Ch.17 Schizophrenia and the Affective Disorders

Copyright 2001 by Allyn & Bacon

Carlson (7e) PowerPoint Lecture Outline

Chapter 17: Schizophrenia and the Affective Disorders

This multimedia product and its contents are protected under copyright law. The following are prohibited by law:•any public performance or display, including transmission of any image over a network;•preparation of any derivative work, including extraction, in whole or in part, of any images;•any rental, lease, or lending of the program.


Schizophrenia

■ Schizophrenia represents a disorder of thought and emotion, but not a “split-personality”● Thought disorder● Hallucinations● Delusions● Bizarre behaviors

■ The incidence of schizophrenia is about 1%● No gender differences in incidence

17.2


Symptoms of Schizophrenia

■ Positive symptoms include delusions, hallucinations and thought disorder● Delusions are beliefs that are contrary to reality

◆ Delusions can involve control, grandeur, or persecution

● Hallucinations are perceptions that occur in the absence of stimuli (often auditory and/or olfactory)

● Thought disorder: disorganized and irrational

■ Negative symptoms involve a loss of normal behaviors, such as● Poverty of speech and low initiative● Social withdrawal and diminished affect

17.3


Heritability of Schizophrenia

■ The heritability of schizophrenia is a strong indicator of a biological basis for schizophrenia● Adoption studies

◆ Adult schizophrenics that were adopted as children are likely to have schizophrenic biological relatives.

● Twin studies◆ Concordance rates for schizophrenia are higher for

identical than for fraternal twins: ● No single gene has been identified for schizophrenia

◆ Genes may pass on a susceptibility to develop schizophrenia

17.4


Genes and Schizophrenia Susceptibility

17.5


The Dopamine Hypothesis of Schizophrenia

■ The “dopamine hypothesis” is that the positive symptoms of schizophrenia involve overactivity of brain dopaminergic synapses● Chlorpromazine (CPZ) was identified as an effective

antipsychotic (AP) agent◆ CPZ was later found to block DA receptors (D2 receptors)◆ Other drugs that block DA receptors also reverse

schizophrenia

● Stimulants such as amphetamine that release DA can produce the positive symptoms of schizophrenia

17.6


DA Activity in Schizophrenia

■ PET studies indicate greater release of dopamine in the striatum of schizophrenics to a test dose of amphetamine● Amount of dopamine released was related to the increase in

positive schizophrenia symptoms■ Studies of dopamine receptors in schizophrenic brain

have provided mixed results● Postmortem studies suggest increased numbers of D2 receptors

in striatum (but may be due to exposure to AP drugs)◆ The striatum is a motor control region: may be the wrong site◆ Schizophrenia may be related to D4 or D3 receptors

● Clozapine is an effective AP drug that does not interact with D2

◆ Clozapine acts on D4 receptors in the accumbens

17.7


Antipsychotic Medications

■ Antipsychotic medications diminish the thought disorder evident in schizophrenia

■ Side effects of antipsychotic medications include● Autonomic problems (dry mouth)● Skin-eye pigmentation● Breast development (increased prolactin release after

blockade of dopamine neurons)● Tardive dyskinesia: facial tics and gestures

◆ TD is due to overstimulation of DA receptors

17.8


Brain Damage and Schizophrenia

■ The negative symptoms of schizophrenia are related to brain damage● The neurological signs evident in schizophrenia include

◆ Eye tracking problems◆ Catatonia◆ Problems with blinking, eye focusing, and visual pursuit

● Schizophrenics exhibit enlarged brain ventricles, which suggests loss of brain cells

● Regions of schizophrenic brain that are abnormal include◆ Prefrontal cortex◆ Medial temporal lobes ◆ Medial diencephalon

17.9


Ventricular Enlargement in Schizophrenia

17.10

Normal Twin Schizophrenic Twin


Causes of Brain Damage in Schizophrenia

■ The neurological symptoms of schizophrenia may be caused by● Birth trauma (obstetrical issues)● Viral infections that impair neural development during the

second trimester◆ Seasonality effects (schizophrenia is more likely for winter births)

● Nutritional issues (Hunger Winter: female offspring were more likely to exhibit schizophrenia than male offspring)

● Maternal stress may compromise the immune system of the mother and lead to a greater chance of contracting a viral infection

17.11


Seasonality and Schizophrenia

■ Children born during the late winter and early spring are more likely to develop schizophrenia● Seasonality effect occurs in

cities but not the countryside■ Seasonality effect may be

related to the mother contracting a viral infection during the second trimester of fetal development

17.12


Hypofrontality and Schizophrenia

■ Hypofrontality refers to the decreased activity of the dorsolateral prefrontal cortex● Damage to the prefrontal cortex impairs behavioral flexibility

(card sorting task)● Schizophrenics show decreased activity in the prefrontal cortex

■ Abuse of PCP produces positive and negative symptoms of schizophrenia● Positive: related to indirect actions of PCP on accumbens DA● Negative: related to decreased DA utilization in prefrontal

cortex following PCP treatment

17.13


Major Affective Disorders

■ Affect refers to emotions, moods, and feelings● Our affect is usually a reflection of our experiences● In the major affective disorders, our emotional

reactions are at the extremes and may not be related to our actual experiences

■ The major affective disorders include● Bipolar disorder - alternating cycles of

◆ Mania: euphoria, delusions◆ Depression: profound sadness, guilt, suicide risk

● Unipolar depression: continuous, episodic

17.14


Biological Bases of Affective Disorder

■ Heritability of affective disorder (AD) has been established in twin studies and family studies● Bipolar disorder may be related to a single gene

■ Depression is amenable to physical treatments including● Pharmacological treatments

◆ MAO inhibitors (e.g. iproniazid)◆ Serotonin reuptake inhibitors (e.g. Prozac)

● Electroconvulsive shock therapy (ECS)● Sleep deprivation

17.15


Monoamine Hypothesis of Depression

■ Depression results from reduced activity of brain monoamines● Reserpine depletes monoamines--> depression● Suicidal depression is related to a low level of 5-

HIAA● Antidepressant meds increase either NE or 5-HT

◆ Usually via blockade of monoamine reuptake● Tryptophan deletion procedure:

◆ Reduces brain 5-HT levels◆ Reinstates depression in former depressed patients

17.16


Antidepressant Medication and 5-HT

17.17


REM Sleep and Depression

■ Sleep pattern is disrupted in depressed persons● Reduced REM latency, reduced stages 3 and 4 sleep

■ REM deprivation improves mood■ Antidepressant drugs suppress REM sleep, and

increase slow-wave sleep■ Persons who have short REM sleep latency are

more likely to develop depression■ REM sleep deprivation is more effective than is

total sleep deprivation (effects last longer)

17.18


Sleep Patterns in Depression

17.19


Mood and Sleep Deprivation

17.20


Seasonal Affective Disorder

■ SAD is a form of depression evident in winter months (short days/long nights)

■ SAD involves● Mood and sleep disturbances● Carbohydrate cravings and weight gain

■ Phototherapy for SAD: increased exposure to light improves mood in SAD (and also for unipolar depression)

17.21

Documents

Ch.17 Schizophrenia and the Affective Disorders