12 - Psychological Disorders Flashcards
Nucleus accumbens
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
Cravings
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)
Tolerance
Decrease in effect as an addiction develops
Drug tolerance is learned
Can be weakened through extinction procedures
Withdrawal
Body’s reaction to absence of the drug eg headache when you don’t have coffee
Predispositions
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
Environmental influences
Prenatal environment contributes to risk for alcoholism
Childhood environment: careful parenting supervision decreases likelihood of developing impulsive behaviour that leads to abuse
Type I alcoholics
Develop alcohol problems gradually, after age 25 - more stress related
Type II alcoholics
Associated with early onset - usually men with a family history of alcoholism
Behavioural predictors of abuse
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
Treatments for alcoholism
Cognitive-behavioural therapy:
Contingency management includes rewards for remaining drug-free
Medication:
Antabuse: results in sickness after drinking
Medications to combat opiate abuse
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
Mood disorders: major depression
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
Genetics and depression
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
Brain activity associated with depression
Decreases activity in the left prefrontal cortex (happy mood)
Increased activity in the right prefrontal cortex
Imbalance stable over the years, despite symptom changes
Categories of antidepressant drugs
Tricyclics
Selective serotonin reuptake inhibitors (SSRIs)
Monoamine oxidase inhibitors (MAOIs)
Atypical antidepressants
Tricyclics
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
SSRIs and SNRIs
Selective serotonin reuptake inhibitors (SSRIs): block the reuptake of the neurotransmitter serotonin
Serotonin norepinephrine reuptake inhibitors (SNRIs): block reuptake of serotonin and norepinephrine
MAOIs
Monoamine oxidase inhibitors
Block the enzyme monoamine oxidase
Results in more transmitters in the presynaptic terminal available for release
Atypical antidepressant drugs
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
Antidepressant drugs - new investigatory substances
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
Why are antidepressants effective?
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!)
Cognitive-behavioural theory & depression
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
Exercise & depression
Shown to have modest antidepressant benefits
Electroconvulsive therapy (ECT) & depression
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
Altered sleep patterns & depression
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
Deep brain stimulation
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
Unipolar disease
Characterised by alternating states of normality and depression
Bipolar disorder (manic-depressive disorder)
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’)
Treatments for bipolar disease
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
Schizophrenia- diagnosis
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
Role of genetics in schizophrenia
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
Efforts to locate a gene link in schizophrenia
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
The neurodevelopmental hypothesis of schizophrenia
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
The neurodevelopmental hypothesis of schizophrenia- evidence
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
Prenatal and neonatal environment influences for schizophrenia
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
Mild brain abnormalities in schizophrenia
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
Early development and later psychopathology
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
Treatments for schizophrenia
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
Dopamine and schizophrenia
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
Glutamate and schizophrenia
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
