Neuropsychology Exam 3

Three components of emotion

1. Behavioral – visible actions like facial expressions or body language.

2. Physiological – changes in the autonomic nervous system.

3. Experiential – internal, subjective experience and cognitive interpretation.

Behavioral

• Facial expression (Paul Ekman)

• Body language

• Language

Our emotions are a big part of interpersonal interactions 

What are Ekman’s six basic emotions?

Anger, Disgust, Fear, Surprise, Happiness, Sadness.

Physiological

Change in autonomic nervous system 

Heart rate, respiration, sweating, pupil dilation — all help us respond to the environment.

Experiential - 2 aspects

• Subjective quality – emotions “happen to us.”

• Cognitive aspect – how we interpret, label, and regulate feelings.

James-Lange (Physiological theory)

• Emotions are our “recognizing” a change in our autonomic arousal level. 

• We see a shark in the ocean, it causes our heart rate to climb, then we feel afraid

Cannon-Baird (Physiological theory)

• Emotion feeling occurs before the physiological response.

• Example: We feel fear → then HR increases.

Stage fright

• Beta blockers stop physical arousal → people report less fear.

• Supports James-Lange, but both theories are partially correct.

Schachter and Singer — Two factor Theory

• Physiological Change

• Cognitive Interpretation

Experiment 

• Cover Story — Vitamin (suproxin) on vision

Injected with .5cc of adrenaline or saline

• 2 groups

Informed - made aware of side effects > HR

Ignorant - no side effect info

• Paired with angry or euphoric confederate

Measures self-report emotional state of subjects

• Ignorant more intense than informed

Behavior Brain area

Patients with lesions in the brain stem (medulla) have been reported to have uncontrolled crying (behavioral emotions)

• Not associated with “feeling” sad

• Dissociation between brain areas that control behavior and the other components of emotion

Hypothalamus

• Controls the push/pull of the autonomic nervous system

• Sympathetic = action

• Parasympathetic = calming

• Control cardiovascular system

• Regulates hormones, heart rate, breathing, sweating.

Amygdala

Made of several sub nuclei

• Central nucleus

• Lateral nucleus

• Basal

Removal of any results in tameness

Stimulation results in fear response 

• Startle

• Avoidance

LeDoux - Fear learning

• Classical conditioning of fear response

• Pair shock (UCS) with a ton (CS) and elicit freezing behavior (UCR)

• Eventually CS alone elicits freezing (CR)

In some studies they recorded electrical activity from amygdala 

• In others they lesioned the amygdala

Fear Conditioning in Humans

• Might underline anxiety disorders and PTSD

• Initially neutral environment stimuli get repeatedly paired with stress producing events

• Eventually these stimuli alone can cause stress response 

• Very resistant to extinction

Patient SM

• Bilateral amygdala damage in late childhood due to Urbach-Withe disease 

• Rare genetic disorder

• SM shows no behavioral or physiological evidence of fear

• Shown fear including stimuli she only shows interest, curiosity, and excitement 

• Unable to reliably report or draw fearful facial expressions

Role of cortex in emotion

• Interpretation of emotions

Judgements involving emotional information

• Regulation of emotions

Role of cortex - laterality

RH appears to play a more important role in 

• LH damage results in more depression

• RH damage more euphoria

RH damage

• Problems judging facial expressions 

• Problems determining and expressing emotion in voice

• A-prosodia

• Problems with comprehending humor

• Problems judging emotional situations (frontal lobes)

Orbitofrontal Cortex (OF)

Evidence suggests it has to do with translating personal consequences of behavior

• Patiens with OF damage can verbalize consequences, but less likely to use this information

• “ If I jump off the roof, I could break a leg”

• Might involve connects with the anterior cingulate gyrus 

• Anterior cingulate involves in inhibitory control

Phineas Gage

Personality changes, less inhibited

Prefrontal Lobotomy

• Jacobson’s chimp had fewer tantrums after frontal lobe removal

• Moinz (neuropsychiatrist) convinced neurosurgeons to try on humans

• Calmed patients and reduced compulsions

Schizophrenia

A serious mental disorder characterized by disoriented thoughts, delusions, hallucinations and other bizarre behavior.

