Chapter 6: Disorders of Cognition and Emotion (Biopsychology of Emotions)

Emotions

complex psychological state

3 Key Components of Emotion

Subjective experience

Physiological response

Behavioral or expressive response

Subjective experience

how a person feels internally (e.g., happiness, sadness, anger).

Physiological response

how the body reacts (e.g., increased heart rate, sweating).

Behavioral or expressive response

how emotions are shown outwardly (e.g., facial of voice expressions, body language, tone)

The Case of Phineas Gage (1848)

– The personality of a foreman changes after a construction accident that damaged his frontal lobe

Darwin’s Theory of the Evolution of Emotion (1872)

In his book, The Expression of Emotions in Man and Animals, emotions are described as reinforced expressions that indicate likely behaviors.James-Lange Theory (1884)

James-Lange Theory (1884)

– autonomic activity and behavior that are triggered by the emotional event produce the feeling of emotion

Cannon-Bard Theory (1872)

– emotional stimuli have 2 independent excitatory effects:

1. They excite both the feeling of emotion in the brain

2. expression of emotion in the autonomic and somatic nervous system

Limbic System Theory of Emotion

Emotional expression is controlled by several interconnected nuclei and tracts that ring the thalamus

limbic system

amygdala, mammillary body, hippocampus, fornix, cortex of the cingulate gyrus, septum, olfactory bulb, and hypothalamus

HIPPOCAMPUS

-  is a curved, seahorse-shaped structure located deep in the medial temporal lobe of the brain, heavily involved in memory and spatial navigation.

• Helps form contextual memories—linking emotions to specific events, places, and times.

FORNIX

A bundle of nerve fibers that acts as a major output tract of the hippocampus.

helps relay contextual memory (from the hippocampus) to emotion-processing regions

MAMMILLARY BODY

Ø   are 2 small, round structures located on the diencephalon

- Helps relay information from the hippocampus to the thalamus, supporting memory formation and recall.

- They play a role in emotional memory

AMYGDALA

Ø  is a small, almond-shaped cluster of nuclei located deep within the medial temporal lobe of the brain.

3 main complexes of amugdala

BASOLATERAL COMPLEX

CENTRAL NUCLEUS

CORTICOMEDIAL NUCLEI

BASOLATERAL COMPLEX

  - Receives sensory input from the thalamus and cortex.

• Involved in processing emotions, especially fear and reward.

CENTRAL NUCLEUS

-  Involved in olfactory (smell) processing.

• Plays a role in social and reproductive behaviors.

CORTICOMEDIAL NUCLEI

   - Main output center of the amydala

• Connects with the hypothalamus and brainstem to trigger physical reactions

CINGULATE GYRUS

-  is a curved fold of brain tissue located in the medial aspect of the cerebral cortex,

• Integrates emotional input from the amygdala with cognitive processing from the frontal lobes helping to decide how strongly to react to emotional events.

SEPTUM

- is a thin, midline structure located deep within the limbic system,

• Acts as a regulator of emotional intensity, having inhibitory effects on excessive emotional responses

OLFACTORY BULB

-  is a neural structure located just beneath the frontal lobes,

• The olfactory bulb links smell directly with the limbic system, making smell one of the most emotionally evocative senses.

HYPOTHALAMUS

-  is a small structure located deep below the thalamus and above the brainstem.

• It plays a key role in regulating many essential functions like hormonal balance, autonomic functions, and emotions.

- integrates emotional experiences with physical responses and helps regulate behaviors related to emotion

Universality of Emotions

A study showed that members of an isolated New Guinea tribe who had had little or no contact with the outside world expressed similar emotions that most people have (Ekman & Friesen, 1971)

6 primary facial expressions

surprise, anger, sadness, disgust, fear, and happiness

Facial Feedback Hypothesis

facial expressions influence our emotional experience

Voluntary Control of Facial Expression

It is possible to inhibit true facial expressions and to substitute false ones. There are many reasons for choosing to put on a false facial expression. Some of them are positive (e.g., putting on a false smile to reassure a worried friend), and some are negative (e.g., putting on a false smile to disguise a lie)

Duchenne Smile

 French anatomist Duchenne said that the smile of enjoyment could be distinguished from deliberately produced smiles by consideration of the 2 facial muscles that are contracted during genuine smiles:

2 facial muscles

Orbicularis Oculi

Zygomaticus Major

Orbicularis Oculi

which encircles the eye and pulls the skin from the cheeks and forehead toward the eyeball

Zygomaticus Major

which pulls the lip corners up. It can be controlled voluntarily, whereas the orbicularis oculi is normally contracted only by genuine pleasure

Hypothalamic-pituitary-adrenal (HPA) axis

-    a crucial neuroendocrine system that regulates the body's response to stress

Hyphothalamus

- detects stress signals and releases corticotropin-releasing hormone (CRH).

Pituitary Gland

CRH stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH).

Adrenal Glands

ACTH travels to the adrenal glands, which then release cortisol and other hormones, preparing the body for a stress response

Cortisol

Helps the body use glucose, protein, and fats

Adrenaline

- makes the heartbeat faster, causes blood pressure to go up and gives you more energy.

