase as the progressive condition worsens Focal lesions trauma, space-displacing lesions, localized infections, cerebrovascular accidents symptoms of diffuse damage almost always accompany focal lesions of sudden onset Clear cut evidence of focal lesions may not appear until later Focal lesions involve only or mostly one hemisphere Brain regions are not isolated they work together as interconnected, distributed neural networks Lesions of prefrontal cortex have been associated with face recognition memory impairment Lesion site is more likely to predict the nature of the accompanying neuropsychological deficits than its size stroke For TBIs, the size of the lesion may be an important determinant of residual functional capacity The depth and extent to which a cortical lesion involves subcortical tissue will alter the behavioural correlates of similar cortical lesions depth of lesion has been clearly related to the severity of impairment of verbal skills Anosognosia Anosognosia with neglect of the paralyzed side lesions of the right optic region of the thalamus Anosognosia with amnesia for or lack of recognition of the affected limbs occurs with lesions penetrating only to the transmission fibres from the thalamus to the parietal cortex Anosognosia with positive symptoms such as confabulations or delusions lesions limited to the parietal cortex Diachisis Diaschisis depression of activity that takes place in areas of the brain outside the immediate site of damage; usually associated with frontal lesions Applies more appropriately to the depression of relatively discrete or circumscribed clusters of related functions than to global dampening Typically viewed as transient Similar to disconnection syndromes as they both involve disrupted neural transmission through subcortical white matter www.notesolution.com
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