1% of population - life long disorder

6 Schizophrenia diagnostics

1. Presence of critical symptoms — divided into:

   • Cognitive: delusions, hallucinations, thought disorder (incoherent speech)

   • Emotional: blunted or flat affect

2. Evidence of deterioration in functioning

3. Symptoms persist for at least 6 months

4. Any affective disorder must be secondary

5. Onset before age 45

6. Not due to an organic brain disorder

Postive schizophrenia symptoms

Hallucinations, Delusions, thought disorder

Negative schizophrenia symptoms

flat effect, lack of speech, Anhedonia (inability to pleasure)

what causes schizophrenia 

overactive dopamine system 

to many dopomaine receptors 

Major neuromodulator in the brain

involved in movement, reward, cognitive functions (STM, working memory and attention)

Evidence for the role of Dopomaine

Neuroleptics (Haldol) is effective treatment for positive symptoms - block dopamine action

Dopamine Agonists (e.g., amphetamine) aggravates and mimic schizophrenia

Amphetamine psychosis

neuroleptics (Antipsychotics)

• Drugs that block dopamine systems to reduce symptoms.

• Affect both dopamine pathways; striatum involvement causes side effects.

• Can lead to tardive dyskinesia — a movement disorder with repetitive muscle movements in the face, neck, arms, or legs due to too many dopamine receptors.

Anti-schizophrenic mediations

• Clozapine doesn’t strongly affect D2 receptors (movement system).

• Instead, it acts on D3 and D4 receptors in the limbic system and frontal lobes, helping control emotion and thought with fewer movement side effects.

what causes negative schizophrenia symptoms

• Neurological damage (possible cause)

• Glutamate hypothesis: underactive glutamate system in the cortex (NMDA receptor hypofunction) — since glutamate is the main fast-acting neurotransmitter in the cortex, low activity may lead to negative symptoms.

How do you get Schizophrenia 

genetic hypothesis, environment hypothesis, combines effects

Diathesis-stress model

It explains how mental disorders develop through an interaction between:

• Diathesis (vulnerability): a biological or genetic predisposition to a disorder.

• Stress: environmental or life stressors that trigger the symptoms.

3 types of depression

1. Reactive

2. Endogenous/unipolar (major depressive disorder)

3. Bipolar -manic/depression

Reactive non-clinical depression

1. “normal” depression

2. response to life events

3. usually passes in relatively short time

Major depressive Disorder symptoms 

Most typical symptoms:

• Low mood

• Inability to experience pleasure in past enjoyable activities

• “Ruminating” over thoughts and feelings of worthlessness 

• Inappropriate guilt or regret

• Helplessness or hopelessness

Other symptoms of depression: 

• Poor concentration

• Withdrawl from being social

• Reduces sex drive

• Irritability

• Insomnia or hypersomnia

• Thoughts of suicide

Major depressive disorder (MDD)

cycles, episodes average 13 months

• 2-3 times more likely in women

• 7-20% of population

• age usually around mid 20s

Major depressive disorder symptoms

• 40% generic

• diathesis-stress model

MDD results from preexisting vulnerability which is activated by environmental stress

Bipolar - manic/depression

• effects men and woman equally

• Elation - delusions and grandiosity

• average age: 30s

• usually lasts 6 months - 8 months without medication

• mania 2 months average

Types of Bipolar

Type 1 - cycles between mania and depression

Type II - cycle between depression and hypomania (less extreme mood elevation)

• harder to diagnose

Cyclothymia Hypomania to mild depression

Bipolar Causes 

• Genetic 

10 times more likely to have it if relative has it 

Concordance is 70% in twins and 20% in fraternal (same if twins are together or apart)

some evidence is due to single dominant gene

Drug Treatment depression

Tricyclic antidepressants - effective in 70% unipolar

Prozac maybe even more

• serotonin agonist, SSRI

Lithium carbonate - effective against mania in bipolar

psychedelic drugs (psilocybin)

ketamine

4 types of Anxiety disorders

1. generalized anxiety disorder (GAD)

2. Panic disorder - phobias

3. post-tramatic stress disorder (PTSD)

4. obsessive compulsive disorder (OCD)

Generalized Anxiety disorder (GAD)

• Excessive, ongoing worry and tension
• An unrealistic view of problems
• Restlessness or a feeling of being "edgy"
– Irritability
• Muscle tension
• Headaches
• Difficulty concentrating
• Longer than 6 months

Panic disorder

Characterized by sudden episodes of intense anxiety, fear, or terror.