Cytokines

a group of peptide hormones that are released by many cells and participate in a variety of physiological and immunological responses, causing inflammation and fever

Stress

reduce dendritic branching in the hippocampus, and to disrupt the performance of hippocampus-dependent tasks.

• These effects of stress on the hippocampus appear to be mediated by elevated glucose and cortisol levels

hippocampus in stress

susceptible to stress induced effects. The reason for this susceptibility may be the particularly dense population of glucocorticoid receptors

Diathesis Stress Model

This model recognizes the interplay between underlying vulnerability (i.e. diathesis) that predisposes someone to illness and environmental stressors.Gene – Environment Correlation Model

• There’s a certain threshold or critical level at which a psychological disorder will develop

Gene – Environment Correlation Model

Describes situations where an individual's genes influence their exposure to certain environments, leading to a correlation between genetic and environmental factors

3 main types of GECM

passive, evocative (or reactive), and active (or selective).

HALLUCINATIONS

are perception-like experiences that occur without an external stimulus.

DELUSIONS

are fixed beliefs that are not amenable to change considering conflicting evidence.

DISORGANIZED THINKING

(formal thought disorder) is typically inferred from the individual's speech

CATATONIC BEHAVIOR

is a marked decrease in reactivity to the environment.

Essential Features of Psychotic Disorders

HALLUCINATIONS

DELUSIONS

DISORGANIZED THINKING

GROSSLY DISORGANIZED OR ABNORMAL MOTOR BEHAVIOR

CATATONIC BEHAVIOR

Genetic Factors of Schizophrenia

Pregnancy and birth complications with hypoxia and greater paternal age

prenatal and perinatal adversities, including stress, infection, malnutrition, maternal diabetes, and other medical conditions

Dopamine Theory of Schizophrenia

1. The antischizophrenic drug reserpine was known to deplete the brain of dopamine and other monoamines by breaking down the synaptic vesicles in which these neurotransmitters are stored.

2. Drugs such as amphetamine and cocaine, which can trigger schizophrenic episodes in healthy subjects, were known to increase the extracellular levels of dopamine and other monoamines

 reserpine

antischizophrenic drug, was known to deplete the brain of dopamine and other monoamines by breaking down the synaptic vesicles in which these neurotransmitters are stored.

amphetamine and cocaine

which can trigger schizophrenic episodes in healthy subjects, were known to increase the extracellular levels of dopamine and other monoamines

Anhedonia

impaired capacity for emotional gratification has long been noted to be due to a selective neuronal degeneration within the norepinephrine reward neural system

phencyclidine

a glutamate antagonist, produces an acute syndrome similar to schizophrenia.

Brain Damage Associated with Schizophrenia

Cerebral Ventricles

Prefrontal Cortex

Temporal cortex

Basal Ganglia

Cerebellum

Cerebral Ventricles

Implies loss of brain cells and correlates with poor cognitive performance and poor adjustment

Temporal cortex

Structural and functional abnormalities and altered connectivity

Prefrontal Cortex

Individuals with schizophrenia show low metabolic rates in prefrontal cortex

Basal Ganglia and Cerebellum

involved in the control of movement

2 broad types of Mood Disorder

•Involves only depressive symptoms

•Involves manic symptoms (bipolar disorders)

DSM-5 depressive disorders

•Major depressive disorder

•Persistent depressive disorder

•Premenstrual dysphoric disorder

•Disruptive mood dysregulation disorder

DSM-5 Bipolar Disorders

•Bipolar I disorder

•Bipolar II disorder

•Cyclothymia

DEPRESSIVE DISORDERS

• the presence of sad, empty, or irritable mood,

• somatic and cognitive changes that significantly affect the individual's capacity to function

What differs among them are issues of: duration, timing, or presumed etiology.

BIPOLAR DISORDERS

• the presence of mania

• Symptoms that are episodic

Monoamine Theory of Depression

holds that depression is associated with underactivity at serotonin and norepinephrine synapses.

Diathesis stress model

based on the finding that people with mood disorders tend to release more stress hormone cortisol

Brain Damage Associated with Mood Disorders

Prefrontal Cortex

Amygdala

Hippocampus

Hypothalamus

Prefrontal Cortex

associated with irrationality and cognitive impairment

Amygdala-

hyperactivity that caused exaggeration to reaction to emotional stimuli

Hippocampus

reduced volume affecting memory and negative bias

Hypothalamus

regulates sleep, appetite, libido, and mood.

ANXIETY

is anticipation of future threat.

FEAR

the emotional response to real or perceived imminent threat

PANIC ATTACKS

- an abrupt experience of intense fear or acute discomfort, accompanied by physical symptoms

Biological Factors in Mood Disorders

Autonomic Nervous System
Neurotransmitters
Genetics

3 major neurotransmitters associated with anxiety

norepinephrine (NE), serotonin, and r-aminobutyric acid (GABA)

Brain Damage Associated with Anxiety

Limbic System

Right Hemisphere of the brain

Frontal Cortex

Right Hemisphere of the brain

abnormal structures that influence emotional processing and intuition

Limbic System in Anxiety

increased activity of certain regions that explains overreaction to stimuli

Frontal Cortex –

overexaggeration of stimuli.