PSYC 211 Chapter Notes -Haloperidol, Endorphins, Morphine

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PSYC211 Chapter 16 Notes
Schizophrenia
The word means “Split mind” but it does not imply a split or multiple personality
Term invented by Eugen Bleuler (1911/1950), intended it to refer to a break in reality with reality cause by disorganization
of the various functions of the mind, such that thoughts and feelings no longer worked together normally
Affects 1% of the world’s population
Very expensive cost to society
There are 3 categories of symptoms
Positive Symptoms (Make themselves known by their presence)
oThought disorders (disorganized irrational thinking)
oHallucinations (Perception of nonexistent object or event)
oDelusions (Belief contradictory to reality)
Negative Symptoms (Absent of behaviours that that are normally present)
oFlattened emotion response
oPoverty of speech
oLack of initiative and persistence
oAnhedonia (inability to experience pleasure)
oSocial withdrawal
oLack of affect
oReduced motivation
Cognitive Symptoms (Closely related to negative symptoms & can be produced by abnormalities in
same brain regions)
oDifficulty sustaining attention
oLow psychomotor speeds (movement of fingers, hands, legs)
oDeficits in learning & memory
oPoor abstract thinking
oPoor problem solving
*Negative and cognitive symptoms are not specific to Schizophrenia; they are seen in many neurological disorders that involve brain
damage especially to the frontal lobe. Negative symptoms are the first to appear followed by cognitive symptoms. The positive
symptoms follow several years later.
Heritability
Schizophrenia is a heritable trait. According to both adoption studies (Kety et al., 1968, 1994) and twin studies (Gottesman
and Shields, 1982; Tsuang, Gilbertson, & Faraone, 1991).
In children with 2 Schizophrenic parents, less than 50% meaning that several genes are involved or that having a
“Schizophrenia gene” imparts a susceptibility to develop Schizophrenia, the disease itself being triggered by other factors.
Carrying a Schizophrenic gene does not mean that a person will necessarily become Schizophrenic.
Another genetic factor is paternal age, children of older fathers are more likely to develop Schizophrenia. (Increased
incidence of Schizophrenia caused by mutations in the sperm)
So far, researchers have found no location of a “Schizophrenic gene”
Walsh et al (2008) suggests that a large number of rare mutations play a role in the development of Schizophrenia
Mutations affecting neural differentiation and growth, guidance of axons during brain development, assembly of
components of neurotransmitter receptors, and factors that control the formation of synapses could be responsible for
susceptibility to Schizophrenia.
Pharmacology of Schizophrenia: The Dopamine Hypothesis
Dopamine Hypothesis
Positive symptoms of Schizophrenia caused by a biochemical disorder (Over activity of synapses between dopaminergic
neurons of the ventral tegmental area and neurons in the nucleus accumbens and amygdala)
Patients with greater amounts of dopamine release showed greater increases in positive symptoms
Effects of Dopamine Agonists and Antagonists
Middle 20th century French surgeon Henri Laborit, developed drug to prevent surgical shock but it also seemed to reduce
anxiety
Later a French drug company made a related compound called, Chlorpromazine – it had dramatic effects on
Schizophrenia
Drug helped keep patients from long hospital visits
Eliminated or helped diminish patients positive symptoms
Hallucinations/delusions went away or became less severe
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Drugs that produced the positive symptoms of Schizophrenia act as dopamine agonists. (They block the reuptake of dopamine)
amphetamine
cocaine
methylphenidate
symptoms of these drugs can be alleviated with antipsychotic drugs, this further strengthens the argument that the
antipsychotic drugs exert their therapeutic effects by blocking dopamine receptors
Consequences of Long-Term Antipsychotic Drug Treatment of Schizophrenia
Causes symptoms resembling those of Parkinson’s disease (For most patients this is temporary)
oSlowness in movement
oLack of facial expression
oGeneral weakness
Much more serious side effect, effects 1/3 of all patients : Tardive Dyskinesia
oMeans, slow/faulty movement
oIt is a late developing movement disorder
oOpposite of Parkinson’s disease
oPatients can’t stop moving
oExplained by super sensitivity –increased sensitivity of neurotransmitter receptors; caused by damage to the
afferent axons or long-term blockage of neurotransmitter release.
*There have been drugs created that do not produce neurological side effects though! They are called Atypical Antipsychotic
medications. It reduces both positive and negative symptoms.
oClozapine – Is the first, (it blocks D4 receptors in the nucleus accumbens) following this drug came, risperidone,
olanzapine, ziprasidone, & aripiprazole
Schizophrenia as a Neurological Disorder
Positive symptoms are unique to Schizophrenia
Negative and cognitive symptoms are similar to those produced by brain damage
Brain abnormalities give rise to increased secretion of dopamine in the nucleus accumbens & the accompanying positive
symptoms
Many studies found evidence of loss of brain tissue in CT & MRI scans of Schizophrenic patients
Ventricle size of the Schizophrenic patients was more than twice as great as that of normal control subjects. Most likely
because of lose of brain tissue
Everyone loses some cerebral grey matter as they age, the rate of tissue loss is greater in Schizophrenia patients
Causes for Brain Abnormalities
Inheritance is a defect that renders people susceptible to some environmental factors that adversely affect the brain
development
Epidemiology – study of distribution & causes of diseases in population
oenvironmental factors, season of birth, viral epidemics, population density, prenatal malnutrition, & maternal
stress
oPeople born in late winter and early spring are more likely to develop Schizophrenia (Seasonality Effect)
