Physiological Basis of Emotion
Phineas Gage: A classic case illustrating how damage to the frontal lobe can change personality and affect emotional regulation, showcasing the importance of the brain in emotional processes.
Theories of Emotion
Darwin’s Theory of Emotion: Suggests that emotional expressions evolved as behavioral signals that indicate an animal's intentions or feelings.
Telegraphed Behavior: Refers to actions that communicate expected behavior.
Principle of Antithesis: States that opposite emotions are expressed through contrasting behaviors, such as submission versus aggression.
James-Lange Theory: Proposes that emotions arise from the brain interpreting physiological responses; for example, we feel fear because our heart races.
Cannon-Bard Theory: Argues that emotional experiences and physiological reactions occur simultaneously but independently; the thalamus sends out emotional stimuli and initiates physiological responses at the same time.
Sham Rage: Observed in cats that have undergone cortex removal, displaying intense rage in response to minor stimuli; indicates the cortex's important role in controlling emotional outbursts.
The Amygdala and Limbic System
Kluver-Bucy Syndrome: Demonstrated in monkeys with damaged amygdalas, making them exceptionally tame and fearless, which highlights the amygdala's role in fear and aggression regulation.
Universal Emotions and Expression
Ekman’s Research: Discovered that basic emotional expressions such as happiness, anger, and fear are universally recognized across cultures, even in isolated communities.
Facial Feedback Hypothesis: Suggests that facial expressions can influence emotional experiences; for instance, smiling can lead to feelings of happiness.
Genetic and Social Influences on Emotion
While genetics form the basis of emotions, cultural factors significantly affect how these emotions are expressed.
Aggression in Rats
Colony Intruder Model: Analyzes how rats act defensively (freezing or fleeing) or aggressively (attacking or adopting a boxing posture) when encountering intruders.
Testosterone's Role: Known to increase aggression, especially in males, which is influenced by social experiences as well.
Fear Conditioning and Brain Areas
Fear Conditioning: A learning process where a neutral stimulus (such as a tone) becomes associated with a frightening event (like a shock), leading to learned fear responses.
Contextual Fear Conditioning: Fear becomes linked to the environment associated with the traumatic event rather than just the stimulus itself; involves the amygdala for fear response and the hippocampus for contextual memory.
Cognitive Neuroscience of Emotion
Emotions arise from the collaboration of multiple brain regions:
Amygdala: Focuses on processing threats and fear.
Prefrontal Cortex: Regulates emotional responses.
Anterior Cingulate Cortex: Important for emotional awareness and pain response.
Stress and Psychoneuroimmunology
Stress Pathways:
Sympathetic Nervous System (SNS): Produces immediate fight-or-flight responses.
HPA Axis: Manages long-term stress through cortisol release.
Psychoneuroimmunology: Investigates how stress impacts the immune system. Chronic stress has detrimental effects, weakening immunity, enhancing illness rates, and resulting in poorer health outcomes.
Chapter 18: Biopsychology of Psychiatric Disorders
Schizophrenia
Characterized by hallucinations, delusions, and disorganized thinking. Subtypes:
Paranoid: Dominated by strong delusions or hallucinations.
Catatonic: Marked by severe movement disturbances.
Disorganized: Involves incoherent speech and chaotic behavior.
Positive Symptoms: Such as hallucinations or delusions that add experiences.
Negative Symptoms: Absences in normal functionality like reduced speech, emotions, or motivation.
Causal Factors of Schizophrenia
Influential factors include genetics, prenatal stress, early brain damage, substance use, and various environmental stressors.
Dopamine Theory of Schizophrenia
Theory: Excessive dopamine activity is thought to precipitate the symptoms.
Supporting Evidence:
Antipsychotic medications that block dopamine receptors alleviate symptoms.
Substances increasing dopamine (like amphetamines) can induce similar symptoms.
Contradictions: Not all patients respond to dopamine blockers, and some symptoms take time to subside even with treatment.
Brain Changes Associated with Schizophrenia
Key findings include enlarged ventricles, reduced sizes of the hippocampus, amygdala, and thalamus, alongside reduced frontal lobe activity (hypofrontality).
Neurological differences can be identified before symptoms manifest.
Depression vs. Bipolar Disorder
Major Depression: Characterized by persistent sorrow, diminished energy, and disinterest.
Bipolar Disorder: Characterized by alternating episodes of depression and mania.
Reactive Depression: Linked to specific life events.
Endogenous Depression: Not specifically associated with external events.
Causal Factors for Depression
Factors involve genetics, childhood trauma, neurotransmitter dysfunction, and chronic stress.
Monoamine Theory of Depression
Suggests that depression is a result of low levels of neurotransmitters like serotonin and norepinephrine.
Supporting Evidence: Antidepressants elevate monoamine levels and are effective in reducing symptoms.
Contradictory Findings: Drug effects are rapid yet mood improvements are gradual; not all depressed individuals exhibit low monoamine levels.
Neuroplasticity Theory
Proposes that depression results from reduced brain plasticity, which antidepressants may help restore.
Treatment of Depression
Common treatments include SSRIs (e.g., Prozac), SNRIs, MAO inhibitors, and tricyclics. Research suggests normalization in activity in brain regions such as the prefrontal cortex and hippocampus with antidepressant use.
Hypomania vs. Mania; Bipolar I vs. Bipolar II
Hypomania: Lesser form of mania, characterized by milder and shorter episodes.
Mania: Marked by extreme energy, high-risk behaviors, and euphoria.
Bipolar I: Involves full manic episodes.
Bipolar II: Characterized by hypomania and depressive episodes without full mania.
Anxiety Disorders
Categories include Generalized Anxiety Disorder, Panic Disorder, Phobias, PTSD, and OCD, all defined by excessive fear or worry alongside behavioral symptoms.
Neural Basis of Anxiety: Involves the amygdala, which plays a central role in fear responses, along with contributions from the prefrontal cortex and hippocampus. Imaging studies typically reveal heightened activity in fear circuits.
Tourette’s Syndrome
Identified by tics (sudden movements or sounds), linked to issues in the basal ganglia and frontal cortex, possibly connected to dopamine imbalances.
Non-Drug Treatments for Disorders
Include Cognitive Behavioral Therapy (CBT), exercise, mindfulness, meditation, Electroconvulsive Therapy (ECT) for severe cases, Transcranial Magnetic Stimulation (TMS), and lifestyle adjustments focusing on sleep, social support, and nutrition.