Ch 14 Psychological Disorders

what percent if adults in us have a "clinically significant" depression

5%

Efforts to locate a gene responsible for schizophrenia

DISC1 consistently linked - controls production of dendritic spines and generation of new neurons at the hippocampus other genes linked to it are important for brain development, transmission to glutamate synapses, and connections btw the hippocampus and prefrontal cortex hypothesis: many cases of schizophrenia arise from new mutations or microdeletion (deletion of a small part of a chromosome)

phenothiazines

a class of neuroleptic drugs that includes chloropromazine

affinity

a drug has this for a receptor if it binds to it (like a key into a lock)

what would a drug that high affinity and low efficacy be like?

a drug that binds to a receptor but fails to stimulate it

efficacy

a drugs tendency to activate the receptor

mesolimbocortical system

a set of neurons which project from the midbrain tegmentum to the limbic system - believed to be area where antipsychotics have their beneficial effects

behavioral predictors of abuse

alcoholism more likely in people who were described as impulsive, risk taking, easily bored, etc in child hood; sons of alcoholics show less than average intoxication after drinking a moderate amount of alcohol, and more decrease in stress as a result of drinking alcohol, than sons of non-alcoholics

psychotherapy

alternate treatment to depression, effects more likely to last than those of antidepressants on avg ppl receiving both psychotherapy and antidepressants improve more than those receiving just one

craving

an insistent search for an activity

treatments of schizophrenia

antipsychotic drugs and dopamine, chlorpromazine

negative symptoms of schizophrenia

behaviors that are absent that should be present normally stable over time and hard to treat

positive symptoms of schizophrenia

behaviors that are present that should be absent

monamine oxidase inhibitors (MAOIs)

block enzyme monamine oxidase, a presynaptic enzyme that metabolizes catecholamine and serotonin into inactive forms

antagonists

block receptors

stimulants

block reuptake of released dopamine, so it releases dopamine instead of producing reuptake

serotonin norepinephrine reuptake inhibitors

block reuptake of serotonin and norepinephrine

what neurotrophin do most people with depression have lower levels of?

brain-derived neurotrophic factor (BDNF)

substance-induced psychotic disorder

characterized by hallucinations and delusions caused by drugs such as cocaine, amphetamine, and LSD, which inc the activity of dopamine synapses in a study people w schizophrenia had about 2x D2 receptors occupied as normal

butyrophenones

class of neuroleptic drugs that includes haloperidol (Haldol)

abnormalities in hemisphere dominance and depression

decreased activity in the left hemisphere and increased activity in the right prefrontal cortex - probably a predisposition to depression rather than a reaction to it

seasonal affective disorder (SAD)

depression that reoccurs seasonally, usually during winter most common in regions closest to the poles, where nights are very long in winter and very short in summer

deep brain stimulation

device implanted into the brain to deliver periodic stimulation to certain brain areas in experimental phase but research is promising

schizophrenia

disorder characterized by deteriorating ability to function in everyday life an by some combination of: delusions, hallucinations, disorganized speech, grossly disorganized behavior, and weak or absent signs of emotion, speech, and socialization

what 2 types of synapses do must abused drugs increase activity

dopamine and norepinephrine

Phencyclidine (PCP)

drug that blocks NMDA glutamate receptors - supports glutamate hypothesis produces effects very similar to schizophrenia drugs used to stimulate glutamate activity very risky - why there are none used to treat schizophrenia

second-generation (atypical) antipsychotics

drugs that alleviate the symptoms of schizophrenia while seldom, if ever, producing movement problems - have less effects on dopamine D2 receptors and stronger effects at D4 and serotonin 5-HT2 receptors more effective at relieving the positive symptoms than typical antipsychotics but do not improve overall quality of life anymore than others

stimulation in what areas increased rats self-stimulation of the brain

electrodes in areas that increased the release of dopamine or norepinephrine in the nucleus accumbens

SAD treatment

exposing person to very bright lights for about an hour either early in the morning or evening

hallucinations

false sensory experiences such as hearing voices

after age 14 is depression more common in males or females

females

Genetics and schizophrenia

genetic basis but not dependent on any one gene more closely you are biologically to someone w schizophrenia the more likely you are to get it: about a 50% concordance(agreement) of schizophrenia in monozygotic twins and 15% in dizygotic adopted children w schizophrenia: more common that their biological relatives have it than their adoptive relatives but also support for environmental influences

Why are antidepressants effective?

increase availability of serotonin and other neurotransmitters BUT ppl with depression do not normally have low levels of serotonin Antidepressant drugs produce their effects on neurotransmitters in the synapses within minutes to hours but it takes weeks before patients experience mood elevation. some patients respond to one drug and not another but no clear evidence that any antidepressant drug produces different effects than any other

opiates

inhibit neurons that release GABA, a transmitter that inhibits the firing of dopamine neurons

propanalol

interferes w protein synthesis and therefore prevents prevents reconsolidation - some initial studies have shown that it can help prevent cravings in cocaine users

genetic influence on addiction

is a genetic predisposition but not in one gene, many genes have small effects

mild brain abnormalities w scizophrenia

less than avg gray and white matter and larger than avg ventricles (fluid-filled spaces within the brain) smaller hippocampus weaker than avg connections btw dorsolateral prefrontal cortex and other brain areas - area that develops slowly - leads to deficits in memory and attention strongest deficits in left temporal lobe (lower activity) and prefrontal areas

cognitive symptoms

limitations of thought and reasoning that are common in schizophrenia trouble maintaining attention taking sayings too literally

bipolar treatment

lithium salts most effective also valproate and carbamazepine consistent sleep schedule may reduce intensity of mood swings

intermediate risk factors

living in city a father over age 55 childhood infection of toxoplasma gondii (having a cat)

disordered thinking

main problem w schizophrenia - results from abnormal interactions between the cortex and thalamus and cerebellum

antabuse

makes it harder to metabolize acetaldehyde, which causes a person to feel sick after drinking; moderately effective as a supplement to a persons commitment to stop drinking

agonists

mimic or increase effects of a neurotransmitter

atypical antidepressants

miscellaneous group of drugs w antidepressant actions and mild side effects

How effective are antidepressants?

