Brain, Mind, and Behavior - Exam 3

Psychiatric disorders

disorders of psychological function sufficiently severe to require treatment

Difficulties in diagnosing psychiatric disorders

1. biological tests for psychiatric disorders are not developed enough to actually diagnose someone

2. we have to rely on patients' symptoms

a. patients with the same disorder may display different symptoms

b. patients with different disorders may display the same symptoms

How does the National Institute of Health deal with psychological disorders?

Instead of diagnosing psychological disorders, it diagnoses people with particular features/symptoms

DSM 5

the current edition of the Diagnostic and Statistical Manual of the American Psychiatric Association

Inclusion criteria

characteristics that patients must have in order to qualify for a specific diagnosis (eg. symptoms of hallucinations and delusions for schizophrenia)

Exclusion criteria

characteristics of patients that prevent them from being given a specific diagnosis (i.e. is there another reason why this patient might have these symptoms)

Three general ways of treating psychopathology

- behavioral methods/counseling

- medication/drug treatment/nutrition

- neurosurgery/stimulation treatments

Schizophrenia

- psychotic disorder involving distortions in thoughts, perceptions, and/or emotions

- affects approx. 1 percent of the population

Schizophrenia positive symptoms

symptoms that seem to represent an excess of typical function

includes delusions, hallucinations, disorganized speech, inappropriate affect (emotions), and other odd behavior

Schizophrenia negative symptoms

symptoms that seem to represent a reduction/loss of typical function

Affective flattening - diminished emotional expression

Avolition - reduction or absence of emotion

Catatonia - remaining motionless for long periods of time

Genetic/environmental influences on schizophrenia

genes have been identified that might predispose individuals to schizophrenia, but environmental influences explain why schizophrenia is eventually developed (typically through epigenetic mechanisms)

Brain changes associated with schizophrenia

- enlarged ventricles

- loss in cortical volume, especially in temporal lobes and dorsal peak

- hypofrontality

- shrinking and disorganization of the hippocampus

Hypofrontality

reduced activation of the cortex of the frontal lobes of the brain

Dopamine hypothesis of schizophrenia

the theory that schizophrenia is caused by too much activation of dopamine (D2) receptors and, conversely, that antipsychotic drugs exert their effects by decreasing dopamine levels

Evidence for dopamine hypothesis

- drug-induced psychosis risk is very high with drugs that increase synaptic dopamine availability: cocaine, amphetamines

- typical antipsychotics were found to affect dopamine activation

Binding affinity

a high affinity means a drug binds strongly to a receptor; the high affinity of competitive antagonists allows them bind to receptors and block neurotransmitters

D2 dopamine receptors

type of dopamine receptor that is suspected to have the greatest impact of parkinson's/schizophrenia

Problems with the dopamine theory of schizophrenia

- antipsychotic drugs don't treat the negative symptoms of schizophrenia

- people with schizophrenia seem to have normal levels of dopamine

- some drugs (like atypical antipsychotics) work effectively without affecting D2 dopamine receptors

Treatments for schizophrenia include

1. antipsychotic drugs

2. psychotherapy

3. cognitive behavioral therapy

Cognitive behavioral therapy

a popular integrative therapy that combines cognitive therapy (changing self-defeating thinking) with behavior therapy (changing behavior)

Antipsychotic (neuroleptic) drugs

drugs used to treat symptoms of schizophrenia and bipolar disorder

Psychosis

psychological symptoms where a person loses contact with reality, experiencing irrational ideas and distorted perceptions (not necessarily caused by schizophrenia)

Typical antipsychotics

the first generation of antipsychotic drugs, which work as dopamine antagonists

Chlorpromazine

a typical antipsychotic that is a competitive antagonist at dopamine receptors; this blockage sends a signal back to the presynaptic neuron to release more dopamine because there is not enough...however, this dopamine will be prevented from binding to the receptor and will get broken down in the synaptic cleft

Haloperidol

competitive antagonist at dopamine D2 receptors

Reserpine

another early antipsychotic drug; the active ingredient of the snakeroot plant; breaks down synaptic vesicles of the dopamine neurotransmitter

Atypical antipsychotics

second generation of antipsychotic drugs; do not have a strong binding affinity with D2 dopamine receptors; generally work by blocking serotonin 5-HT2 receptors

Common atypical antipsychotics include

clozapine and risperidone

Glutamate hypothesis of schizophrenia

proposal that schizophrenia relates to deficient activity at glutamate synapses

Psychotomimetic

a drug that induces a state resembling schizophrenia

Classical hallucinogens

- LSD, mescaline, psilocybin

- agonize serotonin

- mimic schizophrenia's positive symptoms

Dissociative hallucinogens

- ketamine, PCP

- antagonize glutamate

- mimic schizophrenia's negative symptoms

Weinberger's original neurodevelopmental model of schizophrenia

Suggests that the dopamine projection from the VTA to the prefrontal cortex doesn't develop correctly in schizophrenics. This would cause underactivation of PFC, and thus an overactivation of limbic system and specifically the nucleus accumbens (since one of the jobs of PFC is to inhibit the NA).

