NEUR2020 EXAM 3 CONTENT PDF

Neuroscience of Stress, Anxiety and Depression NEUR2020: Neuroscience for Psychologists Lena Oestreich ([email protected]) she, her Acknowledgement of Country The University of Queensland (UQ) acknowledges the Traditional Owners and their custodianship of the lands on which we meet. We...

Neuroscience of Stress, Anxiety and Depression NEUR2020: Neuroscience for Psychologists Lena Oestreich ([email protected]) she, her Acknowledgement of Country The University of Queensland (UQ) acknowledges the Traditional Owners and their custodianship of the lands on which we meet. We pay our respects to their Ancestors and their descendants, who continue cultural and spiritual connections to Country. We recognise their valuable contributions to Australian and global society. Image: Digital reproduction of A guidance through time by Casey Coolwell and Kyra Mancktelow Overview 1. Introduction 2. Stress 3. Anxiety 4. Depression 3  irritability Introduction reactivity insomnia difficulty Anxiety fatigue/ concentrating exhaustion memory tension Stress problems Depression changes in decreased appetite libido 4 Stress Stress: The body’s physiological response to perceived threats Stressor: any experience or event that triggers stress (can be physical or psychological) Stress response: The physiological changes that occur in reaction to a stressor 5  Please download and install the Slido app on all computers you use Is stress good or bad? ⓘ Start presenting to display the poll results on this slide. 6 Adaptive vs. Maladaptive Stress Adaptive Stress (“Good Stress”) Maladaptive Stress (“Bad Stress”) Definition: Stress that is short-term and Definition: Chronic or overwhelming stress motivating that negatively affects health Examples: Meeting a deadline, preparing for Examples: Persistent work pressure, ongoing a presentation, or physical exercise financial issues, or long-term caregiving Benefits: Consequences: Mobilizes energy resources (increased - Impairs cognitive functions (memory focus and alertness) problems, difficulty concentrating) Enhances memory and learning - Weakens the immune system Improves problem-solving and - Contributes to mental health disorders performance like anxiety and depression 7 Good vs bad stress - Good stress Transient and mild Safe environment Plausible but not guaranteed reward Control Alertness and focus - Bad stress Chronic and severe (perceived) lack of control Lack of predictability 8  Please download and install the Slido app on all computers you use Think of a situation that causes you stress. What physical and emotional reactions do you experience? ⓘ Start presenting to display the poll results on this slide. 9 The Fight-Flight-Freeze-(Fawn) Response Definition: The body’s automatic, physiological reaction to perceived threats survival mechanism to Flight: Escape quickly mobilize Fight: Confront the threat the threat physiological and psychological resources Fawn: Appeasing Nervous and Freeze: Become endocrine (hormonal) the threat immobile when the systems rapidly threat seems prepare the body to overwhelming respond 10 Sympathetic Nervous System & Hypothalamic-Pituitary-Adrenal Axis 11 SNS and HPA Axis Sympathetic Nervous System (SNS) Role: Triggers the immediate, automatic fight-flight-freeze-fawn response Effects: Increases heart rate, redirects blood flow to muscles, dilates pupils, accelerates breathing Key Hormone: Adrenaline (epinephrine) Duration: Short-term, immediate response to perceived threats Hypothalamic-Pituitary-Adrenal (HPA) Axis Role: Manages the body’s prolonged response to stress Effects: Sustained release of cortisol, regulates energy, suppresses non-essential functions like digestion and reproduction Key Hormone: Cortisol Duration: Long-term, ongoing response when threat is persistent 12 Modern Life Stressors - All stressors elicit the same stress response - Modern life stressors are typically: Not life-threatening Social, psychological, or emotional Often ongoing or last for extended periods  fight-flight-freeze is often maladaptive in modern contexts 13 Psychoneuroimmunology - Definition: The study of interactions among psychological factors, the nervous system, and the immune system - Acute Stress (SNS activation): Can enhance immune function Eustress = Stress that promotes health - Chronic Stress (HPA axis): Weakens the immune system Distress = Stress that impairs health 14 Psychosomatic Disorders - Medical disorders influenced by psychological factors - Example: Gastric ulcers Typically caused by Helicobacter pylori (H. pylori) bacteria Stress weakens the body’s defences, reducing digestive function H. pylori can then attack the stomach lining, leading to ulcers 15 Psychosocial Short Stature (PSS) - Disorder of short stature caused by extreme stress and emotional deprivation during childhood  temporary growth hormone deficiency (GHD) - Caused by epinephrine release in response to stress - Failure to thrive despite adequate nutrition - GHD can be reversed if child is removed from abusive home 16 Stress and health - Stress can affect behaviors that further decrease immune system function - Behaviors of stressed person can elicit stress or illness in other people - Exposure to stress early in life can have negative effects on brain and endocrine system development 17 Effects of Stress on the Brain: Hippocampus Location & Function: Located in the temporal lobe Critical for learning, memory, and mood regulation Vulnerability: Highly plastic (able to change) but vulnerable due to many glucocorticoid receptors, which bind to cortisol Chronic stress leads to reduced neurogenesis (formation of new neurons) and dendritic branching (connections between neurons) Consequences: Shrinkage of the hippocampus Linked to memory problems, difficulty concentrating, and mood disorders Associated with depression, schizophrenia, Alzheimer’s disease 18 Effects of Stress on the Brain: Amygdala Location & Function: Almond-shaped structure near the base of the brain Critical for the perception of fear and other negative emotions (automatic, unconscious) Strong connections to the medial prefrontal lobes, where fear- evoking stimuli are consciously evaluated Vulnerability: Stress increases dendritic branching and causes enlargement of the amygdala Overstimulation leads to heightened sensitivity and reactivity Consequences: Hyperactivity and hyperreactivity of the amygdala are linked to depression, anxiety, and post-traumatic stress disorder 19 Coping with Stress Parasympathetic Nervous System (PNS): Also known as the “rest and digest” system Opposes the "fight or flight" response of the sympathetic nervous system Helps to bring the body back to a state of calm and balance after stress Importance: Reduces physiological arousal caused by stress Supports long-term health and well-being by counteracting the effects of chronic stress 20  Please download and install the Slido app on all computers you use What activities or techniques do you use to reduce stress? ⓘ Start presenting to display the poll results on this slide. 21 Techniques for Reducing Stress Deep Breathing Mindfulness & Meditation Physical Activity Progressive Muscle Relaxation (PMR) Social Connection 22 BREAK 3. Anxiety - Fear is an adaptive response to threat that is typically transient - Anxiety is a fear that persists in the absence of a direct threat - Fear and anxiety are beneficial for survival because they motivate coping behaviors 24 Fear circuit Amygdala: Detects threats and initiates fear response Prefrontal Cortex (PFC): Regulates and controls emotional responses Anterior Cingulate Cortex (ACC): Monitors emotional conflicts and ensures emotional response if appropriate Implications for Anxiety: Overactivation of the fear circuit leads to exaggerated fear responses and inability to regulate emotional states 25  Please download and install the Slido app on all computers you use Are PTSD and OCD anxiety disorders? ⓘ Start presenting to display the poll results on this slide. 