Week 2 Flashcards

1
Q

Neuroanatomy: medial temporal

A

most important:
Anterior Cingulate cortex (ACC)

also:
fornix
cingulate gyrus
corpus callosum
pineal body
olfactory bulb
optic chiasm
amygdala
pituitary gland
hippocampus
hypothalamus
interthalamic adhesion
brain stem  (cut edge)
thalamus
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2
Q

Memory and Temporal Lobes

damage to medial temporal cortex:

A

Damage to medial temporal cortex (hippocampus) leads to modality specific memory problems

LH problem in learning and remembering verbal material

RH problem in learning and remembering visual material

Both Hemispheres: general amnesic syndrome (profound problem laying down new memories for verbal and visual information)

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3
Q

Wernicke Korsakoff’s Syndrome: Another cause of amnesia

A

Degenerated diencephalon (particularly dorsomedial nucleus of the thalamus & mammillary bodies) due to thiamine deficiency caused by excessive and longstanding alcohol abuse

Slow development: difficult to pinpoint onset of amnesia
Damage often extends to frontal lobes

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4
Q

Memory Disorders

Amnesias

A

Global amnesia (Clive, HM)

Post-traumatic amnesia

Anterograde amnesia (new learning after onset)

Retrograde amnesia (memories pre-onset)

Psychogenic amnesia (“The great escape: a neuropsychological study of psychogenic amnesia”; Kopelman et al., 1994) – see also dissociative fugue

AA – memory impairment for events after ABI. PA – intact anterograde memory, some brief loss of consciousness, major stresses – media attention

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5
Q

HM famous memory case – generalised epileptic seizures

A

1953 William Scoville performed a bilateral medial-temporal lobe resection in an attempt to prevent further seizures

Demonstrated that severe amnesia can result from an injury to a relatively small region of the brain (but is necessary but not sufficient)

HM was left with severe anterograde amnesia
Above average IQ
Normal perceptual ability and language
Retrograde (pre-surgery memory) is good
Socially appropriate – no personality changes

Over 100 studies conducted on this classic case

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6
Q

Herpes Simplex Viral Encephalitis

Clive Wearing

A

Clive was 46 when he developed meningitis-like symptoms (fever, headaches, fatigue and confusion), lasting several months

Finally diagnosed with HSVE and treated with an antiviral drug which saved his life “but left his brilliant mind full of holes” (Wilson, 1999, p. 73)

CT scan – low density in the (L) temporal lobe – extending into inferior and posterior frontal lobe and R medial temporal lobe

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7
Q

Core vs Extended Consciousness

A

Clive experienced predominant damage to the limbic region which enables core consciousness but not autobiographical consciousness, thus leading to a life “being sensed but not really examined” (Damasio, p. 217)

Clive was unable to recognise the existence of his own past consciousness since his illness (severe anterograde amnesia and delusional beliefs)

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8
Q

Psychological effects of damage to the temporal Lobe:

Personality and emotional behaviour

A
Pedantic speech, 
egocentricity, 
fixed beliefs, 
obsessiveness, 
perseveration on conversation topics,
paranoia, 
preoccupation with religion, 
prone to aggressive outbursts
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9
Q

Emotion Processing

A

Amygdala: Role in emotional processing and emotional learning and memory (both implicit/explicit).

Mediates approach and withdrawal behaviour

Fear conditioning – neutral stimuli gets paired with fearful experience and produces fear reaction (phobia and avoidance reactions)

The amygdala interacts with the hippocampal memory system:

  • –Responsible for assigning emotional significance to stimuli and events
  • –Affects the storage of memories and influences recall
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10
Q

Threat Processing Pathways

A

1) Innate and fast-acting thalamo-amygdala pathway, bypasses cortex to elicit immediate autonomic, endocrine and behavioural response (unconscious/implicit processing)

Adv of emotion driven system: adaptive for survival, diverts attention in presence of threat and danger
Disadv of this system: can be too dominating; hasty and potentially irrational reactions that affect goals (e.g., good relationship)

2) Slow acting thalamo-cortical-amygdala pathway that supports cognitive appraisal of the meaning of stimuli within context (LeDoux, 1996) – react in accordance with goals and social needs (conscious processing through prefrontal cortex)

Amydala response triggers hypothalamus – freezing, flight, fight – stress hormones

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11
Q

Role of Orbito-Frontal Cortex

A

Role in regulating emotional expression and inhibition of inappropriate social behaviour

Connections with the limbic system: amygdala may elicit learnt emotional associations – while the OFC corrects/adjusts responses (down regulation)

Reasoning about an
emotional event can reduce
its emotional impact and
alter behaviour

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12
Q

Example: An argument

A

Fast-acting and non-conscious threat response system: quick analysis of emotional meaning of the situation.

