Exam III Revision - Attention and Consciousness PDF

ATTENTION and CONSCIOUSNESS Overt attention: directing our senses and our attention towards the same target (include moving the eyes and head). Covert attention: shift focus of visual attention, e.g., in peripheral vision (without moving your eyes) Inattentional blindness: The failure to perceive...

ATTENTION and CONSCIOUSNESS Overt attention: directing our senses and our attention towards the same target (include moving the eyes and head). Covert attention: shift focus of visual attention, e.g., in peripheral vision (without moving your eyes) Inattentional blindness: The failure to perceive non-attended stimuli that seem so obvious as to be impossible to miss. **Late** selection model: A model of attention in which the attentional bottleneck filters out stimuli **after** even preliminary perceptual analysis has occurred. **Early** selection model: A model of attention in which the attentional bottleneck filters out stimuli only **before** substantial analysis has occurred. Define the meanings differences Timing example of experimental task - Voluntary attention is endogenous, top-down process, which means we shift our attention towards a specific target according to our goal and interest. Slower comparing to involuntary but can maintain for a longer time. Posner cuing task: show an arrow to any direction, then present the target according to the location of the arrow. - Involuntary attention is exogenous (triggered by salient stimuli in the external world), it is bottom-up process, which means it is controlled by sensory inputs that are in lower level of nervous system. Fast, but fades away quickly. Experiment: a high frequency of sound or sudden dash of light that which is presented unexpectedly to trigger a reflex. What other factors modulate attentional selection? - The salience of the stimulus - Where the eye moves and their fixation point - Whether we attend to whole objects or features - Time delay to select a target stimulus in the sensory field - Motivation (reward) - Task, context, predictive components - Link to working memory ERP: directing attention to the correct location enhances neural processing when the stimulus appears, reflected as large enhancements in the P1 and N1 components.  Brain structure involved in attention: - Super colliculus: involved in the movement of the eyes toward objects of attention, especially **overt attention**. - Pulvinar: heavily involved in visual processing and **direction of attention**. - Temporoparietal Junction (TPJ): The point in the brain where the temporal and parietal lobes meet that plays a role in **shifting attention** to a **new** location after target onset and involved in **bottom-up control**. - Lateral intraparietal area (LIP) in monkey: involved in the voluntary, **top-down control** of attention. - Intraparietal sulcus (IPS) in human: involved in voluntary, **top-down control** of attention. - Frontal eye field (EFE): important for establishing gaze in accordance with cognitive goals (top-down processes) rather than with any characteristics of stimuli (bottom-up processes). Brain disorders about attention: - Hemispatial neglect: No attention is paid to the left side of the body or to things presented to that side. Results from damage to the right inferior parietal cortex. - Bálint's syndrome: that may occur after bilateral lesions of cortical attentional systems. - Oculomotor apraxia: difficulty in steering gaze voluntarily - Optic ataxia: difficulty reaching using visual guidance. - Simultagnosia: difficulty paying attention to more than one object at a time Consciousness: The state of awareness of one's own existence and experience. - Easy problem: Mechanisms, processes, and observable correlations - Hard problem: Subjective experience and qualia EMOTIONS Emotion: a subjective mental state usually accompanied by distinctive behaviors and involuntary physiological changes - James-Lange Theory: Emotions result from the interpretation of physiological changes in the body. - Cannon-Bard Theory: Physiological arousal and emotional experience occur simultaneously but independently. - Schacht and Singer Theory: emotion arises from physiological arousal and cognitive labeling of that that arousal, context determines how physiological arousal is labelled Sympathetic nervous system: activates fight and flight Parasympathetic nervous system: activates rest and digest - Emotions/brain regions/neurotransmitters: - Fear: amygdala + limbic system hippoacampus contextualize and learn what is dangerous; two pathways (low: thalamus to amygdala) (high: thalamus to cortex); norepinephrine: increase alertness and physical readiness + GABA inhibitory neurotransmisster helps regulate overreaction of fear response - Happiness: amygdala process emotions Dopamine (rewarding system) + **ventral tegmental area** (produces dopamine and initiates the rewarding pathway), Oxytocin (love hormone, fosters social bond), Serotonin, Endorphin + opioids, androgens/estrogens (sex hormone contributes to mood regulation) - Sadness: the cingulate cortex (process emotional pain and monitors conflict between emotion and cognitive states) and insular cortex (integrates bodily sensations). Low serotonins are associated with depression and reduced dopamine level and elevated cortisol level - Disgust: anterior insula; activated by senses and also social (STOPPED) Brain regions like the amygdala (threat detection), hypothalamus (fight-or-flight), and prefrontal cortex (impulse control) coordinate reactive and proactive aggression, modulated by these chemicals. Acute stress involves autonomic responses like increased heart rate, blood pressure, and cortisol release, while chronic stress dysregulates the