occurs in episodes so even w/o treatment people recover within a few months the best comparisons of the benefits of drugs are comparisons between those who are treated with medication and those who are administered a placebo. Placebo results often overlap with drug group results. One study suggests that for people with mild to moderate depression, there is no clear benefit of a drug over a placebo. Furthermore, even for those with severe depression, antidepressants don't always work. some studies - antidepressants only useful for people w severe depression overall - antidepressants only moderately helpful for most people w depression and not helpful at all for many of them

differential diagnosis

one that rules out other conditions w similar symptoms similar effects to schizophrenia: substance abuse brain damage undetected hearing deficitis Huntington's disease nutritional abnormlaities

bipolar disorder

people alternate between depression and mania (restless activity, laughter, excessive self-confidence, rambling speech and loss of inhibitions) inc glucose activity during mania and decrease during depression

unipolar disorder

people alternate between depression and normality

major depression

people feel sad, helpless, and lacking in energy for weeks at a time

studies on depression

people react normally to sad or frightening depictions but seldom smiled at comedies or pleasant pictures show decreased response to a likely reward

altered sleep patterns

people with depression feel better the next day if they stay up all night combining sleep deprivation w drugs can sometimes be helpful this might work bc sleep deprivations releases a hormone w antidepressant effects

genetics and depression

people with early onset depression have a high probability of other relatives with depression or other disorders (anxiety, bulimia, IBS, etc) people w later onset depression have a high probability of relatives w circulatory problems

bipolar 1 disorder

person has full blown episodes of mania, more common in men

bipolar II disorder

person has much milder manic phases called hypomania

Addiction

pleasures decrease and the risks increase as addiction progresses

prenatal and neonatal environment that inc risk of schizophrenia

poor nutrition of mother during pregnancy, premature birth, low birth weight, and complications during delivery if a mother is Rh- neg and her baby is Rh-pos, the bay's Rh pos blood may trigger an immunological rejection by the mother - 2x chance of getting schizophrenia having a cat in childhood - toxoplasma gondii

environmental influences of addiction

prenatal alcohol exposure; children w careful parental supervision are less likely to develop impulse control problems - even if they have a genetic predisposition to them

tricylics

prevent the presynaptic neuron from reabsorbing dopamine, norepinephrine, or serotonin after releasing them (allows neurotransmitters to remain longer in the synaptic cleft, stimulating postsynaptic receptors)

nucleus accumbens

reinforces experiences of all types , drugs work to increase dopamine in that area via direct (stimulants) or indirect (opiates) means

chlorpromazine

relieves the positive symptoms of schizophrenia

the neurodevelopmental hypothesis

schizophrenia is caused in large part by abnormalities to the nervous system during the prenatal or neonatal periods

glutamate hypothesis of schizophrenia

schizophrenia results from deficient activity at certain glutamate synapses, bc dopamine inhibits glutamate activity in many parts of the brain, much of evidence supporting dopamine hypothesis also supports glutamate hypothesis researches have found that ppl w schizophrenia release lower than normal amounts of glutamate in the prefrontal cortex and hippocampus and have fewer glutamate receptors

dopamine hypothesis of schizophrenia

schizophrenia results from excess activity in certain dopamine synapses - evidence type if drugs that relieve and aggravate the symptoms of schizophrenia

tardive dyskinesia

serious side effect of antipsychotics; characterized by tremors and other involuntary movements; caused by prolonged blockade of dopamine receptors in the basal ganglia

selective serotonin reuptake inhibitors (SSRIs)

similar to tricylics but specific to the neurotransmitter serotonin and milder side effects, ex Prozac

demographic data on schizophrenia

slightly more common in men, in all ethnic groups, about half of 1% suffer from it, more common in cities, older the age of father at time of babies birth increases risk

repeated exposure to addictive drugs disrupts activity in which brain area

the prefrontal cortex - area responsible for restraining impulses

season-of-birth effect

the tendency of people born in winter to have a slightly greater possibility if developing schizophrenia - maybe bc of nutrition during winter, viral infections, etc

what drugs are most effective against schizophrenia

those most effective at blocking dopamine receptors

Electroconvulsive Therapy (ECT)

treatment through an electrically induced seizure - usually applied every other day for about two weeks side effects include memory loss for the few months following the shock about 1/2 of those that respond to ECT relapse into depression within 6 months unless given antidepressant drugs or other therapies to prevent it; typically works faster and helps a higher percent of patients

delusions

unjustifiable beliefs, such as "beings from outer space are controlling my actions"

antipsychotic drugs (neuroleptic drugs)

used for the treatment of schizophrenia, work primarily by blocking dopamine receptors; phenothiazines and butyrophenones

Methadone and LAAM

used to reduce "withdrawal" symptoms and avoid the "high" of heroin and morphine; dont end opiate addiction but satisfy the craving in a less dangerous way

withdrawal

when the body reacts to the absence of a drug

tolerance

when the effects of a drug (especially the pleasurable effects) decrease over time