Chapter 15: Schizophrenia and the Affective Disorders
Lecture Overview
Schizophrenia
Biochemical Bases
Neurological Bases
Major Affective Disorders
Biochemical Bases
Seasonal Affective Disorder
Schizophrenia
Disorder of thought and emotion
Thought disorder
Hallucinations
Delusions
Incidence (about 1%)
No gender differences in incidence
Symptoms of Schizophrenia
Positive symptoms: presence of
Delusions (e.g. control, grandeur, persecution)
Hallucinations (auditory and olfactory)
Thought disorder
Negative symptoms: loss of normal behaviors
Poverty of speech
Low initiative
Social withdrawal
Diminished affect
Heritability of Schizophrenia
The biological basis of schizophrenia is evident in heritability studies:
Adoption studies
Schizophrenics 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 identified for schizophrenia
Negative Symptoms of Schizophrenia
Signs of brain damage
Eye tracking problems
Catatonia
Problems with blinking, eye focusing and pursuit
Ventricular enlargement: loss of brain cells
Reduced activity of frontal lobes
Damage to:
Dorsolateral prefrontal cortex
Medial temporal lobes
Enlarged Ventricles in Schizophrenia
Hypofrontality in
Schizophrenia
PET scans reveal reduced neural activity within frontal lobes of schizophrenics
Explanation for hypofrontality:
Factors That May Produce Neurological Damage
Birth trauma (obstetrical issues)
Viral infections
Seasonality effects (schizophrenia is more likely for winter births)
Nutritional issues (Hungerwinter: female offspring more likely to exhibit schizophrenia than males)
Stress
Positive Schizophrenic Symptoms: The Dopamine Hypothesis
Chlorpromazine (CPZ) was identified as an effective antipsychotic (AP) agent
CPZ was later found to block DA receptors
Drugs that block DA receptors vary in AP effectiveness
Stimulants such as amphetamine release DA
Chronic administration of amhetamine can induce schizophrenia (Griffiths et al 1972 study)
Stimulants can reinstate psychoses in recovered patients
Hypofrontality in turn activates nuc. accumbens
DA Activity in Schizophrenia
Increased DA levels: No convincing data
Increased receptor activity?
Postmortem studies suggest increased D2 receptors
PET studies suggest no change in D2 receptors in striatum
AP drugs may induce observed changes in receptors
Are we looking in the right place? (Nuc. accumbens should be examined)
Clozapine: may interact with D4 receptors in accumbens
Side Effects of Antipsychotic Medication
Autonomic problems (dry mouth)
Skin-eye pigmentation
Breast development (increased prolactin release)
Tardive dyskinesia: facial tics and gestures
TD due to overstimulation of DA receptors in some patients
Major Affective Disorders
Affect: emotions, moods, and feelings
Major affective disorders:
Bipolar disorder - alternating cycles of
Mania: euphoria, delusions
Depression: profound sadness, guilt, suicide risk
Unipolar depression: continuous, episodic
Biological Bases of Affective Disorder
Heritability of AD has been established in twin studies
No clear linkage to a single gene
Physical treatments for depression
Pharmacological treatments
MAO inhibitors (e.g. iproniazid)
Serotonin reuptake inhibitors (e.g. Prozac)
Electroconvulsive shock therapy (ECS)
Sleep deprivation
Monoamine Hypothesis of Depression
Depression results from reduced activity of the monoamines NE or 5-HT
Reserpine depletes monoamines--> depression
Antidepressants meds increase either NE or 5-HT
Via blockade of reuptake
Tryptophan deletion procedure:
Reduces brain 5-HT levels
Reinstates depression in former depression patients
Not effective in persons treated with NE reuptake drugs
Links Between REM Sleep and Depression
Sleep patterns in depressed persons
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
Seasonal Affective Disorder
SAD: form of depression evident in winter months (short days/long nights)
Mood and sleep disturbances
Carbohydrate cravings and weight gain
Phototherapy for SAD: increased exposure to light improves mood in SAD (and also in unipolar depression)