26 Are PTSD and OCD anxiety disorders? Post-traumatic stress disorder (PTSD): failure to recover after experiencing or witnessing a terrifying event Obsessive compulsive disorder (OCD): recurring, unwanted thoughts, ideas or sensations (obsessions) that may trigger the drive to do something repetitively (compulsions) 27 Neurobiology of OCD and PTSD Similarities between anxiety disorders, OCD and PTSD: All three conditions exhibit amygdala hyperactivity, leading to heightened fear responses, PFC underactivity, which prevents effective emotional regulation and ACC dysfunction, leading to difficulties in modulating anxiety Differences: PTSD: hippocampal volume reduction, impairing memory and context discrimination OCD: orbitofrontal cortex (OFC) overactivity, contributing to obsessive thinking and compulsive behaviours 28  Pharmacological treatments for anxiety disorders Benzodiazepines (e.g., Diazepam, Xanax, Temazepam etc.) Enhance effect of gamma-aminobutyric acid (GABA) Counters anxiety by sending calming effects from brain to body Typical short-term use (addictive, dangerous in higher doses) Serotonin agonists (Buspirone & selective serotonin reuptake inhibitors (SSRIs)) Increases serotonin circulation in brain 2-4 weeks to feel effect Long-term use No sedating effects 29 Behavioral interventions for anxiety disorders - Cognitive Behavioral Therapy (CBT) most effective psychotherapy for Generalised Anxiety Disoder - Psychoeducation helpful for all anxiety disorders - Relaxation/ breathing/ mindfulness techniques - Exposure therapy for specific phobias 30  Please download and install the Slido app on all computers you use What are common symptoms and experiences of depression? ⓘ Start presenting to display the poll results on this slide. 31 4. Depression - Major Depressive Disorder (MDD): persistent feelings of sadness and hopelessness and loss of interest in activities once enjoyed -  interferes with daily living - Anhedonia: inability to experience pleasure - Apathy: lack of interest, enthusiasm, or concern - Reactive depression: depression triggered by a negative experience - Endogenous depression: depression with no apparent cause 32 Depression - Genetic component  heritability ~ 40%  no individual genes linked to depression - Early exposure to stress increases likelihood of developing MDD in adulthood - Epigenetic factors  stress  traumatic event 33 Subtypes of MDD Seasonal affective disorder: episodes of depression recur during a particular season (usually winter)  Worse in countries with longer winter days  Light therapy can reduce symptoms Peripartum/ postpartum depression: depression experienced during pregnancy, after childbirth, or both  Physical changes (hormones) and stress (sleep deprivation, exhaustion, anxiety)  Observed in 19% of pregnancies 34  Reward system - System of subcortical structures that are connected to frontal lobe via white matter tracts - Grey matter volume reductions in prefrontal cortex, hippocampus, amygdala and cingulate cortex common in MDD - fMRI studies provide evidence for abnormal communication within this network associated with depression 35 Brain Changes in Depression Prefrontal Cortex (PFC): - Reduced activity, affecting emotional regulation and decision-making - Inability to suppress negative thoughts and emotions Hippocampus: - Decreased volume, impairing memory and context processing - Chronic stress worsens depressive symptoms 36 Monoamine theory of depression - Depression is caused by reduced levels of monoamines (serotonin, norepinephrine, dopamine) - Postmortem studies found increased number of serotonin and norepinephrine reuptake transporters on presynaptic neurons in MDD patients compared to healthy controls transport neurotransmitters back into presynaptic neuron Fewer neurotransmitters in circulation 37  MDD treatments based on monoamine theory Monoamine oxidase inhibitors (MAOIs, e.g., isocarboxazid, phenelzine): increase levels of monoamine neurotransmitters by inhibiting MAOs Tricyclic antidepressants (e.g., amitriptyline, imipramine): block reuptake of serotonin and norepinephrine Selective Serotonin-Reuptake Inhibitors (SSRIs; e.g., fluoxetine, citalopram): block reuptake of serotonin Atypical antidepressants (e.g., mirtazapine, bupropion): effects on different neurotransmitters like dopamine, nicotinic acetylcholine, melatonin N-Methyl-D-aspartate (NMDA)-receptor antagonist (e.g., ketamine): blocks glutamate reuptake 38  Effectiveness of drug treatments for MDD MAOI, tricyclic antidepressants and SSRIs effective in about 25-50% of patients with MDD Antidepressants are more effective for severe depression MDD patients with treatment resistant and severe depression typically benefit from ketamine treatment 39 Neuroplasticity theory of depression Depression results from a decrease of neuroplastic processes in various brain regions (e.g., hippocampus)  Stress is associated with changes in neuroplasticity  Prolonged stress can trigger MDD  Reduced synthesis of neurotrophins (proteins that support neurons) leads to decreased adult hippocampal neurogenesis 40 MDD treatments based on neuroplasticity theory - Treatments that increase brain-derived neurotrophic factor (BDNF) improve depressive symptoms Drugs like antidepressants or ketamine stress management, exercise, social interactions High protein diet, fasting Increases synaptogenesis and adult hippocampal neurogenesis 41 Neuroinflammation theory of depression - Stress leads to an increased release of pro-inflammatory cytokines  bidirectional feedback loop between cortisol and cytokines - Reward system vulnerable to prolonged inflammation  reduced serotonin - Depression often comorbid with autoimmune disorders and highly prevalent after brain injury (e.g., stroke, traumatic brain injury) MDD treatments based on neuroinflammatory theory: - Antidepressants - Fish-oil, diet high in omega-3 - non-steroidal anti-inflammatory drugs (ibuprofen, aspirin, naproxen) 42  Behavioral interventions for MDD - Cognitive behavioral therapy (CBT) most effective psychotherapy for MDD - Mindfulness/ breathing techniques - Exercise (does not have to be high impact!) - Interpersonal therapy focuses on past and present social roles and interpersonal interactions 43 Transcranial magnetic stimulation (TMS) - Noninvasive delivery of repetitive magnetic pulses to prefrontal cortex  improved activity in limbic system - 20-30 sessions over consecutive weekdays - 10–30-minute treatments - Often effective for treatment resistant depression 44 Deep brain stimulation (DBS) - Brain stimulation through surgically implanted electrode - Tip of electrode implanted in white matter connecting to anterior cingulate gyrus - Implanted under skin - Delivers continual electric pulses - Typically, only performed in very severe and treatment resistant depression - Highly effective 45 Anxiety and depression comorbidity - anxiety and depression are the two most prevalent psychiatric disorders and are highly comorbid (> 50%) - similar brain systems and triggers - most identified genes are implicated in depression AND anxiety  complex traits are typically polygenic - both respond to similar treatments and can be triggered by stress 46 Psychedelic therapies - in 1950s and 1960s, > 1,000 scientific articles on using psychedelics as psychiatric treatment  banned due to recreational use - Assumption: People get locked into disorders like depression and anxiety (rumination and worry)  psychedelics help break that cycle and enhance neuroplasticity - 71% of patients with treatment resistant MDD who took psilocybin improved and half entered remission - 3,4-methylenedioxymethamphetamine (MDMA) highly effective treatment for PTSD - advantages over traditional treatments  not addictive  only one or few sessions needed  more likely to achieve remission 47 Thank you Dr Lena Oestreich | Senior Research Fellow School of Psychology and AIBN [email protected] @LenaOestreich CRICOS code 00025B Acknowledgement of Country The University of Queensland (UQ) acknowledges the Traditional Owners and their custodianship of the lands on which we meet. We pay our respects to their Ancestors and their descendants, who continue cultural and spiritual connections to Country. We recognise their valuable contributions to Australian and global society. Image: Digital reproduction of A guidance through time by Casey Coolwell and Kyra Mancktelow NEUR2020 Neuroscience for Psychologists Lecture 10 Semester 2, 2024 Emotions Alan Pegna Key definitions Emotion: A complex psychological state that involves experiential, behavioural, and physiological elements. Motivation: The process that initiates, guides, and maintains goal-oriented behaviours. Reward: Positive reinforcement that follows a particular behaviour, influencing its future occurrence. 