Perceptual representations link external stimuli (e.g., comment, angry face) with internal affective and physiological states

Immediate and emotionally driven responses initially dominate or disrupt higher order goal systems (carefully thought out reactions congruent with goals and social needs).

Working memory system registers that the self is under threat and supports processing of information at the implicational level (OFC) - or what this may mean for one’s self and the future to guide goal-directed behaviour (LeDoux, 2000)

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13
Q

Pre-frontal cortex: Executive functions

COOL EF

A

Dorso-lateral region: ‘Cool EF:

–Cognitive flexibility, problem-solving, planning, working memory, prospective memory and complex attention

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14
Q

Pre-frontal cortex: Executive functions

HOT EF

A

Ventro-medial region: ‘Hot EF’

  • Emotional decision making
  • Reward based learning
  • Perspective taking - ToM
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15
Q

Pre-frontal cortex: Executive functions

Orbito-frontal region

A

Regulating social and emotional behaviour

Learning from experiences (stimulus-response)

Olfaction - smell

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16
Q

Deficits arising from Dorsolateral damage

A

Cognitive impairment in the areas of:

  • Planning and organisation
  • Problem-solving (novel)
  • Alternating and divided attention
  • Mental flexibility
  • Sequencing
  • Rule following and strategy formation
  • Working memory and on-line monitoring
  • Response suppression/inhibition
17
Q

Effects of OPFC & VMPFC Damage

A

Behavioural dysregulation:

  • Social disinhibition (e.g., lack of tact)
  • Lack of spontaneity and stimulus bound behaviour
  • Reduced social skills (e.g., reading and responding to social cues)

Personality changes:

  • Lack of empathy and poor mentalising ability
  • Increased or decreased emotional responsivity
  • Relatives may perceive the person as “no longer himself”
18
Q

Empathy

Emotion recognition:

A

Fusiform Gyrus and amygdala

19
Q

Empathy

Emotional contagion

A

Shared Emotion

Inferior frontal, inferior parietal & insula

20
Q

Empathy

Theory of mind and perspective taking

A

Temporo-parietal junction and medial PFC

21
Q

Empathy:

Affective Response

A

Anterior cingulate and medial PFC - emotional and social response (“are you okay?”)

–Mirror neuron networks in inferior frontal, ventral and dorsal premotor, and inferior parietal regions

—Simulates other’s mental states by directly mapping other’s thoughts, actions, and intentions to the self

22
Q

Empathy:

Understanding self and others

A

difficulty identifying and understanding one’s own emotional state is linked to empathy deficits (Valdespino et al., 2017)

23
Q

The Insula and its role in emotional response

A

The insula processes emotional response to self and others’ experience of pain(physical and emotional)

People who ruminate have excessive activity in the insula region.

Those with alexithymia have reduced activity.

Alexithymia is a subclinical phenomenon involving a lack of emotional awareness or, more specifically, difficulty in identifying and describing feelings and in distinguishing feelings from the bodily sensations of emotional arousal (Nemiah et al., 1976).

