Exam 4 Flashcards by Isabella Wilton

Prevalence of Schizophrenia

12% of population
1 in 5 in USA
more women than men

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Positive symptoms of schizophrenia

Psychosis
Hallucinations
Delusions
Disorganized thought and speech

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Negative symptoms of schizophrenia

Lack of emotional expression
Reduced facial expression
Anhedonia
Alogia
Social withdrawal

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Anhedonia

no pleasure in things that are normally enjoyable

Symptom of schizophrenia

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Alogia

Lack of spontaneous speech

Symptom of schizophrenia

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Cognitive symptoms of schizophrenia

Memory impairment
Poor attention span
Difficulty making plans
Reduced decision-making
Poor social cognition

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Twins and schizophrenia

Concordance rate in identical twins is 50%, down to 17% in fraternal

Shows that there is some genetic factor, but environment is also involved

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Features of twin with schizophrenia

Lower birth weight, more physiological distress, more sensitive behavior, subtle neurological signs

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Schizophrenia and eye movement

People with schizophrenia display difficulty with smooth movement of the eyes

Smooth pursuit
Free-viewing
Saccade
Fixation stability

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Integrative model of schizophrenia

More than 100 genes influence it, including DISC1

Paternal age is an epigenetic factor

INTERACTION BETWEEN GENETIC FACTORS AND STRESS

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Stressors that may lead to schizophrenia

Transition from childhood to adulthood
Prenatal stress
Maternal illnesses
City Living

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Influence of cities on schizophrenia

Population influences risk of developing it

Also what age you move there and how long you stay there

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Schizophrenia vulnerability and development

Onset in males 2-3 years earlier
Some women get it during menopause
Increase in symptoms during synaptic rearrangement

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Brain abnormalities in patients with schizophrenia

Enlarged lateral ventricles
Structure/function of corpus callosum
Accelerated cortical thinning
Reduced subcortical volume

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DISC1 mutation and lateral ventricles

Mice with a mutated DISC1 gene developed enlarged lateral ventricles, just like schizophrenia patients

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Schizophrenia and frontal lobes

reduced metabolic activity in frontal lobes

Decreased blood flow to frontal lobes

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Hypofrontality hypothesis

frontal lobes are underactive in people with schizophrenia

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Historical treatment for schizophrenia

lobotomy

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First effective medication for schizophrenia

Chlorpromazine - antipsychotic
Reduced positive symptoms
Targets dopamine receptors

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Dopamine hypothsis

Schizophrenia is caused by an excess of either dopamine release or dopamine receptor

More likely related to dopamine SYNTHESIS, not receptors

Problems with the dopamine hypothesis

Drugs block D2 receptors faster than symptoms are reduced

Some effective atypical neuroleptics actually increase dopamine levels

Side effects of antipsychotics

Dyskinesia
Tardive Dyskinesia
Supersensitivity psychosis

Dyskinesia

Side effect of antipsychotics

initial, maladaptive motor symptoms, disappear when dose is reduced (dose dependent)

Tardive Dyskinesia

Side effect of antipsychotics

late onset, repetitive, involuntary movements, irreversible, may be due to dopamine receptor supersensitivity

Supersensitivity psychosis

marked increase in positive symptoms of schizophrenia upon discontinuation of antipsychotic drugs

Second-Generation antipsychotics

atypical antipsychotics have lower affinity for D2 receptors, their highest affinity is for serotonin receptors Clozapine

Glutamate hypothesis of schizophrenia

Schizophrenia is caused by an under activation of glutamate receptors Prompted by effects of PCP and ketamine

PCP and schizophrenia

PCP is an NDMA receptor antagonist Prevents glutamate from acting normally Noncompetitive antagonist Produces schizophrenia like symptoms

Depression is characterized by:

Unhappy mood Loss of interest/reduced energy Changes in appetite Disrupted sleep patterns Difficulty in concentration Restless agitation or torpor Pessimism and thoughts of death

Prevalence of mental illness among college students

32% of college students report having mental illness (female>male)

Presence of mental illness greater in women

Patterns of seeking help Gender differences in endocrine physiology, related to the reproductive cycle Postpartum and postmenopausal depression

Brain changes associated with depression

Increased activation in: -prefrontal cortex during cognitively demanding tasks -Amygdala during emotional processing Decreased activity on: -Hippocampus -Anterior cingulate cortex

Habenula and depression

Habenula is dysfunctional in people with depression Mediates low mood and loss of pleasure Stimulation reduces depressive behavior

Pharmacological treatment for depression

Monoamine oxidase inhibitors Tricyclics SSRIs

Monoamine Oxidase (MAO) Inhibitors

MAO is an enzyme that inactivates the monoamines Inhibit MAO = increase monoamines at the synapse Pharmacological treatment for depression

Monoamine hypothesis of depression

Depression is due to reduced monoamine activity

Tricyclics

Pharmacological treatment for depression Second generation of antidepressants Inhibits reuptake of monoamines

SSRIs

Pharmacological treatment for depression Bock reuptake of serotonin

Problems with SSRIs

SSRI benefits are often not much different than placebo Not everyone responds to SSRIs Long lag time between treatment and reduction of symptoms Anti-depressant discontinuation syndrome

Non-traditional pharmacological treatments of depression

Ketamine Psychedelic drugs that target 5-HT

Ketamine as a treatment for depression

Non-traditional NMDA receptor antagonist Can be administered via inhaler at ER Rapid reduction in suicide ideation

Psychedelic drugs as a treatment for depression

Non-traditional Targets 5-HT Psilocybin LSD

Non-pharmacological treatments for depression

Electroconvulsive shock therapy (ECT) Repetitive transcranial magnetic stimulation (rTMS) - alters cortical electrical activity Deep brain stimulation (DBS) - surgically implanted electrode Cognitive behavioral therapy Exercise

Bipolar disorder

Characterized by alternating periods of mania and depression Men and women equally affected Type I and Type II

Mania symptoms

Expansive mood Excessive talkativeness Grandiosity Increased energy/reduced sleep

Rapid cycling in bipolar disorder

Four or more cycles / pear (some people have several per day)

Treatment of bipolar disorder

Lithium Affects serotonin and dopamine activity Increases gray matter Must be carefully monitored for toxic side effects

Brain changes in bipolar disorder

Brain changes akin to those in schizophrenia Enlarged ventricles and reduced gray matter

Side effects of lithium

Tremors Weight gain Flattened mood Cognitive impairment