3 Some history William James in 1884 first suggested a relation between brain-body function and emotional states  physiological states influence neocortex and determine emotional experience. This view is shared by Lange (1887) and for this reason is usually called the James-Lange theory.  What are emotions?  What are emotions?  What are emotions?  What are emotions?  What are emotions?  William James (1842-1910) The body plays an important role in the generation of emotional responses and emotional subjective feelings The perception of the bodily response IS the emotion “If we fancy some strong emotion and then try to abstract from our consciousness of it all the feelings of its characteristic bodily symptoms we find that we have nothing left behind"  The sequence of an emotional response  Walter Cannon (1871-1945) Body changes are too slow Surgical removal of viscera from brain do not impair emotional behaviour The central nervous system must mediate emotions (Cannon-Bard theory of emotions) Diencephalon produces emotional expression by projecting to peripheral organs, and emotional experience by projecting to the neocortex.  Three main theories of emotions Basic emotion theories (biological basis, universal in all humans across cultures) Constructivist theories (man-made concepts; is arousal + cognition) Appraisal theories (it’s the what we see in the situation, e.g., water when you are thirsty)  James Papez(1883-1958) Papez (1937) suggests an anatomical framework for the Cannon-Bard theory. He proposes the first major theory for the neurology of emotions. The structures involved are integrated into “Papez’s circuit”. Hippocampus  fornix  mammillary bodies  thalamus  cingulate gyrus  hippocampus Papez viewed the cingulate gyrus as the cortical area for emotional experience. Papez’s circuit  The limbic system MacLean extended Papez’s model in the 1950s. He integrated the amygdala, orbito-frontal cortex, and septum into the Papez circuit. He suggested that this system, the limbic system, was the circuit for emotion, the hippocampus being the key element. The limbic system is still often used synonymously for emotional system. Papez’s circuit and the limbic system  The limbic system Two major problems invalidate the limbic system theory of emotion. From the anatomical point of view, there is no reason to put these structures together  From the functional point of view: the amygdala seems more important for emotion than the hippocampus. Furthermore, the hippocampus is now known to be implicated in other functions as well (explicit, episodic memory above all)  Role of the amygdala in emotion In 1939, Heinrich Kluver and Paul Bucy fortuitously notice that bilateral anterior temporal lobectomy (including the amygdala) produce a particular behavioural syndrome in monkeys. Emotional behaviour is greatly impaired.  The Kluver-Bucy syndrome hypoemotionality (monkeys become tame, no fear) hyperorality/hyperphagia (explore everything with their mouths, eat anything including previously disliked foods, wrapping paper, etc.) hypersexuality (increased autoerotic, homosexual and heterosexual behaviour, inappropriate object choice) Also often associated: visual agnosia memory disorders  Role of the amygdala in emotion A rare patient (SM) presenting a bilateral amygdala lesion (Urbach-Wiethe syndrome) showed an unusual deficit in face processing (Adolphs et al. (1994) Nature). Adolphs et al. (1994) Nature  Amygdala responds to fear Data shows that the amygdala responds to fear. Evidence is unclear as to whether it responds to other emotions?  Amygdala responds to fear In healthy controls, fearful faces activate the amygdala Canli et al. (2001) Science  Role of the amygdala in fear conditioning Joseph Le Doux (2000) focused on fear: the amygdala is necessary for fear response. In monkeys, there exists an innate fear of snakes. Amygdala damage makes it disappear (Kluver-Bucy syndrome)  Amygdala damage also prevents acquired fear: fear conditioning does not occur following amygdala damage.  Role of the amygdala in fear conditioning An electric shock (unconditioned Conditioned response stimulus –US-) produces unconditioned 25 Control Mean arterial blood pressure (mmHg) Amygd lesion responses (US) e.g., an increase in 20 blood pressure. When a tone is 15 presented repeatedly before the US, the 10 response will also appear following the 5 tone alone (conditioned response). This 0 1 2 3 4 5 6 7 8 9 10 seconds fear-conditioning is attenuated in animals following amygdala lesions. LeDoux et al., (1990)  Role of the amygdala in fear conditioning In 1911, the Swiss neurologist and psychologist Edouard Claparede, observed that an amnesic lady kept forgetting she ever saw him. On one occasion he hid a needle in his hand when he shook hands with her. On the next occasion, she still couldn’t Edouard Claparede (1873-1940) remember him, but refused to shake hands (although she didn’t know why). Bechara et al., (1995) Science  Role of the amygdala in fear conditioning In 1995, Bechara and coll. repeated a similar experiment in 3 patients with different lesions: a) Bilateral amygdala damage b) Bilateral hippocampal damage c) Bilateral hippocampal AND amygdala damage Episodic memory and fear conditioning were measured in each patient. Bechara et al., (1995) Science  Role of the amygdala in fear conditioning Experiment: An US (a 100dB boat horn ) was coupled with (1) a blue colour slide (visual conditioning) or (2) a computer sound (auditory conditioning) which served as the as the CS. time Bechara et al., (1995) Science  Role of the amygdala in fear conditioning  DV for conditioning was the electrodermal response (EDR)  DV for episodic memory was the response to 4 questions: How many different colours? Name the colours. How many colours were associated with the horn? Name the colours that appeared after the horn. Bechara et al., (1995) Science  Role of the amygdala in fear conditioning Amygdala damage Hippocampal Amygdala + Intact hippocampus damage Hippocampal Intact amygdala damage Fear conditioning (EDR)  KO  OK  KO Episodic Memory (Questions)  OK  KO  KO Bechara et al., (1995) Science  Role of the amygdala in fear conditioning Amygdala damage Hippocampal Amygdala + Intact hippocampus damage Hippocampal Intact amygdala damage Fear conditioning (EDR)  KO  OK  KO Episodic Memory (Questions)  OK  KO  KO Amygdala responsible for fear conditioning Bechara et al., (1995) Science  Role of the amygdala in fear conditioning Amygdala damage Hippocampal Amygdala + Intact hippocampus damage Hippocampal Intact amygdala damage Fear conditioning (EDR)  KO  OK  KO Episodic Memory (Questions)  OK  KO  KO Hippocampus responsible for episodic memory Bechara et al., (1995) Science  Role of the amygdala in fear conditioning Amygdala damage Hippocampal Amygdala + Intact hippocampus damage Hippocampal Intact amygdala damage Fear conditioning (EDR)  KO  OK  KO Episodic Memory (Questions)  OK  KO  KO Double dissociation for amygdala and hippocampus in conditioning and memory Bechara et al., (1995) Science  The role of the prefrontal cortex in emotion Lesions in basomedial (or ventral orbital) regions  changes in personality First case described: Phineas Gage in 1848 (see Damasio, Descartes’ error, chapter 1 for detailed description). Patients are socially inadequate, disinhibited, dysphoric, show impairments of social behaviour.  The role of the prefrontal cortex in emotion The 13th septembre 1848, an accidental explosion blows a tamping iron through Phineas Gage’s skull. The patient survived and his physician (Dr Harlow) describes the clinical case in 1848 then in 1868. Phineas Gage (1823-1860)  The case of Phineas Gage The rod (about 1m10 long with a diameter of 3cm) enters the left cheek, comes out at the top of the skull and lands some 25m away. Phineas Gage appears not to have lost consciousness even though his left and possibly right frontal lobes were destroyed.  