12 - Psychological Disorders

Question 1

Nucleus accumbens

Answer 1

Located at the base of the forebrain
Involved in addiction
Nearly all abused drugs and other addictive activities (eg gambling) increase dopamine release in the nucleus accumbens

Question 2

Cravings

Answer 2

Insistent search for the activity/substance - distinctive feature of addictions
Even after long periods of abstinence, visual cues can trigger a craving
Studies in rats show repeated exposure to an addictive substance alters receptors to become more responsive to the addictive substance (less responsive to other types of reinforcement)

Question 3

Tolerance

Answer 3

Decrease in effect as an addiction develops
Drug tolerance is learned
Can be weakened through extinction procedures

Question 4

Withdrawal

Answer 4

Body’s reaction to absence of the drug eg headache when you don’t have coffee

Question 5

Predispositions

Answer 5

Genetic influences
Twin studies confirm strong influence of generics on vulnerability to alcohol/drugs
Many addiction-linked genes have been identified, each with a small effect

Question 6

Environmental influences

Answer 6

Prenatal environment contributes to risk for alcoholism
Childhood environment: careful parenting supervision decreases likelihood of developing impulsive behaviour that leads to abuse

Question 7

Type I alcoholics

Answer 7

Develop alcohol problems gradually, after age 25 - more stress related

Question 8

Type II alcoholics

Answer 8

Associated with early onset - usually men with a family history of alcoholism

Question 9

Behavioural predictors of abuse

Answer 9

Monitoring response of young people to predict risk of later problems
Research findings:
Sons of alcoholics show less than average intoxication after drinking a moderate amount of alcohol
Alcohol decreases stress for most people, but more so for sons of alcoholics

Question 10

Treatments for alcoholism

Answer 10

Cognitive-behavioural therapy:
Contingency management includes rewards for remaining drug-free
Medication:
Antabuse: results in sickness after drinking

Question 11

Medications to combat opiate abuse

Answer 11

Methadone as a safer alternative
Similar to heroine and morphine
Activates same brain receptors and produces same effects
Can be taken orally, absorbs slowly, and leaves the brain slowly - ‘rush’ and withdrawal both reduced

Question 12

Mood disorders: major depression

Answer 12

Symptoms:
Person feels sad and helpless most of the day, every day, for long periods of time
Person does not enjoy anything and cannot imagine enjoying anything
Fatigue, feeling of worthlessness, or contemplation of suicide
Trouble sleeping and concentrating

Question 13

Genetics and depression

Answer 13

No one gene has been identified as clearly linked to depression
People with early-onset depression (before age 30) are most likely to have relative with depression
Genetic influence varies with environment
Short form of the serotonin transporter gene influences reaction to stressful events

Question 14

Brain activity associated with depression

Answer 14

Decreases activity in the left prefrontal cortex (happy mood)
Increased activity in the right prefrontal cortex
Imbalance stable over the years, despite symptom changes

Question 15

Categories of antidepressant drugs

Answer 15

Tricyclics
Selective serotonin reuptake inhibitors (SSRIs)
Monoamine oxidase inhibitors (MAOIs)
Atypical antidepressants

Question 16

Tricyclics

Answer 16

Block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release
Also block histamine receptors, acetylcholine receptors, and certain sodium channels
Side effects: drowsiness, dry mouth, difficulty urinating, and heart irregularities

Question 17

SSRIs and SNRIs

Answer 17

Selective serotonin reuptake inhibitors (SSRIs): block the reuptake of the neurotransmitter serotonin

Serotonin norepinephrine reuptake inhibitors (SNRIs): block reuptake of serotonin and norepinephrine

Question 18

MAOIs

Answer 18

Monoamine oxidase inhibitors
Block the enzyme monoamine oxidase
Results in more transmitters in the presynaptic terminal available for release

Question 19

Atypical antidepressant drugs

Answer 19

Miscellaneous group of drugs with antidepressant effects and milder side effects
E.g. Bupropion
Inhibits the reuptake of dopamine and to some extent norepinephrine, but not serotonin

Question 20

Antidepressant drugs - new investigatory substances

Answer 20

Ketamine 
Blocks NMDA type glutamate receptors 
Produces rapid antidepressant effects in people who don't respond to other medications
Not suitable (produces delusions and hallucinations) but may lead to something similar

Question 21

Why are antidepressants effective?

Answer 21

People with depression have lower than average brain-derived neurotrophic factor (BDNF): important for synaptic plasticity, learning
As a result, people with depression show:
Smaller than average hippocampus
Impaired learning
Reduced production of hippocampal neurons
Some studies show antidepressants increase BDNF (but not all!)