• Physical symptoms: heart palpitations, rapid breathing, dizziness.

• With agoraphobia: fear of open or public places (can trigger attacks).

• Without agoraphobia: panic occurs without a specific trigger.

Rates and causes of anxiety

2% rate men and women

Age: 35

Genetic factor 

Higher rate in 1 st degree relatives (30%)
– Higher in monozygotic than dizygotic twins
• High comorbidity with Major Depressive Disorder

Caused by not enough or Blocked GABA receptors

Treatment Anxiety

Behavioral therapy
– Systematic desensitization
• Benzodiazepines (e.g., Valium)
– GABA agonist
– GABA is major inhibitory neurotransmitter

PTSD

• Caused by experiencing or witnessing a traumatic event.

• Involves recurrent dreams, memories, or flashbacks of the trauma.

• Leads to avoidance of reminders, social withdrawal, and emotional numbness.

• Also causes hypersensitivity to noise or movement and a heightened startle reflex.

what goes wrong in anxiety disorders?

• The amygdala activates the hypothalamus, triggering the stress response.

• The amygdala itself is activated by the cortex and learned associations (e.g., classical conditioning).

• Overactive frontal cortex circuits may overstimulate the amygdala.

• Benzodiazepines help by reducing frontal overactivity, which in turn reduces the stress response.

Disorders Arising from Damage/Disfunction
to the central nervous system

1. Cerebrovascular disorders

2. Traumatic brain injury (TBI)

3. Epilepsy

4. tumors

5. Headache

6. Degenerative 

7. “other”

What are Cerebrovascular Disorders?

• Among the most common causes of death and chronic illness in the Western world.

• Caused by a disruption of blood flow to the brain (known as a stroke or Cerebral Vascular Accident – CVA).

• Severity depends on the size of the affected blood vessel.

• A Transient Ischemic Attack (TIA) is a temporary or mild stroke warning of possible future strokes.

Traumatic Brain Injuries (TBI)

Is the most common brain injury in people under 40

sport activities are the cause of 20% of TBI

higher chance of head trauma on males 15-30 years old

What does Traumatic Brain Injuries cause on the brain?

Immediate

• Immediate injuries: contusion (bruising) where the brain hits the skull, hematoma (bleeding), and axonal tearing.

• Secondary injuries: brain swelling (edema), glutamate excitotoxicity causing cell death, and blood-brain barrier disruption.

concussions - mild (TBI)

A mild traumatic brain injury (mTBI).

Glasgow Coma Scale (15-point test) checks eye, verbal, and motor responses — scores 13–15 = mTBI.

• Neurological exam tests vision, hearing, reflexes, and strength.

• Sport Concussion Assessment Tool (SCAT) evaluates:

  • Symptoms: headache, nausea, fogginess, irritability

  • Cognition: memory, concentration, orientation

  • Balance & coordination

Chronic Traumatic Encephalopathy (CTE)

• A neurodegenerative disease caused by repeated head injuries.

• Symptoms appear years later and affect behavior, mood, and thinking.

• Considered a form of dementia.

Epilepsy

A brain disorder marked by recurrent seizures.

Two types:

• Symptomatic seizures: have a known cause (e.g., TBI).

• Idiopathic seizures: occur spontaneously with no clear cause.

Affects about 4–10 people per 1,000.

Epilepsy symptoms

Three main symptoms:

1. Aura: warning sign before a seizure

2. Loss of consciousness

3. Motor movements: body shaking or jerking

Diagnosis is confirmed with an EEG (electroencephalogram).

Seizure 

The active component of epilepsy

manifested by a abnormal, excessive, and hypersynchronous electrical discharge of neurons in the brain.

two types - focal and generalized

Focal Seizures (partiel)

Begins in one place (a focus point) and spreads

Generalized Seizures

Affect both sides of the brain (bilaterally symmetrical).

Type: Grand mal (tonic-clonic) seizure.