The case of Phineas Gage A few months after the accident, probably around mid 1849, Phineas tries to work again. His character had changed so much that his employers no longer want to hire him. Before the accident he was said by his colleagues to be a most efficient and capable foreman… a shrewd, smart business man, very energetic and persistent in executing all his plans of operation. Afterwards he became fitful, irreverent... capricious and vacillating. He became impatient and obstinate, would be rude to others, did not manage to hold a job and became an alcoholic. He seemed incapable Reconstruction by of realizing the consequeneces of his actions. Damasio et al., 1994. His friends said he “was no longer Gage”.  Symptoms of Frontal Lobe Lesions Impaired social and sexual behavior ◦ Changes in personality ◦ Pseudodepression ◦ Appears after lesions of the left frontal lobe ◦ Outward apathy, indifference, loss of initiative ◦ Reduced sexual interest, Little or no verbal output ◦ Pseudopsychopathy ◦ Appears after lesions of the right frontal lobe ◦ Immature behavior, lack of tact and restraint ◦ Promiscuous sexual behavior ◦ Coarse language, lack of social graces, increased motor activity  Effect of ventral prefrontal lobes on emotion: psychosurgery Initiated by Moniz in 1935, frontal lobotomies were even performed to diminish symptoms in psychiatric patients (without any systematic scientific study to back the findings.  Effect of ventral prefrontal lobes on emotion: psychosurgery In 1945, Freeman developed a simplified (10 minute) procedure called “transorbital leucotomy”, which was widely used to “alleviate” psychiatric symptoms. It became know as the ice-pick lobotomy and was used on tens of thousands of persons. Insula responds to disgust In another study (Phillips et al. (1998) Proc Roy Soc) tried to identify regions responding to vocal and facial expressions of fear, as well as disgust. Phillips et al. (1998) Proc Roy Soc Insula responds to disgust Activation of facial expressions of fear were compared to baseline (neutral faces). As expected, fearful expressions activated the amygdala Phillips et al. (1998) Proc Roy Soc Insula responds to disgust Activation of facial expressions of disgust were then compared to baseline (neutral faces). This time, expressions of disgust activated the insula Phillips et al. (1998) Proc Roy Soc Insula responds to disgust Makes sense: The gustatory cortex is located in the insula. Electrical stimulation of the insular region can cause nausea Epileptic auras presenting as a “bad taste” or as nausea often originate in the insula Disgust is associated with bad food Hemispheric asymmetries and emotion  Hemispheric asymmetry in emotions In the early 1960s, the emotional responses during Wada tests were observed. Right inactivation  euphoric-maniacal reactions Left inactivation  depressive-catastrophic reactions So the left hemisphere was thought to house positive emotions while the right hemisphere was the seat of negative emotions inactivate left right or negative emotions inactivate right-left or positive emotion  Hemispheric asymmetry in emotions A decade later, an Italian neurologist, Guido Gainotti observed the same thing in brain-damaged patients: Patients with left hemisphere lesions tend to show catastrophic reactions when confronted with their difficulties (only 10% in right hemisphere lesions) Right lesioned patients are more often indifferent. They can be unaware of their difficulties, are more disinhibited, can joke or be sarcastic, even euphoric. They may deny their illness (called “anosognosia”) and even confabulate about a paralysed limb (e.g., “that hand belongs to my wife, she left it in my bed”) Gainotti’s hypothesis of asymmetrical representation of emotion Hemispheric asymmetries have been observed in emotional processing: the left hemisphere lesionsdepression, while the right hemisphereeuphoria. However, maybe the emotional response following right hemisphere lesion is inappropriate and only this hemisphere processes emotion (i.e., having a brain lesion is always a cause for depression…).  Hemispheric asymmetry in emotions: facial expressions How about people with not brain damage? Is there any asymmetry in the expression of emotion (Sackheim, 1978) ?  Hemispheric asymmetry in emotions: facial expressions Yes ! The left half of a face (right hemisphere controlled) is more expressive. Two left halves Normal face Two right halves  Hemispheric asymmetry in emotions: facial expressions Left and right brain lesions were tested on their capacity to express facial emotions. Facial expressions 60 50 Kolb & Milner (1981) show that both Mean no. expressions right and left brain damage reduce 40 facial expression. 30 But the right frontal group is more 20 impaired (Borod, et al., 1986) 10 0 Left frontal Right Left Right Left Right frontal temporal temporal parietal parietal  Hemispheric asymmetry in emotions: speech The amount of spontaneous speech was measured in right and left brain damage. Spontaneous speech 14 Kolb & Taylor (1981) 12 show that both right Mean frerquency of talking frontal damage 10 increases spontaneous 8 speech while left brain 6 damage reduces it. 4 2 0 Left frontal Right Left Right Left Right frontal temporal temporal parietal parietal  Hemispheric asymmetry in emotions Left and right brain lesions were tested on their capacity to express different emotions in their voices The right brain damaged patients were more impaired (Kent & Rosenbeck, 1982) The right brain damaged patients are more impaired in their capacity to recognise facial emotions The right brain damaged patients were more impaired comprehend emotional prosodies in actors’ voices from Borod et al. (2000) Hemispheric asymmetry 1 2 3 Right brain The right brain The right brain damaged patients damaged patients damaged patients are more impaired are more impaired were more in expressing in their capacity to impaired emotions in their recognise facial comprehend voices (Kent & emotions emotional Rosenbeck, 1982) prosodies in actors’ voices from Borod et al. (2000) SUMMARY: Hemispheric asymmetry in emotions  Right hemisphere probably more involved in emotion.  Theory that left- hemisphere=positive and right- hemisphere=negative emotion not entirely ruled out. Disorders of Emotion Major Depressive Disorder (MDD): Characterized by persistent sadness and lack of interest Bipolar Disorder: Marked by fluctuating mood states between mania and depression Generalized Anxiety Disorder (GAD): Encompasses chronic and excessive worry Post-Traumatic Stress Disorder (PTSD) : Stress and fear after a traumatic event ------------------------------------------------------------------------------------------------------------------------- Hyperactive amygdala leads to heightened fear and emotional response (PTSD, GAD) Changes in prefrontal cortex activity can lead to emotional impulsivity and mood instability Serotonin and norepinephrine imbalance (in bipolar disorder) NEUR2020 Neuroscience for Psychologists Semester 2, 2024 Frontal lobes Alan Pegna  The frontal lobes constitute about 1/3 of the brain’s total weight 3 subdivisions: The frontal lobe Motor region Premotor region Prefrontal region o dorsolateral o ventromedial or orbital o medial  The frontal lobe BA 6, 8, 44 : premotor region BA4 : Primary motor region BA 9, 10, 11, 45 : prefrontal region The frontal lobe Central or rolandic fissure The prefrontal area The prefrontal area is larger (proportionally) in humans: From: Walsh, Clinical Neuropsychology, 1997 The prefrontal area Anterior cingulate orbitofrontal http://dericbownds.net/uploaded_images/orbitofrontal.gif  The prefrontal area This region of the frontal lobe receives input from the dorsomedial thalamic nucleus Divided functionally into 3 separate parts: the prefrontal dorsolateral cortex the orbitofrontal (ventromedial) cortex The medial frontal cortex (cingulate gyrus ) These regions are essentially multimodal The prefrontal area: - what does it do? Supervisory functions o Working memory - o Inhibition o Flexibility o Planning o Reasoning o Problem solving Personality and behaviour --  Phineas Gage: a “dysexecutive” patient On September 13th, 1848, Phineas Gage was working as a foreman in Vermont when an accident shot a steel rod through the front of his skull. Not only did Gage survive the blow, he reportedly got to his feet and walked away. But with a significant part of his frontal lobe destroyed, Gage underwent a dramatic personality shift.  