hypothalamic-pituitary-adrenal (HPA) axis, impairing recovery. Chronic stress weakens the immune system by suppressing lymphocyte production, increasing susceptibility to infections and inflammatory diseases. PSYCHOPATHOLOGY - **Schizophrenia** is a complex psychiatric disorder marked by positive symptoms (e.g., hallucinations, delusions), negative symptoms (e.g., flat affect, social withdrawal), and cognitive impairments (e.g., attention and memory deficits). It involves dopamine dysregulation, with hyperactivity in the mesolimbic pathway linked to positive symptoms and hypoactivity in the mesocortical pathway contributing to negative and cognitive symptoms. Antipsychotic drugs, such as Clozapine, primarily act as D2 receptor antagonists, blocking dopamine activity to reduce positive symptoms, and some also block serotonin receptors, which may help alleviate negative symptoms. Brain regions implicated include the prefrontal cortex, hippocampus, and ventricles, often showing structural abnormalities like reduced gray matter and enlarged ventricles. Schizophrenia is highly heritable (\~80%) and treatment combines antipsychotics with psychosocial therapies. It is almost equally prevalent in men and women. - Depression is characterized by persistent sadness, loss of interest, fatigue, and changes in appetite or sleep, often accompanied by feelings of worthlessness or suicidal ideation. It has a high heritability, with genetic factors like polymorphisms in the serotonin transporter gene contributing significantly to risk. Key brain regions involved include the prefrontal cortex (reduced activity), amygdala (hyperactivity), parietal and temporal cortex, and hippocampus, which often shows reduced volume due to impaired neurogenesis and potential synaptic loss. Depressed individuals exhibit differences in brain activity and connectivity, particularly in the default mode network (DMN) and reward pathways, compared to controls. Dysregulation of neurotransmitters like serotonin, dopamine, and norepinephrine underlies many symptoms. Treatments include antidepressants (e.g., SSRIs, SNRIs), psychotherapy (e.g., CBT), and newer approaches like transcranial magnetic stimulation (TMS), while gender, cultural norms, and stigma influence prevalence and treatment, with women at nearly double the risk due to hormonal and social factors. - Depression is more frequently diagnosed in women than in men, but this higher rate may not fully reflect greater prevalence. Increased use of mental health services and willingness to report emotional distress among women can lead to higher diagnosis rates compared to men, who may underreport due to stigma. Biological factors, such as the hormonal fluctuations associated with pregnancy, childbirth, and the postpartum period, play a significant role in triggering mood disorders in women, including postpartum depression. Additionally, hormonal imbalances, such as shifts in estrogen and progesterone levels during the menstrual cycle, pregnancy, and menopause, can increase vulnerability to depression by affecting neurotransmitter systems and stress regulation. Together, these biological, psychological, and sociocultural factors contribute to the observed gender differences in depression rates. - Bipolar disorder is characterized by alternating episodes of mania (elevated mood, impulsivity, hyperactivity) and depression (low mood, energy, motivation), with core theories including loss of brain homeostasis, neuronal loss, and disruptions in chronobiology (circadian rhythms). Neuroimaging studies reveal differences in brain activity between manic and depressive states, enlarged ventricles, and structural and functional differences in the limbic system (e.g., amygdala and prefrontal cortex). Dysregulation of multiple neurotransmitters, including dopamine, serotonin, and glutamate, is linked to symptoms, and pharmacological treatments. Bipolar disorder has strong heritability, though the genetics remain unclear; interestingly, lithium responsiveness also shows heritability. Gender and cultural factors influence symptom presentation, with women more likely to experience depressive episodes and rapid cycling. - Anxiety disorders encompass conditions like phobic disorders (intense fear of specific stimuli), generalized anxiety disorder (GAD) (persistent, excessive worry about everyday life), and panic disorder (sudden, intense fear accompanied by physical symptoms like chest pain or shortness of breath). These disorders involve overactivity in the amygdala, reduced regulation by the prefrontal cortex, and neurotransmitter imbalances, including low GABA (an inhibitory neurotransmitter) and abnormalities in serotonin receptor densities (5-HT1A). GABA agonists, such as benzodiazepines (BZs) like Valium, Xanax, and Halcion, are common anxiolytics; they enhance GABA's action, increasing chloride ion influx into neurons, causing hyperpolarization and reducing neural excitability. Valium, one of the most prescribed drugs in history, exemplifies the popularity of this treatment. Other anxiolytics include buspirone, a serotonin receptor agonist targeting 5-HT1A receptors. Psychotherapy, especially cognitive-behavioral therapy (CBT), often complements pharmacological treatments, addressing underlying thought patterns, while cultural and gender differences influence the prevalence and expression of these disorders. - Post-Traumatic Stress Disorder (PTSD) is characterized by symptoms such as intrusive memories, hyperarousal, emotional numbing, and avoidance of trauma-related stimuli. It involves brain regions like the amygdala (overactivation in fear processing), hippocampus (reduced volume affecting memory and context), and prefrontal cortex (impaired regulation of fear responses). Neurotransmitters such