1. Tonic stage (10–20 sec): muscles stiffen.

2. Clonic stage (1–3 min): rhythmic jerking movements.

3. Postictal phase: tiredness, confusion, soreness, headache, and no memory of the seizure.

Petit Mal (absence) seizure

A type of generalized seizure with loss of awareness.

• Little or no movement — may blink, roll eyes, or stare blankly.

• Person may stop speaking briefly (10–30 seconds).

• Quick recovery afterward.

• Most common in children.

Treatment for Epilepsy

Anticonvulsant drugs - Dilantin, phenobarbital, Carbamazepine (Carbatrol, Tegretol, others)

• Surgery (especially in drug resistant cases)

• Deep brain stimulation (DBS)

Tumors

A tumor is a mass of new tissue that grows independently of normal cells.

• Benign tumors

• Malignant tumors

Benign tumors

do not usually return after removal

Malignant tumors

Recur, grow progressively, and can be life-threatening.

Headaches: Migrane

Begins with an aura lasting 20–40 minutes (caused by vasoconstriction in the occipital cortex).

Followed by a headache due to vasodilation in the dura.

• Pain is intense, often on one side of the head.

• May include nausea and vomiting.

Degenerative CNS disease 

• Parkinson’s disease (PD)

• Dementia 

Alzheimer’s disease (AD)

• Multiple Sclerosis (MS)

• Huntington’s Disease 

Parkinson’s Disease (PD)

A progressive central nervous system (CNS) disorder that mainly affects movement.

• Early symptoms: tremors, muscle rigidity, slow movement, and walking difficulty.

• Later symptoms: worsening movement issues and possible dementia.

Causes of Parkinson’s disease

Caused by the death of dopamine-producing cells in the substantia nigra.

• Results from a mix of genetic and environmental factors.

• 15% have a close relative with the disease; 5–10% have a gene mutation.

• About 60,000 new cases per year in the U.S.

Treatment for Parkinson’s Disease

Levodopa (L-DOPA): increases dopamine; often the first treatment.

Dopamine agonists: used when L-DOPA becomes less effective.

Deep Brain Stimulation (DBS): electrodes implanted in the thalamus can reduce symptoms in late-stage patients

Dementia 

A progressive syndrome that impairs memory, thinking, and behavior.

Interferes with daily functioning and independence.

Other symptoms may include emotional problems, language difficulties, and low motivation.

Types of Dementia

• Alzheimer’s (AD)

• Frontal-temporal (FTD)

• Lewy body (related to parkinson’s)

• Vascular

Alzeimers’s Disease (AD)

A chronic, progressive neurodegenerative disease that worsens over time.

Causes 60–70% of all dementia cases.

Affects about 6.5 million people in the U.S.

Risk increases with age.

• life expectancy 3-9 yrs

• Always fatal no cure

Amnesic MCI

Frequently forgetting recent events

(important appointments, conversations, or social engagemnts)

Repetition: asking the same questions, telling the same stories

Misplacing items and being unable to find them

Getting lost in familiar places 

Symptoms of Alzheimer’s

Early: trouble remembering recent events (mild cognitive impairment – MCI).

Later: worsening memory, language difficulties, disorientation, mood swings, loss of motivation, and poor self-care

Cause of Alzheimer

70% believed to be inherited

Likely many genes are involved

Increase risk in depression (MDD) And hypertension (high blood pressure)

Brain basis of Alzaimer’s

Brain pathology is associated with:

• intracellular neurofibrillary tangles

• Amyloid Plaques

Amyloid Hypothesis (Altzeimer’s)

• Cause: Build-up of amyloid beta (Aβ) plaques outside brain cells

• Gene: APP gene on chromosome 21 → extra copy in Down syndrome (trisomy 21) → early Alzheimer’s symptoms (~age 40)

• Risk Factor: APOE4 form of Aβ → increases risk for early-onset AD (40s–50s)

Tau Hypothesis (Alzheimer’s)

• Cause: Abnormal tau proteins trigger disease process

• Effect: Tau proteins stick together → form neurofibrillary tangles inside neurons

• Result:

  • Microtubules break down

  • Cytoskeleton collapses

  • Neuron’s transport system fails

Cycles (circadian Rhythms)

A pattern of cyclical body activities lasting about 24 hours 

• Physical, behavioral and internal biological changes.