Phineas Gage: a “dysexecutive” patient Phineas Gage survived and his physician (Dr. Harlow) described his observation in 1848 and again in 1868. Experts say a photograph owned by a Maryland couple, Jack and Beverly Wilgus, depicts Phineas Gage 11  Phineas Gage: a “dysexecutive” patient The bar (about 1.10m long and 3 cm in diameter) entered the left cheek, emerged from the top of the skull and landed about 25m away. Phineas Gage did not lose consciousness despite the lesion. Reconstruction performed by Damasio and al. 1994.  Phineas Gage: a “dysexecutive” patient He was now fitful, irreverent, and grossly profane, showing little deference for his fellows. He was also impatient and obstinate, yet capricious and vacillating, unable to settle on any of the plans he devised for future action. His friends said he was “no longer Gage." Irritable and often confused, he was unable to perform the duties that made him a successful foreman. But he did work as a coach-and-six driver in Chile for six years. In February 1860, he began to have epileptic seizures and died on 21st May 1860 from Macmillan, 2000  Prefrontal ventromedial area: personality Inadequacy Apathy Disinhibition, Indifference Disorders of "social intelligence" Irritability, aggression Euphoria Poor social control, inappropriateness Anosognosia Poor planning, self-direction Apathy Distractibility Pseudo-depression At the motor level, object manipulation and imitation are observed. Ventromedial (=orbital) prefrontal regions  personality changes  Prefrontal area: planning Anecdotal reports – patients were ‘stimulus-bound’: reacted to whatever was in front of them and did not respond to imaginary situations, rules, or plans for the future. Some gained significant weight, and / or became sexually promiscuous Could not form / sustain goals Distracted by circumstances Dorsolateral prefrontal areas  cognitive deficits  Prefrontal area: cognitive difficulties Damage seems to also cause problems on a cognitive level – abstraction – planning – Selection of appropriate responses – Poor self-direction – Distractibility – Impaired working memory Behaviour is “reflexive”, elicited by environmental circumstances, and purposeless : stimulus-driven Cannot interpret the environment based on previous knowledge  Prefrontal area: cognitive difficulties Damage seems to also cause problems on a cognitive level – abstraction – planning – Selection of appropriate responses – Poor self-direction – Distractibility – Impaired working memory Behaviour is “reflexive”, elicited by environmental circumstances, and purposeless : stimulus-driven Cannot interpret the environment based on previous knowledge  Prefrontal area: cognitive difficulties Convergent vs. divergent thinking – Convergent thinking: one possible answer to a question (5 + 4 =?) – Divergent thinking : many responses possible (How many different things can you do with a piece of string?) – Frontal lobe injury disrupts divergent thinking Decreased spontaneity in behaviour – verbal fluency – figural fluency – Behaviour reduced overall The dorsolateral prefrontal area: divergent thinking Example of verbal fluency in a patient (Write as many possible words starting with S and C) The dorsolateral prefrontal area: divergent thinking Example of verbal fluency in a patient Produce as many different drawings as possible  The dorsolateral prefrontal area: inhibition red green blue yellow green blue red yellow red blue yellow red blue green blue red yellow red yellow green blue red yellow blue green blue green yellow red blue yellow green yellow green blue red green yellow green red blue green blue yellow red yellow blue green In this test, called the Stroop test, the colour of the font must be read as fast as possible (not the word). Perret (1974) showed that patients with a left frontal lesion are impaired (but imaging studies show activation on the right !!) The dorsolateral prefrontal area: concept formation The Wisconsin Card Sorting Test The dorsolateral prefrontal area: concept formation by number (e.g., 2) In this test, a deck of cards must by shape be (e.g.,triangle) Or by colour classified: (e.g., red)  The dorsolateral prefrontal area: concept formation Milner (1963) showed that patients with prefrontal dorsolateral lesions were impaired (BA ~ 9). Patients could not find all the criteria and/or could not shift from one to another when required to (perseverated and The Wisconsin Card Sorting Test became “stuck in a set”)  The dorsolateral prefrontal area: concept formation Stuss et al (2000) tested groups of patients with brain lesions and explored the types of errors  The dorsolateral prefrontal area: concept formation Patients with right and left (RDL and LDL) dorsolateral frontal damage, as well as superior medial frontal damage (SM) were most impaired. They switched categories the least often, and perseverated on the preceding category the most.  The dorsolateral prefrontal area: planning The Tower of Hanoi (or London or Toronto): must be rebuilt on another post using the fewest possible number of moves. Ss move one piece at a time, and must never place a larger piece on a smaller one. Dysexecutive patients are impaired at this task.  The dorsolateral prefrontal area: planning The Rey-Osterrieth complex figure: must be reproduced (redrawn) as accurately as possible. Both accuracy and planning are scored.  The dorsolateral prefrontal area: planning The Rey-Osterrieth complex figure: Patients with frontal lobe damage are impaired in their ability to plan and organise the figure correctly  The dorsolateral prefrontal area: planning The Rey-Osterrieth complex figure: Patients with frontal lobe damage are impaired in their ability to plan and organise the figure correctly The dorsolateral prefrontal area working memory Baddeley and Hitch in 1974 described working memory which involved elements (bits), kept in short-term memory over short periods, on which mental operations are performed The dorsolateral prefrontal area: working memory On-line manipulation of information is conceptualised as WORKING MEMORY: Information may be old, Reorganise: new, or mix of old and new –Q 1 C D 7 3 Internal – In alphanumeric order representation, –C D Q 1 3 7 ie imaginary situation  The dorsolateral prefrontal area: working memory McCarthy et al 1994 – Spatial working memory task – fMRI – Spatial wm task: respond when a stimulus appears at a location that has been used previously – Control colour task: respond when a red object appears – Same display Stimulus display ++ + + + + Spatial working memory task Respond Control colour task Respond  Location: “working memory” task Activates dorsolateral PFC more Dorsolateral prefrontal cortex (PFC) activation during the working memory task McCarthy et al (1994) PFC: temporal organization of memory – Patients with FL lesions – Arranging sequence for cooking meals – Could remember ingredients – Could not arrange her actions into a proper sequence, switching preparation from one dish to another, or mix up which ingredients belonged together – Could not generate a plan to achieve a coherent goal Arnold Pick In 1892, he described a man who had presented in life with progressive loss of speech and dementia. When the patient died his brain was found to be atrophied. This shrinkage had been caused by brain cells dying in localized areas. This feature of localization is very different to Alzheimer's disease where the atrophy is more generalized. Neuropathology associated with Pick’s Frontotemporal atrophy with "knife- like" thinning of the gyri in frontal lobes and temporal lobes.  