The Drug Revolution for Mental Health Medicine for Madness
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Demonic Possession St. Zenobius exorcises devils (seen fleeing
from the mouths of the possessed)
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A hole in the head: Trepannation
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Benjamin Rush (1745-1813) Treated mentally ill at Pennsylvannia
hospital Madness as disease Used talk therapy Humane treatment
Holistic approach
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Phillipe Pinel (1745-1826) Treatise on Insanity 1791 Removed
chains from mental ill patients at Paris asylum (1792)
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Pinel freeing patients
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Dorothea Lynde Dix (1802-1887) Found mentally ill housed in
jails (MA) Helped found hospitals in 15 states & Canada Humane
care Supervised nursing corp: US Civil War
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Early Treatment The spinning chair One of Rushs invention
Treatments not very effective
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Early 20 th century treatments Insulin coma Lobotomy First
generation shock treatment Restraints Restrictions Warehousing
State hospitals growing every year
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Deinstitutionalization KW 6-9
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Mental health movement Move patients to less restrictive
environments (out of state hospitals) Follow up with community
mental health Monitor continued drug treatment Patient rights
Change in commitment laws
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Drug can Modify KW 6-5
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Mood Disorders characterized by emotional extremes Major
Depressive Disorder no apparent reason, experiences two or more
weeks of depressed moods, feelings of worthlessness, and diminished
interest or pleasure in most activities
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Depression Major Depressive Disorder Defined-long-term sadness
and helplessness Demographics Observed more often in women than men
Peak frequency between 25 and 44 About 19% of all people suffer a
bout of depression at least once in their lives Genetics Depression
does have a genetic link Gene has not been located
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Gender Differences in Depression 12-17 18-24 25-34 35-44 45-54
55-64 65-74 75+ Age in Years 10% 8 6 4 2 0 Percentage depressed
Females Males
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Mood Disorders- Suicide 15-24 25-34 35-44 45-44 55-64 65-74
75-84 85+ Suicides per 100,000 people 70 60 50 40 30 20 10 0 Males
Females The higher suicide rate among men greatly increases in late
adulthood
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Depression Reactive Related to traumatic life event Can be
triggered by an event (ex: death of a loved one, birth of a child,
etc) Endogenous Source from within More likely to be related to
neurochemical differences
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Depression Physiology of Depression Two Conclusions Mood
depends on the effects of a combination of transmitters Different
depressed people have somewhat different transmitter abnormalities
Video
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Mood Disorders- Depression Altering any one component of the
chemistry- cognition-mood circuit can alter the others Brain
chemistry Cognition Mood
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Depression Drug Treatments Antidepressants Tricyclics-prevent
reuptake of serotonin or norepinephrine/epinephrine MAO
Inhibitors-block MAO from breaking down serotonin and
norepinephrine/epinephrine SSRIs-Selective Serotonin Reuptake
inhibitor: inhibits reuptake of serotonin
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Routes of action of antidepressants Tricyclics block the
reuptake of dopamine, norepinephrine, or serotonin. SSRIs
specifically block the reuptake of serotonin. MAOIs block the
enzyme MAO, which converts dopamine, norepinephrine, or serotonin
into inactive chemicals.
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Serotonin and Depression KW 6-11
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Prozac
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MDMA Casues Cell Damage MDMA Changes the density of serotonin
axons in monkeys Normal brain on left Brain on right 18 months
following treatment
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Depression: Other treatments ECT Applied every other day for
two weeks Muscle relaxants and anesthetics minimize discomfort
Memory loss can be a side-effect (limited if shock is given to
right hemisphere only Altered Sleep Patterns Treat patient like
someone with difficulty adjusting to changing time zones
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Biomedical Therapies Electroconvulsive Therapy
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Seasonal Affective Disorder Defined-depression that regularly
recurs in a particular season Usually treated by bright light
therapy
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Mood Disorders Manic Episode a mood disorder marked by a
hyperactive, wildly optimistic state Bipolar Disorder alternates
between the hopelessness of depression and the overexcited state of
mania formerly called manic-depressive disorder
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Bipolar Disorder Defined-alternate between mania and depression
Demographics May last only days or for a year or more 1% of people
have a mild case at some time in life Average age of onset is early
20s Genetics Concordance rate is.50 No specific gene has been
identified
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Mood Disorders-Bipolar PET scans show that brain energy
consumption rises and falls with emotional swings Depressed
stateManic stateDepressed state
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Bipolar Disorder Treatments Lithium Stabilizes mood Mechanism
unknown Side effect: toxicity Anticonvulsant drugs (like Depakote)
Mechanism of action on cortex (lower activity)
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Schizophrenia Definitions Schizophrenia literal translation
split mind a group of severe disorders characterized by:
disorganized and delusional thinking disturbed perceptions
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Schizophrenia Symptoms Delusions false beliefs, often of
persecution or grandeur, that may accompany psychotic disorders
Hallucinations false perceptual experiences such as seeing
something without any external visual stimulus
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Prevalence Schizophrenia affects about 1% of the population and
range in severity. Occurs in all parts of the world, but is 10 to
100 times more common in the United States and Europe than in
third-world countries. More common in men than in women by a ration
of about 7 to 5. More severe and earlier age of onset for men
(early 20s versus late 20). Likelihood increases as the age of the
father increases.