What controls circadian rhythms

Controlled by two influences:

1. Environmental cues – mainly sunlight.

2. An internal clock (endogenous oscillator) in the brain.

The internal clock can free-run without light cues (e.g., in darkness).

With a regular light source, the clock becomes entrained (synced) to it.

• Special retinal ganglion cells (RGCs) send light signals to the suprachiasmatic nucleus (SCN) — a small area in the hypothalamus above the optic chiasm that regulates daily rhythms.

What are circadian rhythms for?

pacemakers of daily activity

arousal, metabolism, and hormonal activity 

Suprachiasmatic nucleus (SCN)

The SCN has two parts: core and shell.

• Core neurons receive input from M1 retinal ganglion cells (RGNs) that contain melanopsin, activated by light.

• Light → activates M1 RGNs → activates core neurons → activates shell neurons.

• Shell neurons hold the internal circadian clock.

• This process allows external light to entrain (sync) our circadian rhythms.

How does Suprachiasmatic nucleus(SCN) control sleep?

SCN shell neurons send signals to the pineal gland.

The pineal gland releases melatonin, a hormone that promotes drowsiness.

Melatonin helps regulate sleep and maintain circadian rhythms throughout the brain.

Why do we Sleep?

evolutionary or conservation theory

restorative theory

Evolutionary theory (sleep)

Sleep to conserve energy and for protection

Restorative theory (sleep)

Replenishes neurotransmitters.

Resets synaptic receptors to optimal sensitivity.

Enhances memory consolidation (strengthening of learned information).

What is sleep?

part of circadian cycle

state of altered consciousness

physiologically made of sequence of stages (stages defined as electroencephalogram EEG)

Four types of EEG

Defined by frequency

1. Beta - 13 to 20 Hz

2. Alpha - 8 to 12 Hz

3. Theta - 4 to 7 Hz

4. Delta - 1 to 4 Hz

Sleep spindles - 12 to 14 Hz 

Sleep stages using EEG

Stage 1: wide awake to alpha

Stage 2: Alpha to Theta

Stage 3: Has both Theta and some Delta

Stage 4: Mostly Delta (slow wave sleep)

REM sleep

REM sleep

Period of brain arousal (paradoxical sleep)

Each episode last 10-20 minutes

Behaviorally characterized by rapid eye movement

What is REM sleep?

Most people awakened from REM report dreaming

dreaming can occur on other stages (but mostly REM)

REM is associated with paralysis of the body

What is dreaming?

Cortical activity during sleep

associated with images, ideas and emotions

• may or may not remember after waking

• more likely remember if awakened during REM

Dreams aren’t walking thoughts (frequently have bizarre quality)

Freud “Interpretation of dreams”

Dreams reflect the unconscious mind, showing hidden desires and anxieties, often from childhood.

Psychoanalysis uses dream interpretation to uncover repressed desires.

There is little scientific evidence supporting this theory

Dream theories

• Dreams may reflect memory formation processes during sleep.

• The prefrontal cortex (responsible for executive functions) is inactive during REM, which explains why dreams often seem bizarre or illogical.

Sleep Disorders

Since we spend about 25% of life asleep, many neuropsychological disorders affect sleep.

Two main categories:

1. Dyssomnias – problems with the amount, quality, or timing of sleep.

2. Parasomnias – abnormal behaviors or experiences during sleep.

Dyssomnia

A category of sleep problems characterized by a direct problem with the sleep process itself 

Hypersomnia 

Insomnia 2 types

Narcolepsy

Sleep apnea 2 types

Hypersomnia

sleeping too much or sleeping at inappropriate times.

Insomnia 2 types

1. Onset insomnia: problems getting to sleep

2. Maintenance insomnia: problems staying asleep

Can result in poor sleep hygiene, drugs and anxiety

Narcolepsy

A disorder causing excessive daytime sleepiness and sudden sleep episodes.

Episodes may be triggered by strong emotions.

The normal sequence of sleep stages is disrupted.

Sleep Apnea 2 types

1. Obstructive: caused by blockage of upper airway - reduction in blood oxygen

2. Central: problem in brain stem respiratory area that regulates breathing