Biological - Other Flashcards
Give some facts about neurotypical development, including:
Prevalence, onset, why, what happens.
- Prevalence – 15-20%
- Onset during infancy or childhood.
- Impairment or delay of functions related to biological maturation of the central nervous system.
- Steady course that does not involve remissions and relapses.
- Common family history of similar or related disorders (genetic factors).
- Possible change in pattern with age.
- Heterogeneity
What is dyslexia?
- The learning difficulties result in significant impairment in the
individual’s academic, occupational or other important areas of
functioning. If functioning is maintained, it is only through significant additional effort. - The term “dyslexia” was originally used to describe the loss of the ability to read as a result of brain damage.
- Samuel Orton introduced “developmental dyslexia”.
Persons with dyslexia perceive illusory effects more strongly than non-dyslexics.
Mechanism:
-The lateral inhibition is stronger
Or
-They experience more global integration of the contrast response.
What is the Single Cognitive Deficit Model of developmental
disorders? And evidence against it.
- The single cognitive deficit model – looks for a specific ‘cause’ of a syndrome and suggests a simple cause-effect relationship, e.g.:
- Dyslexia – phonological deficit
- ADHD – inhibition deficit
- Autism – theory of mind deficit
- Single cognitive deficit model guided, either explicitly or implicitly, much of the early work on developmental disorders.
- Theory of mind deficit provides a good explanation of the problems in social interaction and communication in autism, but
- does not explain the third autism core symptom: repetitive behaviours and restricted interests;
- does not explain some of the cognitive strengths found in autism (e.g. in visual perception).
- Single deficit theory of dyslexia may be restricted to the English
language and thus lack generalizability.
Give some examples of comorbidity of syndromes?
- 87% of persons with ADHD have one or two other
neurodevelopmental conditions (Kadesjö and Gillberg, 2001). - 21% of persons with ADHD have three or more other
neurodevelopmental conditions (Andrews et al., 2002). - 25-90% of children diagnosed with developmental language disorder
exhibit symptoms of dyslexia (Tomblin et al., 2000). - Each neurodevelopmental disorder has a narrow set of defining
symptoms (e.g. dyslexia – writing and reading difficulties). - And several co-occurring symptoms
- It is unclear whether these other symptoms
- are causally related to the core symptoms of the syndrome,
- are the result of a common cause,
- or are outcomes of the syndrome.
What are some common additional symptoms in developmental disorders?
- Visual stress
Visual stress in response to
bright, contracting stimuli - Common in autism spectrum
- Co-occurring in dyslexia
Coping strategies - Avoiding strong light
- Reducing contrast
- Auditory Processing Disorder
- normal hearing pure tone sensitivity but experience auditory
processing difficulties in everyday life that are indexed by reduced
performance in other more sophisticated audiometric tests such as speech audiometry in noise or complex non-speech sound
perception; - difficulty processing brief, rapidly presented stimuli and/or making
frequency discriminations.
*Difficulty following verbal instructions
*Need instructions to be repeated
*Slow to process verbal information
*Easily overloaded with auditory information -> daydreaming,
distracted
*Difficulty sustaining attention on speech - Atypical Executive Functions
- Planning
- Monitoring
- Correcting
- Executing
- Prefrontal cortex, slow maturation
- Time management problems
- Difficulties in visual/auditory processing of transient stimuli
What is the Multiple Cognitive Deficit model of developmental disorders?
- In multifactorial causation, more than one causal factor is required to yield a given outcome.
- Can the single cognitive deficit model account for comorbidity?
- Example: A phonological deficit theory in dyslexia and an inhibition deficit theory in ADHD
- Dyslexia is defined by cognitive tests whereas ADHD is defined by behaviour ratings (usually from teachers and parents), the comorbidity is not due to
definitional overlap. - Traditional boundaries between typical and atypical are arbitrary
(based on standard deviation) - Neurodiversity paradigm and Multiple Cognitive Deficit Model
suggests diffused boundaries between typical and atypical). - the etiology of complex behavioural disorders is multifactorial and involves the
interaction of multiple risk and protective factors; - these risk and protective factors alter the development of cognitive functions
necessary for typical development; - no single etiological factor is sufficient for a disorder;
- comorbidity among complex behavioural disorders is to be expected because of
shared etiologic and cognitive risk factors; - vulnerability is often continuous and quantitative, rather than being discrete and
categorical.
What is the neurodiversity paradigm?
- The Neurodiversity paradigm rejects the assumption that typical
brains function correctly while atypical brains function incorrectly.
Since people with typical development are more numerous, the world is organised according to their needs. - In education, typical individuals are privileged, while the needs of
atypical individuals are misunderstood and unnoticed. That does not imply that the representation of the world created in atypical brains is inferior or incorrect. It is simply different.
What is an emotion?
An internal process that modifies the way an organism responds to
certain kinds of external stimuli.
What type of nervous system do emotional situations arouse?
Autonomic nervous system
What are the two branches of the autonomic nervous system?
- The sympathetic nervous system
- The parasympathetic nervous system
Sympathetic Nervous System
Prepares the body for brief, vigorous “fight-or-flight” responses.