as cortisol (dysregulated stress response) and norepinephrine (hyperarousal) are implicated, and heritability studies suggest a genetic predisposition to PTSD, linked to smaller hippocampal volumes. Treatments include exposure therapy (including virtual reality-based methods) to target maladaptive fear conditioning pathways, along with medications like SSRIs. Gender differences show women are more susceptible, possibly due to hormonal and social factors, and cultural norms influence symptom expression and treatment access. The diathesis-stress model highlights the interplay between genetic vulnerabilities and environmental stressors in PTSD development. - Obsessive-Compulsive Disorder (OCD) is characterized by intrusive thoughts (obsessions) and repetitive behaviors (compulsions) that interfere with daily life. Brain regions implicated include the orbitofrontal cortex, cingulate cortex, and caudate nuclei, where increased metabolic rates are observed, as well as overactivity in a circuit involving the prefrontal cortex, striatum, and thalamus. Serotonin dysfunction is central, as evidenced by the effectiveness of SSRIs like Prozac, Luvox, and Anafril in reducing symptoms. Cognitive Behavioral Therapy (CBT) is another primary treatment. Genetic links suggest heritability and comorbidity with Tourette's syndrome, further implicating shared neural pathways. Cultural and gender differences influence symptom presentation, with women often reporting contamination fears and men more symmetry-related obsessions. This underscores the need for tailored approaches in treatment. MEMORY - Long term memory - Declarative verbal (explicit) - Episodic (experiences) hippocampus, medial temporal lobe, neocortex - Semantic (general knowledge and facts) lateral and anterior temporal cortex, prefrontal cortex - Non-declarative non-verbal (implicit) - Skill learning striatum - Priming neocortex - Classical conditioning amygdala and cerebellum - Non-associative learning reflex pathways - Spatial memory hippocampus and cortex - Short term memory sensorimotor and prefrontal cortex 3 steps of memory: - Encoding: sensory information into short term memory - Consolidation: short term memory/working memory into long term memory - Retrieving: stored information is used Patient H.M. underwent surgery to alleviate epilepsy, involving the removal of both sides of the anterior temporal lobe, including the amygdala and hippocampus, which resulted in anterograde amnesia---an inability to form new declarative memories (e.g., facts and events). Despite this deficit, H.M. retained non-declarative memory (e.g., procedural skills), demonstrating the distinction between memory systems. His case profoundly advanced our understanding of the roles of the hippocampus in declarative memory formation and the independence of implicit memory processes. Patient N.A. experienced anterograde amnesia, similar to H.M., following an injury that damaged the medial temporal lobe and structures in the midline diencephalic region, including the thalamus, hypothalamus, and mammillary bodies. Unlike H.M., who underwent surgical removal of the amygdala and hippocampus, N.A.\'s damage was accidental and primarily affected the diencephalic memory network. Patient K.C. (Kent Cochrane) is a landmark case in cognitive neuroscience, providing critical insights into the nature of memory. After a motorcycle accident caused extensive damage to his **medial temporal lobes**, particularly the **hippocampus**, and additional cortical damage, K.C. developed a unique memory impairment. He has severe episodic memory loss, and preserved semantic memory, and normal procedural memory. The **sensory buffer** is a component of memory that temporarily holds sensory information after it is perceived, allowing for initial processing. It consists of **iconic memory** for visual stimuli and **echoic** **memory** for auditory stimuli. The **delayed non-matching-to-sample task** tests **declarative** memory in **monkeys** by requiring them to recognize and choose a **new** **object** after a delay to find a food reward. Monkeys with **hippocampus** and surrounding temporal lobe damage are severely **impaired** on this task, while removal of the amygdala alone does not affect performance, showing that the hippocampus is crucial for this type of memory. The task demonstrates how the hippocampus and medial temporal structures support memory for objects and events, making it a valuable model for studying memory and conditions like amnesia. Exceptions: - **Savants** like Stephen Wiltshire, who can recreate highly detailed scenes from memory. (artist that draw the city) - **Hyperthymesia**: people who vividly recall personal life events but often have poor factual memory. - **Mnemonists** use specific strategies to remember arbitrary information. The **neural mechanisms of memory storage** involve **synaptic plasticity**, where synapses strengthen or weaken in response to activity, enabling learning and memory. Physiological changes include an **increase in synaptic transmitters** released and **interneuron modulation**, enhancing communication between neurons. Structural changes, such as the **formation of new synapses** and **rearrangement of synaptic inputs**, support long-term memory storage and adaptability. The **engram** represents these changes as the physical memory trace, distributed across neural networks. **Hebbian synapses** (\"cells that fire together wire together\") exemplify how repeated activation strengthens synaptic connections. **Long-term potentiation (LTP)**, a key mechanism, involves persistent strengthening of synapses, driven by increased activity and molecular processes like protein synthesis and dendritic spine growth, solidifying memories over time.