Marked atrophy with ventricular dilation. Neuropathology associated with Pick’s Swollen brain cells (Pick cells) with abnormal tau protein inclusions  Frontotemporal dementia (FTD / Pick’s) Abnormal spontaneous behaviours during examination – Inappropriate jocularity – Echolalia (repeating the examiner's words), echopraxia (repeating the examiner's gestures) – Disinhibited approach or utilization behaviours – Unkempt, depressed in early stages – Primitive reflexes such as grasp, suck, and snout, toes 39  Pick’s disease: clinical course During the first 2 years Psychiatric abnormalities related to the “classic” frontal lobe syndromes: – orbitofrontal dysfunction: aggressive and social inappropriateness (may steal or demonstrate obsessive or repetitive stereotyped behaviours), apathy and disinhibition – dorsomedial or dorsolateral dysfunction: a lack of concern, apathy, or decreased spontaneity.  Pick’s disease: clinical course Speech and language – Abnormalities often begin early and progress fast. – Memory impairment relatively less severe than speech/language and behavioural changes – Verbal output that is often nonfluent, with poor naming of objects Movement disorders – Akinesia, plastic rigidity, or paratonia on motor examination – Perseveration  Anterior Cingulate Cortex Was thought to be part of the limbic system (modulation of autonomic responses) Now shown to have attentional / monitoring functions Considering and evaluating appropriate goals and subgoals on the basis of affective feedback 42  Anterior Cingulate Cortex Input from limbic structures, including Anterior cingulate amygdala, the thalamus and the striatum, as well as the brainstem Output to prefrontal cortical areas 43  Anterior Cingulate Cortex C Corbetta and colleagues – Ss asked to selectively attend to a single visual feature (colour, shape, motion) = PASSIVE – Or monitor changes in all three features at the same time = DIVIDED ATTENTION – Passive – enhanced activity in feature-specific regions – Divided attention – ACC activation – So, keeping track of more than one piece of info 44  The Orbitofrontal Cortex Social and emotional judgement ! Social and emotional decision-making Choosing how to act: integrate incoming info with pre-existing info about goals, values and current social situation Experience Individual differences 45 The Orbitofrontal Cortex and decision- making 46  The "Gambling Task” (also called “Iowa The Gambling Task”) was developed by Bechara Orbitofrontal and Damasio in 1994 Cortex and decision-  they suggested that we use emotional making experience to guide our behaviour ("somatic markers" hypothesis).  The prefrontal area (basomedial) The gambling task PICK A CARD Credit: 500$ A B C D  The prefrontal area (basomedial) The gambling task Credit: 500$ A B C D  The prefrontal area (basomedial) The gambling task YOU WIN 500 $ !! Credit: 1000$ A B C D  The prefrontal area (basomedial) The gambling task PICK A CARD Credit: 1000$ A B C D  The prefrontal area (basomedial) The gambling task Credit: 1000$ A B C D  The prefrontal area (basomedial) The gambling task YOU WIN 5 $ !! Credit: 1005$ A B C D  The prefrontal area (basomedial) The gambling task PICK A CARD Credit: 1005$ A B C D  The prefrontal area (basomedial) The gambling task Credit: 1005$ A B C D  The prefrontal area (basomedial) The gambling task YOU LOSE 1000 $ !! Credit: 5$ A B C D  The prefrontal area (ventromedial) The gambling task PICK A CARD Credit: 5$ A B C D  The prefrontal area (ventromedial) These 2 decks give high winnings. But overall the loss is greater A B C D  The prefrontal area (ventromedial) These 2 decks give lower winnings. But overall the gain is greater A B C D  The prefrontal area (ventromedial) The gambling task After a playing for a while:  Skin conductance (emotion)  before selecting B and C  Choices increase for decks A and D This happens although we cannot yet explain our choice. In patients with frontal lesion: The galvanic skin response persists (as in controls)  However the patients continue to choose B and C  and continue to lose... The "frontal" patients  cannot use emotional information (reward and punishment) to guide their behaviour  The prefrontal area (ventromedial) These observations lead to Damasio’s "Somatic marker hypothesis”. Primary emotions exist that are pre-established and innate (amygdala and anterior cingulate) Secondary emotions (prefrontal) are acquired and depend on the individuals’ life experience. The somatic marker confers a physiological state, a bodily sensation, to an image. The "gambling task" reveals whether a person uses his somatic state to predict and evaluate situations.  The prefrontal area (ventromedial) Risk taking during the Iowa gambling task activates the amygdala and orbito-frontal cortex. Lesions in the orbito-frontal cortex push the subject to take greater risks (bad risk assessment).  The frontal lobe: summary From an anatomical point of view, motor, premotor and prefrontal regions can be distinguished. From a functional perspective, the prefrontal area can be divided into basomedian, dorsolateral, and medial regions. On a neuropsychological level, one can distinguish movement disorders (motor, premotor), abstract thinking (planning, abstraction, etc.) and behaviour / personality (basomedial) depending on the areas affected.  From an anatomical point of view, motor, premotor and prefrontal regions can be distinguished. The frontal From a functional perspective, the lobe: prefrontal area can be divided into ventromedial, dorsolateral, and medial summary regions. (1)  A range of behaviours – Apathy – Irritability, aggression – Poor social control, inappropriateness – Poor planning, self-direction The frontal – Distractibility lobe: – Hyper-responsive to stimuli in the environment summary Functions (2) – Working memory and flexibility – Temporal ordering of memories – Planning and selection of goals – Social and emotional decision- making The frontal lobe: summary (3) NEUR2020 Neuroscience for Psychologists Lecture 11 Semester 2, 2024 Attention Alan Pegna  Plan Properties of Attention Capacity, selectivity Early / late selection Distractor interference Selectivity Overt, covert attention Disengagement, shifting, engagement Endogenous, exogenous cues Spotlight / Zoom lens of attention Inattention blindness, change blindness Neglect and extinction as examples of impaired mechanisms of attention The concept of attention ‘Everyone knows what attention is. It is the taking possession by the mind, in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought. Focalization, concentration, of consciousness are of its essence. It implies withdrawal from some things in order to deal effectively with others…’ William James (1907) Attention: working definition Processes that enable a person to recruit resources for processing selected aspects of the incoming sensory information more fully than non-selected aspects. Includes allocating resources to relevant aspects of the environment, ‘locking on’ / engaging, shifting, re- engaging, a well as inhibiting irrelevant information  Attention is NOT: Alertness and arousal Reticular activating system (RAS) in the brain stem - most basic ‘attention’ function Low => poor extraction of information from environment Nervous system has to be receptive to stimulation Diffuse connections to most regions of the cortex Damage: coma (unresponsiveness to most external stimuli), stupor, chronic vegetative state  Arousal and EEG The electro- encephalogram (EEG) provides an electrophysiological measure of arousal. Healthy individuals at different stages of sleep: different behavioural and EEG characteristics  Arousal and EEG The electro-encephalogram (EEG) provides an electrophysiological measure of arousal Coma shows different, EEG patterns (recognizable to the trained eye) Simons & Chabris’ experiment Simons & Chabris (1999) Perception, 28, 1059-74  Two important properties of attention Capacity: is the amount of perceptual resources varies with the task and available for a task / process. individual. Selectivity: at any given moment the fixed attention is selective in perceptual resources can be allocated to different terms of what gets subsets of information in a flexible way. processed at what does not.  