Parasympathetic Nervous System
Increases digestion and other processes to save energy and prepare for later events. Often the systems operate together.
James-Lang theory of emotion, with evidence for and against.
Emotional experience is the by-product of autonomic responses.
You experience fear because your heart is pounding and you are
running away – bottom up theory.
Suggestion that emotions are EMBODIED. That is that they are
linked to bodily responses. eg pen held in lips or teeth study.
Predicts that:
1. People with weak autonomic or musculo-skeletal responses will feel less emotion
2. Causing or increasing someone’s action/response should enhance an emotion.
Pure Autonomic Failure: failure of output from autonomic nervous
system to the body – ANS no longer regulates heart rate and other
organs. Patients have little difficulty identifying emotions others might experience but FEEL their emotions less intensively than before.
People with paralysis through damage to the spinal cord are unable to instigate fight or flight behaviours.
However, most report experiencing emotion at the same level as before
their injury
Cannon-Bard theory of emotion, with evidence for and against.
Top down theory.
Emotional stimulus SIMULTANEOUSLY triggers autonomic response AND emotional experience in the brain.
Because:
1. Autonomic nervous system responds too slowly to account for
rapid onset of emotional experience. For example, a blush is an
autonomic response to embarrassment that takes 15-30
seconds to occur (long after the experience of feeling embarrassed)
2. People have problems detecting changes in autonomic activity
(e.g., heart rate) so how can this lead to a change in the experience of emotion?
3. If non-emotional stimuli (temperature rise) causes the same
pattern of autonomic activity that emotion does then why don’t we
feel afraid when we have a fever?
4. Not enough unique patterns of autonomic activity to represent
the array of unique emotional experience we have.
Removing the cortex in cats led to spontaneous fight or flight
responses – SHAM RAGE
Sensory information is relayed to the thalamus where it bifurcates.
One route goes to the cortex
One route to the hypothalamus (controls bodily responses)
Sham rage suggests that the cortex has a role in inhibiting emotional
responses.
Schacter & Singer theory of emotion, with evidence for/against.
Emotion dependent on Physiological arousal (e.g., increased heart rate, sweating) and Cognitive interpretation (or labeling) of that arousal based on the context.
In experiment gave a situational context (angry/non-angry actor), and a physiological stimulus: saline (does nothing), adrenaline and informed, and adrenaline but not informed.
Participants given an adrenaline shot but not informed of this “interpreted” their change in physiological state differently.
This theory increased the importance of brain processes in experienced emotion.
Lazarus theory of emotion, with evidence for/against.
It is the cognitive interpretation which mediates emotional experience.
Impact of memory in shaping emotional experience affects interpretation, which then leads to physiological state.
Importance of memory – unconscious or conscious
Function of the amygdala, with evidence?
Amygdala receives input from pain, vision and hearing centres. Well
suited for establishing conditioned responses. Some cells respond to
reward and others to punishment.
Projects to hypothalamus and to the
prefrontal cortex. Also projects to midbrain regions that link to Pons
which generates the startle behaviour.
A light is then paired with a shock repeatedly. Finally light precedes the loud noise and increases the startle response. In rats with amygdala damage there is still a startle reflex but no increase from the light stimulus. Suggestion that these animals may have difficulty interpreting signals with emotional consequences.
Toxoplasma gondii parasite.
The host cat excretes the parasite’s
eggs and these are released into the
ground. These infect burrowing
animals like rats. The parasite attacks and damages the amygdala such that the rat shows no fear when approaching cats (perhaps
because it fails to interpret the
emotional significance of a cat).
The cat eats the rat and so the
parasite completes the cycle back into the host.
What is psychic blindness?
An inability to recognize “the emotional importance of events”.
Surgically removed the temporal
lobes and some of the limbic system
(including amygdala).
Monkeys with amygdala damage attempt to pick up lighted matches and other objects they would normally avoid. They are also less fearful of snakes and more dominant monkeys.
What did Whalen argue about amygdala activation?
Comparing Fearful Faces with Neutral
Faces shows bi-lateral Amygdala activation.
B. Comparing Angry Faces with Neutral Faces also shows Amygdala activation.
Other studies found this happen with happy and neutral faces though.
Whalen et al. (2001) argue that the pattern of activation found
for the amygdala may not reflect the processing of negative
emotion/threat per se, but more about detecting ambiguity in the
face and how that relates to predictability of the other persons
actions.
If you see an angry person, you know what will happen, quick response. A fearful face is more ambiguous, you don’t know what she’s frightened of.
What is Urbach-Wiethe Disease?
Individuals with this disease accumulate calcium in the amygdala
and it atrophies.
One patient: Viewed 10 clips from scariest movies and only reports excitement. Stated she hates snakes but was happy to hold a snake.
In a Haunted House instead of screaming at monsters she laughed.
Her fearlessness became a danger to her. She was held at gun
point, at knife point and was physically abused. When describing
the events, she expresses anger but not fear.
She can draw most facial emotions
with the exception of fear.
When pressed to do so, she draws
someone crawling away with their hair standing on end like in cartoons.
SM fails to look at the eyes. For
fearful emotions the eyes are very
important signals.