Factors responsible for Seasonality Effect : Women more likely to contract viral illness during a critical
phase in child’s development
In cities, rarely found in country side (more diseases in highly dense populations)
Vitamin D deficiency – plays important role in brain development
Brain damage later in life
Obstetric Complications – can lead to Schizophrenia
Diabetes of mother
Rh incompatibility between mother & fetus
Bleeding
Edema
Abnormal fetal development
Complications of labour and delivery >interruption of blood or oxygen supply to the brain
Evidence of Abnormal Brain Development
Abnormal prenatal development is associated with Schizophrenia
Schizophrenic children compared to their siblings have a more negative facial expression and abnormal movements
Displayed less sociability and deficient psychomotor functioning
Minor physical anomalies: high-steepled palate or especially wide-set or narrow-set eyes
In Monozygotic twins, one with Schizophrenia usually has a larger lateral & third ventricles, anterior hippocampus was
smaller & grey matter in left temporal lobe was reduced
Monozygotic twins : two types, monochromatic (twins share a single placenta) & Dichorionic (each has its own)
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Concordance rates of Schizophrenia is higher in monochromatic twins than Dichorionic ones
Rapid loss of brain volume occurs at young adulthood, process of Schizophrenia but lies dormant until puberty when
something triggers the neurons
Relationship between Positive and Negative Symptoms: Role of the Prefrontal Cortex
Negative symptoms caused by hypofrontality, decreased activity of frontal lobes
Schizophrenic patients do poorly on neuropsychological tests that are sensitive to prefrontal damage
Hypofrontality is caused by the release of dopamine in the prefrontal cortex
Destruction of the dopaminergic input to the prefrontal cortex lowers its metabolic rate & leads to cognitive dysfunctions
Injection of dopamine antagonists into the prefrontal cortex caused behavioural deficits like those produced by prefrontal
lesions
Drugs, Ketamine (Special K) & PCP (phencyclidine/angel dust) can cause positive, negative & cognitive symptoms of
Schizophrenia
Negative & cognitive symptoms produced by the drugs above are caused by a decrease in metabolic activity of the frontal
lobes
Remembering back to chapter 4, PCP is an indirect antagonist of NMDA-receptors (so is ketamine) by inhibiting the
activity of NMDA receptors, PCP suppresses the activity of several regions of the brain notably the dorsolateral prefrontal
cortex
NMDA & dopamine receptors play an important role in the production of negative/cognitive symptoms: suppression of
these receptors cause hypofrontality
Prefrontal hypoactivity causes hyperactivity of mesolimbic dopaminergic neurons
Excitatory glutamatergic neurons of the prefrontal cortex send axons to the ventral tegmental area, where they form
synapses with dopaminergic neurons that project back to the prefrontal cortex
Drugs that act as NMDA agonists to reduce symptoms of negative/cognitive symptoms
Direct agonists cannot be used because they increase the risk of seizures
Glycine & D-serine bind to one of these sites and act as indirect agonists
Atypical anti-schizophrenic drugs do the impossible: increase dopaminergic activity in the prefrontal cortex & reduce it in
the nucleus accumbens
Aripiprazole is a partial antagonist (drug with very high affinity for a particular receptor but activates that receptor less than
the normal ligand does, serves as an agonist in regions of low concentrations of the normal ligand & as an antagonist in
the regions of high concentrations.)
Major Affective Disorders
There are 2 principal types of major affective disorders, first type is characterized by alternating periods of mania and depression- a
condition called bipolar disorder.
Affects men & women in equal amounts
Episodes of mania last a few days or several months
Episodes of depression that follow generally last 3 times as long as mania
The second type is major depressive disorder (MDD), characterized by depression without mania.
It may be continuous & unremitting or may come in episodes
Mania without periods of depression occur but it is rare
Extreme feelings of unworthiness, and strong feelings of guilt
Risk of suicide
Very little energy, move/talk slow
Pace around aimlessly
May cry a lot, may not be able to experience pleasure
Loss of appetite for food and sex
Sleep disturbed
Body functions disturbed: constipation/secretion of saliva decreases
Episodes of mania:
characterized by a sense of euphoria
exhibit nonstop speech and motor problems
Talk from topic to topic
Often have delusions
Lack the severe disorganization that is seen in Schizophrenia
Usually defensive when contradicted
Go for long periods of sleep
Work on projects which are often unrealistic
Heritability
There is a tendency to develop an affective disorder is a heritable characteristic
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Document Summary

The word means split mind but it does not imply a split or multiple personality. Term invented by eugen bleuler (1911/1950), intended it to refer to a break in reality with reality cause by disorganization of the various functions of the mind, such that thoughts and feelings no longer worked together normally. Negative symptoms (absent of behaviours that that are normally present) Cognitive symptoms (closely related to negative symptoms & can be produced by abnormalities in. *negative and cognitive symptoms are not speci c to schizophrenia; they are seen in many neurological disorders that involve brain damage especially to the frontal lobe. Negative symptoms are the rst to appear followed by cognitive symptoms. According to both adoption studies (kety et al. , 1968, 1994) and twin studies (gottesman and shields, 1982; tsuang, gilbertson, & faraone, 1991). In children with 2 schizophrenic parents, less than 50% meaning that several genes are involved or that having a.

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