Newer dopamine imbalance theory

Also says that schizophrenia results from an underactive prefrontal cortex and an overactive limbic system. However, this theory argues that this is a result of a faulty glutamate system. Since the descending signals from PFC to NA are mediated by glutamate, synapsing on GABAergic interneurons in the NA, then it will poorly inhibit this structure

Major depressive disorder

depression that is so severe that it is difficult for the patient to meet the essential requirements of daily life (aka. clinical/unipolar depression)

Symptoms of major depressive disorder

-Decreased energy, interests, concentration

-Altered sleeping and eating behavior

-Irritability, physical exhaustion, continuous anxiety

-Anhedonia

Anhedonia

not finding pleasure in things anymore

Reactive depression

depression triggered by an obvious negative experience

no longer an exclusion criteria on the DSM-5!

Cell loss in patients predisposed to depression

amygdala and medial prefrontal cortex

Cell loss in patients diagnosed with depression

besides the previous areas, also the hippocampus and cingulate gyrus

Treatments for depression

- counseling and psychotherapy

- antidepressant medication

- stimulation techniques like electroconvulsive shock therapy, transcranial magnetic stimulation, and deep brain stimulation

Monoamine theory of depression

the theory that depression is due to deficient activity at serotonin and norepinephrine synapses in the brain (developed after observing how some antidepressants worked)

Up-regulation

a compensatory increase in receptor availability at the synapses of a neuron where there was an insufficient amount of it

Problems with monoamine theory of depression

- not everyone is helped by monoamine-targeting medication (studies show slight effectiveness of this type of medication)

- medication can take weeks to have effects

- atypical antidepressants can be effective

Monoamine Oxidase Inhibitors (MAOIs)

antidepressant medications that indirectly agonize monoamines like serotonin and norepinephrine by blocking their breakdown

Cheese effect

dangerous side effect of MAO inhibitors caused by an inability to break down tyramine-rich foods such as wine, cheese, and pickles

Iproniazid

the first MAO inhibitor

Tricyclic antidepressants

antidepressant drugs that block the reuptake of serotonin and norepinephrine

Imipramine (Tofranil)

commonly prescribed tricyclic antidepressant

Selective Serotonin Reuptake Inhibitors (SSRIs)

antidepressant drugs that agonize serotonin by blocking its reuptake; currently primary medication for depression

Common SSRIs

Prozac, Paxil, Zoloft, and Luvox

Selective Norepinephrine Reuptake Inhibitors (SNRIs)

antidepressant drugs that are similar to SSRIs, except they block the reuptake of norepinephrine

Common SNRI

Reboxetine

Atypical antidepressants

catch-all class of antidepressant drugs that have many modes of action

Bupropion (Wellbutrin or Zyban)

atypical antidepressant that blocks dopamine and norepinephrine reuptake and antagonizes nicotinic acetylcholine receptors

Ketamine

dissociative hallucinogen that also works as an atypical antidepressant by antagonizing the glutamate NMDA receptor

Neurogenesis theory of depression

an explanation of depression that proposes that neurogenesis, the growth of new neurons in the hippocampus is suppressed during depression, and can be resumed by increasing serotonin or norepinephrine

BDNF (brain-derived neurotrophic factor)

regulates neuronal survival and differentiation during development and is associated with depression (targeted by new depression therapies)

Neurotrophins

chemicals that attract/repel Axon growth, help prevent cell death, and/or promote Axonal branching

neuroplasticity theory of depression

Depression results from a decrease of neuroplastic processes in the prefrontal cortex, hippocampus, amygdala, and other brain structures which leads to neuron loss and other forms of neural pathology

Electroconvulsive shock therapy

a biomedical therapy for severely depressed patients in which a brief electric current is sent through the brain of an anesthetized patient

Transcranial magnetic stimulation (TMS) in depression

involves the delivery of repetitive magnetic pulses to enhance or depress specific cortical areas in an effort to relieve depression; usually in the prefrontal cortex