Question 22

Cognitive-behavioural theory & depression

Answer 22

Shown to be equally effective for all levels of depression
Causes increased metabolism in same brain areas as antidepressant
More likely to reduce relapse months or years later

Question 23

Exercise & depression

Answer 23

Shown to have modest antidepressant benefits

Question 24

Electroconvulsive therapy (ECT) & depression

Answer 24

Electrically induced seizure used for the treatment of severe depression
For patients who have not responded to antidepressant medication
Side effects include memory impairment
High risk of relapse without continued treatment
How ECT relieves depression is unknown
Proliferates neurons in the hippocampus

Question 25

Altered sleep patterns & depression

Answer 25

Disruption of sleep patterns is common in depression
Typically fall asleep but awaken early and are unable to get back to sleep
Enter R.E.M. Sleep within 45 mins
Sleep pattern disruption in young people increases the likelihood of depression
Combining periodic sleep deprivation with antidepressant drugs sometimes helpful

Question 26

Deep brain stimulation

Answer 26

Physician implants battery powered device into the brain to deliver periodic stimulation
Targets brain areas that increase activity as a result of antidepressant drugs
Alternative: optogenic stimulation - can control individual connections

Question 27

Unipolar disease

Answer 27

Characterised by alternating states of normality and depression

Question 28

Bipolar disorder (manic-depressive disorder)

Answer 28

Characterised by alternating states of depression and mania
Mania: restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibition
Bipolar I (‘full-blown’ manic episodes)
Bipolar II (hypomanic - less ‘full-blown’)

Question 29

Treatments for bipolar disease

Answer 29

Lithium: a salt that stabilises mood and prevents relapse in mania or depression
Other drugs: valproate and carbamazepine
All of the drugs work by:
Decreasing glutamate activity
Blocking the synthesis of the brain chemical (arachidonic acid) which is produced during brain inflammation

Question 30

Schizophrenia- diagnosis

Answer 30

Positive symptoms ('too much of'):
Behaviours that are present that should be absent
Examples: hallucinations, delusions, disorganised speech, and disorganised behaviour

Negative symptoms (‘too little of’):
Absent behaviours that should be present (weak emotion, speech, and socialisation)
Usually stable over time and difficult to treat

Question 31

Role of genetics in schizophrenia

Answer 31

Research suggests a genetic component, but does not depend on a single gene
Monozygotic twins have a much higher concordance rate than dizygotic twins
But monozygotic twins only have a 50% concordance rate

Question 32

Efforts to locate a gene link in schizophrenia

Answer 32

Many genes more common in individuals with schizophrenia
Large number of more common genes produce small effects
Possibly caused by new gene mutations or microdeletion of chromosome

Question 33

The neurodevelopmental hypothesis of schizophrenia

Answer 33

Abnormalities occur in prenatal or neonatal nervous system development
Leaves the developing brain vulnerable to disturbances later in life
Result: mild abnormalities of brain anatomy and major abnormalities in behaviour

Question 34

The neurodevelopmental hypothesis of schizophrenia- evidence

Answer 34

Prenatal difficulties are linked to later schizophrenia
People with schizophrenia have minor brain abnormalities that originate early in life
Abnormalities of early development could impair behaviour in adulthood

Question 35

Prenatal and neonatal environment influences for schizophrenia

Answer 35

Intermediate risk factors:
A father over 55 years old
Toxoplasma gondii (a parasite that infects humans, courtesy of house cats)

Low risk factors:
Poor maternal nutrition
Complications during delivery
Head injuries in early childhood
Extreme stress of mother during pregnancy 
Season-of-birth effect
Blood type differences

Question 36

Mild brain abnormalities in schizophrenia

Answer 36

Less grey matter and white matter
Larger than average ventricles
Smaller hippocampus
Deficits of memory and attention consistent with damage to the prefrontal cortex
Lateralisation differences in people with schizophrenia:
Right planum temporale slightly larger

Question 37

Early development and later psychopathology

Answer 37

Most cases of schizophrenia are not diagnosed until age 20 or later
Problems often observed in childhood: impulse control, attention, and memory
Dorsolateral prefrontal cortex one of the slowest brain areas to mature
Area shows consistent signs of deficit in schizophrenia patients

Question 38

Treatments for schizophrenia

Answer 38

Antipsychotic/neuroleptic drugs
Category of drugs tend to relieve schizophrenia and similar conditions
Two chemical families of antipsychotic drugs used to treat schizophrenia:
Phenothiazines
Butyrophenones

Question 39

Dopamine and schizophrenia

Answer 39

Dopamine hypothesis of schizophrenia:
Schizophrenia results from excess activity at dopamine synapses in certain areas of the brain
Substance-induced psychotic disorder:
Hallucinations and delusions resulting from repeated large doses of amphetamines, methamphetamines, or cocaine
Each prolongs activity at dopamine synapse

Question 40

Glutamate and schizophrenia

Answer 40

The glutamate hypothesis:
Deficient activity at glutamate synapses, especially in the prefrontal cortex
In many brain areas, dopamine inhibits glutamate release
Alternatively, glutamate stimulates neurons that inhibit dopamine release
Increased dopamine thus produces the same effect as decreases glutamate