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Characteristics of Schizophrenia Characteristics Deteriorating
ability to function Accompanied by delusions, hallucinations,
thought disorder, movement disorder and inappropriate emotional
expression Behavioral Symptoms Positive Symptoms-behavior that are
present that should be absent Delusions, hallucinations, thought
disorders Negative Symptoms-behavior that is absent that should be
present Weak social interactions, emotional expression, speech, and
working memory
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Probabilities of developing schizophrenia The closer the
genetic relationship to someone with schizophrenia, the higher the
probability of developing it oneself.
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Schizophrenia and Genetics Genetics Concordance rate is 50%
However, genes are not the only influence A gene has not been
located for schizophrenia
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Hypotheses of Causation in Schizophrenia Neurodevelopmental
Either genes or difficulties early in life impair brain development
in ways that lead to schizophrenic-like symptoms in early adulthood
Dopamine Hypothesis-Excess dopamine activity causes behavioral
changes associated with schizophrenia Supported by drug treatments
that target dopamine Glutamate Hypothesis-the problem is deficient
glutamate activity
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Neurodevelopmental The neurodevelopmental hypothesis suggests
abnormalities in the prenatal or neonatal development of the
nervous system. Leads to subtle abnormalities of brain anatomy and
major abnormalities in behavior. Abnormalities could result from
genetics, difficulty during birth, or a combination of both.
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Causation Supporting evidence for the neurodevelopmental
hypothesis includes: Several kinds of prenatal or neonatal
difficulties are linked to later schizophrenia. People with
schizophrenia have minor brain abnormalities that originate early
in life. Abnormalities of early development could impair behavior
in adulthood.
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Prenatal Risk Factors Prenatal risk factors increasing the
likelihood of schizophrenia include: Poor nutrition of the mother
during pregnancy. Premature birth. Low birth weight. Complications
during delivery. Head injuries in early childhood are also linked
to increased incidence of schizophrenia.
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Season of Birth Certain viral infections may be an alternative
or supplement genetic influences. The seasoned-of-birth effect
refers to the tendency for people born in winter to have a slightly
(5% to 8%) greater probability of developing schizophrenia. More
pronounced in latitudes far from the equator. Might be explained by
complications of delivery, nutritional factors, or increased
likelihood of viral infections
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Schizophrenia and Brain S chizophrenia is associated with mild
brain abnormalities: Strongest deficits found in the left temporal
and frontal lobe of the cortex. Larger than normal ventricles.
Especially common in those with complications during birth. Areas
that mature slowly such as the dorsolateral prefrontal cortex.
Schizophrenics have deficits in working memory.
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MRI Scans of Schizophrenia Normal Twin Schizophrenic Twin
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CBF in Schizophrenia
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Treatment Antipsychotic/neuroleptic drugs are drugs that tend
to relieve schizophrenia and similar conditions. Chlorpromazine
(thorazine) is a drug used to treat schizophrenia that relieves the
positve symptoms of schizophrenia. Relief usually experienced 2-3
weeks after taking the drug, which must be taken indefinitely.
Dopamine hypothesis The dopamine hypothesis of schizophrenia
suggests that schizophrenia results from excess activity at
dopamine synapses in certain areas of the brain. Substance-induced
psychotic disorder is characterized by hallucinations and delusions
resulting from repeated large doses of amphetamines,
methamphetamines, or cocaine. Each prolongs activity of dopamine at
the synapse, providing further evidence for dopamine
hypothesis.
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Pathways affected The mesolimbocortical system is a set of
neurons that project from the midbrain tegmentum to the limbic
system. Site where drugs that block dopamine synapses produce their
benefits. Drugs also block dopamine in the mesostriatal system,
which project to the basal ganglia. Result is tardive dyskinesia,
characterized by tremors and other involuntary movements.
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Fig. 15-20, p. 479
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SGAs Second-generation antipsychotics (atypical antipsychotics)
are a class of drugs used to treat schizophrenia but seldom produce
movement problems. Examples: clozapine, risperidone. More effective
at treating the negative symptoms and are now more widely used.
Have less effect on dopamine D 2 receptors and more strongly
antagonize serotonin type 5-HT 2 receptors.
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TGAs? Third Generation Antipsychotics. Abilify (aripiprazole)
Act on both dopamine and serotonin. Regulates, rather than blocks,
dopamine. May help both positive and negative symptoms. Side
effects: restlessness, constipation, sleepiness, involuntary
movement.
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Schizophrenia Conclusions Schizophrenia cannot be explained by
a single gene or single transmitter. Dopamine and glutamate may
play important roles in schizophrenia to different degrees in
different people. Schizophrenia involves multiple genes and
abnormalities in dopamine, glutamate, serotonin and GABA.