Cocktail Party Effect Focus on one source of information, amongst many Bored? Listen to someone else’s conversation Or we overhear something important So, attention can be re-directed, and information selected in a couple of ways  Selective attention Broadbent (1958) suggested that attention functions as an early filter  information is filtered out early on Effectors Limited capacity Sensory registers Output system processor Stimuli Filter Long term memory Broadbent (1958) Perception and Communication. London: Pergamon Press.  Cocktail Party Effect Cherry (1953) used dichotic listening tasks A different stream heard in each ear Ss could follow sensible message even when it switched ears Would hear their names or an emotional word like “murder” (salience) So some stimuli can “intrude”… so there’s no filtering out  Selective attention  But what about the “Cocktail party effect” (Cherry, 1953)?  If your name is mentioned, it attracts your attention  Same if someone hears an emotional word (“murder”)  This means that attention is filtered later Semantic processing Effectors Output system Sensory registers Stimuli Filter Long term memory Cherry (1953) JAMA, 25, 975–979. Deutsch & Deutsch (1958)  Early vs. Late Selection When does the gate get shut ? – the ‘filter’ / bottleneck What is the fate of unattended info? Does it alter performance to targets? Early Late But how can early If selection occurs selections be made later after extensive without any processing, why processing? bother selecting at all?  Early Selection Late Selection Cherry; Broadbent (1950s/early 1960s) Treisman; Deutsch & Deutsch 1960s Sensory input Sensory input Vision; Audition, Vision; Audition, Somatosensory, etc. Somatosensory, etc. Sensory registration Implies increased Sensory registration } interference from irrelevant Attentional info (bc more time bottleneck to process info) Perceptual analysis Semantic meaning } Perceptual analysis Implies reduced Semantic meaning Attentional interference Bottleneck from irrelevant happens later info Higher analysis Higher analysis Awareness Awareness Response selection Response selection  It’s a bit of both (early and late) Depends on task (instructions; type of task,…) We know this because unattended info slows reaction times; reduces accuracy to targets Effectors Limited capacity Output system Filter-attenuator Sensory registers processor Stimuli Long term memory Cherry (1953) JAMA, 25, 975–979. Treisman (1964) Br Med Bull, 20, 12-16.  Example: distractor interference Baseline: no distractor Neutral distractor Opposite distractor Two targets, always appear centrally mapped on two hands: H S H S E H E H – right hand E – left hand Irrelevant information slows resp onses to the target (increased response time) Particularly when the opposite response needs to be inhibited Baseline Neutral distractor Opposite distractor  Visual search o Dealing with busy scenes o Several attention mechanisms engaged in such a context  Overt (making eye movements) vs covert  Shifting attention and the spotlight of attention  Top-down / bottom-up  Zoom lens  Parallel / serial search Overt vs covert attention Overt deployment of attention Eye movement to shift attention Covert deployment of attention Move your attention but not your eyes  Attention shifting: 3 components Disengagement One must disengage from current target Shifting Attention then has to be directed to new target Engagement After reaching new target, attention must be re-engaged  Shifting requires 3 different processes, done by 3 brain regions  Attention shifting: 3 brain areas Disengagement Parietal lobe Shifting (and eye movements) Superior colliculus Engagement thalamus  Each process is selectively impaired after damage to specific brain areas Neural substrates of shifting attention Disengagement Damage to the parietal lobe (especially the right) results in loss of disengagement. Movement / shifting Damage to the superior colliculus impedes movement. Eye movements are also compromised. Engagement Damage to regions in the thalamus compromises this function. Therefore, moving attention from one point to another requires the coordinated action of three separate brain areas.  Attention shifting: 3 brain areas Posner initiates a series of studies on attention shifting and covert attention. The paradigm is often used with his name (Posner’s paradigm) The task is the following:  Attention shifting: Posner’s paradigm Press the left or right key in response to the side where the square appears. The arrow indicates the most likely side of appearance of the square. Respond as rapidly as possible. +  Voluntary and involuntary shifts in attention 1. “Endogenous cues” (symbolic cues - central arrow) Attention must be voluntarily pushed from the central cue to the cued location. 2. “Exogenous cues” Attention is drawn to the location of the cue. Is usually a flash or movement. Cannot be ignored (involuntary). Attention shifting: Posner’s paradigm Healthy control group 580 Right 560 Left 540 520 500 480 460 440 420 400 Valid cue Invalid cue (Posner, Nissen & Ogden, 1978).  cost and benefit of cueing attention to forthcoming target – from Posner cueing paradigm 450 cost 400 Response times (msec) benefit 350 300 250 200 150 valid trial neutral trial invalid trial Enhanced processing in the attended area, a cost with the unattended area receiving less processing.  Attention shifting: Posner’s paradigm These studies showed that 1) Covert and overt (=with eye movements) are dissociated 2) Attention shifting takes time 3) Covert attention moves moves, like a “spotlight”  ERPs recorded during attention shifting N = negative P = positive ERPs are recorded here over the right occipital cortex in healthy controls. Observer covertly attends to either the left or right location as cued by the experiment. Valid cues (green line) associated with enhanced P1 and N1 ERPs relative to invalid cues (red line). – enhanced processing of the validly cued target  Voluntary and involuntary shifts in attention Top-down / bottom-up Exogenous / endogenous cues The interface between external environment and internal states (goals, expectations). Always an interaction between the two states  Zoom lens of attention Zoom lens (Eriksen & St James, Klein): Attention is loosely likened to a zoom lens on a camera that has variable spatial scope. However, the wider the field, the coarser the detail. Narrow field = fine resolution. Local/Global tasks support the zoom lens metaphor.  Distributed vs Focused Attention Distributed attention involves parallel processing and visual “pop out” Visual processing occurs simultaneously over the whole visual field. Focused Attention involves serial processing. Selecting a bit of the environment at a time Visual processing is a series of attentional “fixations” each covering a different region of the visual field. Target detection X T T Find the T Treisman & Gelade, 1980 Target detection T T X X T T Find the T Treisman & Gelade, 1980 Target detection X T T X T X X T X T Find the T Treisman & Gelade, 1980 Target detection X T X T X T T X T X X X X T T Find the T Treisman & Gelade, 1980 Target detection X T T X X T X T X T T X T T X X X X X T X T X T X X X X X X T X T T T T X T Find the T Treisman & Gelade, 1980  Target detection Target detection takes time. Time increases with the number of distractors (~20-40 ms/item) Search is serial Detection Vitesse speed de détection (ms) (ms) 2600 2400 2200 Mean reaction time (ms) 2000 1800 1600 1400 1200 1000 800 600 Temps de réac 400 200 Targetprésente present 1 5 15 30 Cible Cible absente Target absent Number Nombre de of distracters distracteurs Treisman & Gelade, 1980 Target detection X T X Find the T Treisman & Gelade, 1980 Target detection X T X X X X Find the T Treisman & Gelade, 1980 Target detection X X X X X T X X X X Find the T Treisman & Gelade, 1980 Target detection X X X X X X T X X X X X X X X Find the T Treisman & Gelade, 1980 Target detection X X X X X X X X X X X X X X X X X X X X X X X X X X X X X X T X X X X X X X Find the T Treisman & Gelade, 1980 Target detection Vitesse de speed Detection détection (ms) 1300 1200 Mean reaction time (ms) 1100 1000 900 800 700 600 500 Temps de réacti 400 1 5 15 30 Serial search Recherche sérielle Pop-out Non-sérielle Nombre Numberde ofdistracteurs distractors Treisman & Gelade, 1980  Distributed vs Focused Attention Distributed attention involves parallel processing and visual “pop out” (also called ‘feature search’) Visual processing occurs simultaneously over the whole visual field. Focused Attention involves serial processing. Selecting a bit of the environment at a time Visual processing is a series of attentional “fixations” each covering a different region of the visual field.  