Deep brain stimulation

antidepressive measure in which electrical stimulation is applied through surgically implanted electrodes that are usually implanted in the anterior cingulate cortex or the prefrontal cortex

Cingulotomy

lesions that interrupt pathways between the anterior cingulate cortex and the prefrontal cortex in order to treat depression (and other psychopathology)

Bipolar disorder

a category of psychiatric disorders that involves alternate bouts of depression and mania or hypomania

Hypomania

a mild mania characterized by a reduced need for sleep, high energy, and positive affect

Mania

hypomania taken to extreme; also involves delusions of grandeur, overconfidence, and distractibility

Bipolar disorder type I

involves alternate bouts of depression and mania

Bipolar disorder type II

involves alternate bouts of depression and hypomania

Rapid-cycling bipolar disorder

characterized by at least 4 mood cycles in a year

Cyclothymia

disorder that consists of mood swings from moderate depression to hypomania

Treatments for bipolar disorder

psychotherapy and mood stabilizing medication

Mood stabilizing medications

1. Lithium

2. Anti-convulscant medications

3. Anti-psychotic medications

Lithium

an accidentally discovered mood stabilizer that is thought to work by agonizing serotonin

Possible causes of bipolar disorder

1. HPA-axis dysregulation

2. Circadian rhythm dysfunction

3. Monoamine and amino acid neurotransmitter dysregulation

HPA axis dysregulation

includes the hypothalamus, pituitary, and adrenal glands; causes an abnormal pattern of cortisol release

Reward hypersensitivity theory of bipolar disorder

bipolar disorder results from a dysfunctional brain reward system that overreacts to rewards or the lack thereof, explains that repeatedly rewarding individuals with BPD for their activities leads to excessive goal seeking and mania or hypomania, and explains that when people with bipolar disorder fail to achieve their goals this leads to an excessive decrease in reward seeking and depression.

Anxiety disorder

anxiety so severe that it disrupts functioning; associated with feelings and with physiological responses (ex. high heartbeat)

Generalized Anxiety Disorder (GAD)

extreme feeling of anxiety or fear about a large numbers of activities or events

Specific phobias

strong fear or anxiety about a specific object or situation

Panic disorder

recurrent rapid-onset attacks of extreme fear and severe symptoms of stress; the severe physiological symptoms of stress can also occur with the previous three disorders

Treatments for anxiety

- psychotherapy

- behavioral therapy

- anti-anxiety medication

Anxiolytic (anti-anxiety) drugs include

- benzodiazepines

- SSRIs

- buspar

Benzodiazepines

common anxiolytic that stimulates GABA-A receptors primarily in the hippocampus and amygdala (eg. Valium, Xanax)

Buspar

anxiolytic drug that is a direct 5-HT-1A serotonin agonist

Causes of anxiety

- underactivity of similar brain areas as depression, although little brain shrinkage is observed

- an overactive amygdala

Learning

a relatively permanent change in behavior due to experience

Non-associative learning

learning about a stimulus, such as sight or sound, in the external world; includes habituation and sensitization

Habituation

reduced response intensity with repeated presentation (ex. tuning out the sound of a fan)

Sensitization

increased response due to a salient event (ex. becoming jumpy after receiving an electric shock)

Dishabituation

the restoration to full strength of a response after a change of stimulus that had previously become weakened through habituation

Other-race effect in infants

infants can better detect changes in facial features in faces belonging to their own race; they also habituate quicker to faces belonging to their own race

Associative learning

learning the relationship between two pieces of information; includes classical and operant conditioning

Classical conditioning as a concept

when we learn that a stimulus predicts another stimulus

Ivan Pavlov

Russian scientist who discovered classical conditioning through his work with dog salivation

Classical conditioning mechanisms

if you pair a neutral stimulus (NS) with an unconditioned stimulus (US) that already triggers an unconditioned response (UR) that neutral stimulus will become a conditioned stimulus (CS), triggering a conditioned response (CR) similar to the original unconditioned response

Neutral stimulus (NS)

in classical conditioning, a stimulus that elicits no response before conditioning

Unconditioned stimulus (US)

in classical conditioning, a stimulus that unconditionally—naturally and automatically—triggers a response (meat powder)

Unconditioned response (UR)

in classical conditioning, the unlearned, naturally occurring response to the unconditioned stimulus (US) (dogs salivating to the meat powder)

Conditioned stimulus (CS)

in classical conditioning, an originally irrelevant stimulus that, after association with an unconditioned stimulus, comes to trigger a conditioned response (the bell)