24
Q

Psychological Disorders: Problems relating to one’s self and others

A

Autistic Spectrum Disorder
Attention Deficit Hyperactivity Disorder

Conduct Disorder and Oppositional Defiant Disorder

Brain injury and dementia

Narcissistic and Antisocial Personality Disorders

Schizoid Personality Disorder and schizophrenia

Borderline Personality Disorder

25
Emotion Regulation Cognitive reappraisal
reinterpreting an emotion-eliciting event to effectively change its emotional impact - thoughts are altered or the emotion-eliciting stimuli are re-evaluated: DLPFC (develop cognitive strategy to reframe affective experience); MPFC and ACC (revaluate internal states and the external stimuli (changes intensity of emotion and physiological response)
26
Emotion Regulation: Expressive suppression:
actively inhibiting the observable expression of the emotional experience by controlling or neutralizing emotional behavior. OPFC involved in inhibition of inappropriate social and emotional behaviour
27
Amygdala: role in depression
Abnormal increase in resting activity of the amygdala stimulates cortisol release or stress response (Hypothalamic-pituitary adrenal circuit) – particularly relevant to mood disorders Severity of mood symptoms correlates with increase in glucose metabolism in amygdala PET findings indicate hypermetabolism or overactivity of orbito prefrontal cortex, insula and amygdala of people with major depression
28
Neurobiological Correlates
Carriers of the short-form 5-HTTLPR (serotonin transporter) poly-morphism were more likely to develop major depression or PTSD IF they had high exposure to a stressful event AND had low social support
29
Developmental model of depressionBeck (2008), p. 974
Genetic diathesis (predisp.) > reactive amygdala > cognitive biases > exaggeration of stressful events > activation of hypothalamic-pituitary adrenal axis > Dominance of limbic activity over prefrontal function > deficient reappraisal of negative cognitions > depressive symptoms Genetic diathesis also can Increase likelihood of HPA activation Exaggeration of stressful events also leads to a dominance of limbic activity over prefrontal function
30
Anxiety and phobias
Abnormal interactions between the amygdala and PFC Greater amygdala activation in anxious adults and children, compared to healthy controls, when presented with brief threatening stimuli.: - ---A positive correlation between amygdala activation and anxiety symptom severity. - --Increase in amygdala response in anxiety occurs in the absence of a compensatory increase in modulation by the PFC. Fast-acting thalamo-amygdala pathway dominates, leading to impulsive instinctive behaviours
31
Amygdala & PTSD
Does a damaged amygdala protect from developing PTSD? Koenigs et al. (Nature Neuroscience, 2008): A study of 133 Vietnam veterans Veterans with damage to either the amygdala (n = 15, 0%) or OPFC (n = 40, 18%) were much less likely to develop PTSD than those with no brain damage or damage in other areas (45% incidence) Note: differences due to less intense symptoms rather than complete lack of symptoms
32
What about the hippocampus?
Early abuse, war and other extreme stress can impair the activity of the hippocampus, a structure very sensitive to stress Hippocampal volume is reduced in PTSD, and correlates with PTSD symptom severity and ‘combat exposure’ Trauma exposure without PTSD may be associated with hippocampal volume deficits (see meta-analysis by Woon et al., 2010) Possible that hippocampal dysfunction leads to distortion and fragmentation of memories Psychotherapy (integrate and process meaning of events) and pharmacotherapy applications
33
What is Neuroplasticity?
The brain’s ability to reorganise its structure, function and connections in response to internal or external stimuli The lifelong capacity of the brain to change and rewire itself in response to learning and experience. Neurogenesis = ability to create new neurons and connections between neurons (synaptogenesis)
34
Double Edge of Neuroplasticity
Occurs in response to positive and adverse life experiences eg, DV, Heroin addiction, learning to read, playing piano
35
Brain’s Vulnerability to Stress
Trauma and maltreatment activates a prolonged biological stress response through the limbic-hypothalamic-pituitary-adrenal axis The developing brain is particularly vulnerable: prolonged activation of this system leads to structural and functional brain changes (esp. in PFC and limbic system). Children: Accelerated loss of neurons, abnormal pruning of axons, and a decreased level of brain growth factors for neural development (De Bellis, et al., 2002).
36
Legacy of Child Abuse
Structural, functional and behavioural effects are worse for those with longer duration of trauma and younger age of onset (De Bellis & Kuchibhatla, 2006). Neglect or absence of parental responsiveness (e.g., attachment, play, learning, safety) results in delayed myelination of axons – linked to executive dysfunction and poor self-regulation (De Bellis, 2005). Exposure to violence is associated with smaller cerebral and PFC volumes and corresponding increase in CSF. Functionally, externalising (aggression, self-harming) and internalising (depression, anxiety) disorders 
37
Resilience
Children are not equally affected by abuse; variations in "neuroplasticity“ may account for differential response Early intervention for children who have suffered maltreatment can mitigate adverse behavioural, learning and cognitive effects (De Bellis, Keshavan, Shifflett et al., 2002). Sustained positive carer-child interactions can reduce the activity of the HPA axis, modifying behavioural and endocrine responses to stress e.g., attachment-based therapy, therapeutic day care
38
Early adversity and risk of dementia
Radford et al. 2017, Am J Geriatr Psychiatry 25:10, October 2017 296 Aboriginal and/or Torres Strait Islander Australians aged 60–92 years, NSW Life course survey of health, well-being, cognition, and social history including the Childhood Trauma Questionnaire (CTQ)  After controlling for multiple risk factors, higher levels of childhood stress and adversity were associated with depression, anxiety, suicide attempts, dementia diagnosis, and, specifically, Alzheimer disease.