Parallel Search (“Pop out”) single feature difference Task: detect target Note number of ‘distractors’ Target: tilted black bar. Target: white bar.  Distributed vs Focused Attention Distributed attention involves parallel processing and visual “pop out” Visual processing occurs simultaneously over the whole visual field. Focused Attention involves serial processing. Selecting a bit of the environment at a time Visual processing is a series of attentional “fixations” each covering a different region of the visual field.  Serial Search Look for the black bar tilted top right. More than one feature difference (also called ‘conjunction search’)  Parallel and Serial Search Parallel Serial 800 800 Absent Present Reaction Time (msec) Reaction Time (msec) 600 600 400 400 200 200 0 0 2 16 2 32 Number of distractors Number of distractors Neural substrates of pop-out and serial search Serial Engages predominantly the parietal lobes; slow process Popout (parallel) Engages mainly early perceptual areas (striate and extrastriate cortex); rapid process. Parallel search doesn’t require spatial attention shifting.  Summary so far Properties of attention Mechanisms Capacity, selectivity Distractor interference Distributed, focused Overt, covert Early vs late filter monitoring Disengage, shift, engage shifts: exogenous, endogenous When attention ‘fails’  Change Blindness Small changes in the visual display not detected (described by Rensink et al., ~1995)  To summarise Attention helps us avoid sensory overload “Illusions” reveal the presence of the “filter” Demonstrates the capacity limitations of attention, not the limitations of vision Disorders of attention  Unilateral Spatial Neglect Patients do not acknowledge stimuli on the left Sensory, spatial, motor and attentional factors: multimodal Also distinguish from visual field deficits such hemianopia and quadrantanopia  Unilateral Spatial Neglect Occurs after damage to one side of the brain (usually the right hemisphere) Patients behave as if the affected side of space (the contralesional side) has ceased to exist: – ignore food on one side of their plate – fail to shave/make-up one side of their face – bump into objects on one side – fail to read text from one side of the page – or one side of word Most common and severe after damage to the parietal lobe (but can arise from cortical and subcortical damage elsewhere) Frequently co-occurs with hemiplegia and visual field deficits Unilateral Spatial Neglect Line bisection Line crossing  Unilateral Spatial Neglect Line bisection Line cancellation Copying Circle cancellation Drawing from Star memory cancellation Unilateral Spatial Neglect  Eye movements in neglect (scanning of the visual environment) Scan paths (= gaze of patients with unilateral spatial neglect during active visual search (black lines) and at rest (grey lines) (left panel), compared to controls (right panel). Fruhman-Berger (2008) Deviation of eyes vs head  Lesions causing neglect: parietal lobe Middle cerebral artery Basicmedical Key Left unilateral neglect is most frequent Caused by strokes affecting the middle cerebral artery (MCA) on the right  Attentional control with left vs. right parietal lesions Why is unilateral spatial neglect essentially on the left?  It’s likely that the right hemisphere is more involved in spatial attention. Left parietal Right parietal lesion lesion Attentional control with left vs. right parietal lesions Left visual field Right visual field Healthy individuals Left hem Right hem Left visual field Right visual field Left visual field Right visual field Left hem Right hem Left hem Right hem Left parietal lesion Right parietal lesion Emotion and Threat 1. Affect & Attention: In-Class Behavioural Experiment 2. Affect & Memory: Neuroimaging study Affect and Emotion used synonymously here. Definitions? Differences? Relation between affect/emotion and cognition. Specifically, two functions of cognition:  Attention  Memory  Threatening stimuli capture our attention  For example – the angry face in the crowd effect  People are faster to find an angry face amongst other expressions Pinkham et al. 2010  Facilitated attention: We detect threatening stimuli faster than non- threatening stimuli  Difficulty disengaging: We struggle to move our attention from threatening stimuli  WARNING There will be photos of creatures in the experiment, including snakes and spiders. If this will cause you distress please do NOT run the experiment or look at others’ screens.  Learning Resources  Tutorials  Emotion and Threat  Download and UNZIP the experimental folder onto the desktop. 1. Open the ‘Dot Probe Main Task’ file in Matlab 2. Make sure you are in the editor tab and click the green run arrow 3. Follow instructions. Open the data file in excel Some stimuli are frequently associated with danger in the natural environment – these are termed fear-relevant.  Certain animals, such as snakes and spiders, can be dangerous – bites can cause illness or death.  It aids survival for these fear-relevant animals to have priority in our attentional and cognitive systems. Lipp & Derakshan (2005) showed that fear- relevant animals can capture spatial attention.  Our experiment is a miniature version of one conducted by Lipp and Derakshan (2005). First, fixation in centre….. + Second, distractor images – a snake and lizard OR a spider and beetle. Snake/Spider + Lizard/Beetle Third, the target appears on the left OR right. + - Do you think people should be faster or slower to detect the target when it appears in the same place as the fear-relevant animal? Why? If fear-relevant animals capture attention, then: We should be faster to detect the target when it appears on the same side as the fear- relevant animal (valid condition) than the non- feared animal (invalid condition).  345 Invalid: Target appears on opposite 340 side to probe 335 * Valid: Target appears on same side as probe Probe Detection time (ms) 330 325 320 * People faster overall when 315 target is on the right because 310 they are right- handed. 305 300 Left Right Probe Location Invalid Valid Did snakes capture your attention? Did spiders capture your attention? Remember, your attention was captured if your reaction times are FASTER (i.e., lower) for valid condition than invalid condition. Strengths – come up with at least 2 strengths of our experiment Limitations – come up with at least 2 limitations Strengths  Spiders and snakes paired with similar-looking non-dangerous creatures. Limitations  Didn’t measure people’s fear of snakes/spiders (or lizards/beetles)  Some scary creatures were camouflaged. Standard procedures - these are standard procedures rather than notable strengths – would not get good marks in Lab Report 2  Had half the targets on the left and half on the right to eliminate handedness effects (this is more a standard procedure than a notable strength – don’t use this in assignment)  Randomised the order of trials – to avoid doing all the snakes first or all the spiders first or all the left-targets first  While fear-relevant stimuli have broad effects, stronger effects are typically found in subjects with greater levels of fear  For example – fearful participants are often struggle more to disengage from threatening stimuli  Spiders as targets Task: Visual Search where spiders could be the target or distractors Spider Fearful participants showed generally more attentional capture and distraction by spider stimuli than non-fearful controls Spiders as Distractors Note