Download Tour of the Brain Afternoon 7

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The Neurobiology of Mental Illness
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Neurobiology
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The Neurobiology of Mental Illness
Untangling Cause and Effect
The study of the neurobiology of an illness looks at genetic, physical & environmental aspects of
behavioral disease
Studying these three aspects of a disorder gets us much closer to the real causes of these disorders
Nature v Nurture is dead
Mental Disease is a complex interaction of both genes and environment
Schizophrenia
Mood disorders
Anxiety disorders
Substance Use
Dementia
Autism
ADHD
Personality disorders
OCD
Aggression
Eating Disorders
Menstrual Cycle disorders
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A Word About Genes
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Genetic Differences in Identical Twins
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A Word About Environment
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John B. Watson
All medical and behavioral disorders have a genetic basis
Sensitivity to environmental factors is genetic
Having a gene is not the same as expressing it
Stress often “turns on” a unexpressed gene
The genes you have when you are born are not always the genes that you have when you die
Your genes change with time
Even the genes of identical twins will diverge across time
As they age, twins grow more genetically distinct
Epigenetics is the study of environmental impact on genes
There are no genes without an environment
A harsh environment will overcome a good gene
A severe genetic abnormality will undercut the best environment
Most of us are in the middle
People with dopamine disorders have a harder time in even the best of environments
A child psychologist who thought that physical affection was bad for children
A generation of children were denied affection because of his teaching
This may have led to many dysfunctional adults still alive today
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The Germ Theory of Infection
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How To Think About Genes
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Genes Are Like Computer Programs
We have forgotten about the effects of infectious disease
800,000 in the US died in the 1918 flu epidemic
9,000 people died every day for 3 months
20 - 50 million died world-wide in less than one year
Genes are encoded instructions on how to build a specific person/animal/plant
Some routines play in development, but many are unexpressed until specific triggers cause them to
activate
So, you can be born with a gene and not express it until later in life
Or you can engage in behaviors that change your DNA
Some are programmed to come up when you boot your computer, but others are in there for you to call up
when you need them
You can begin to “express” a gene anytime in your life
You can begin to “express” a gene anytime in your life
Bipolar disorder often develops after a stressful event
It’s still a genetic disorder
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DNA Genes & Chromosomes
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Nuclear Disasters
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Copy Number Repeat Diseases
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Are Mental Disorders Increasing?
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Cause of Autism
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Genetic Anticipation
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Schizophrenia & Bipolar Disorder
Will Genetic Research Influence the Treatment of Mental Disorders?
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The Neurobiology of Schizophrenia
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A Long Time Ago
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What Is Schizophrenia?
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Schizophrenia
Chromosomes are comprised of long strings of DNA wrapped around histones
Genes are segments of DNA plus the histones
Histones can be altered by environmental factors
We are learning that there have been many more Russian nuclear disasters than previously known
The cumulative radiation released into the world’s atmosphere is much greater than experts believed
Many psychiatric disorders are due to erroneous numbers of genes copied into the genome
Fragile X syndrome
Huntington’s
Spinocerebellar Ataxia
Lower infant mortality rate
6 million released from state hospitals in the 1950’s
Resulting in 12 million children by 1980
Resulting in 24 million children by 2000
People marry later in life increasing the likelihood of germ cell mutations
Eric Kandel
Psychiatrist - Nobel Laureate
“Genetic anticipation” refers to the deterioration of genetic material as it is copied down the generations
For some mental illnesses the age of onset decreases and the symptoms gets more severe in each new
generation
Parents of bipolar children may be unfairly blamed for worsening disease actually due to genetic
anticipation
Genetic data will provide information for the development of new drugs
Will help remove stigma
Decrease erroneous thinking r.e. causality
Increase personal responsibility for disease management
It will not effect therapies that rely on the interpersonal relationships
The Physics of Thought
Schizophrenia was thought to be a “mental” disease because no structural differences were seen in the
brains of schizophrenics
Things have changed. We can now easily see the structural and chemical changes that exist in the brain
tissue of schizophrenics
SZ is not a single disease but a collection of genetic disorders that alter cognition and perception
SZ has a range of severity and multiple causes
Subtypes? Variations?
Best thought of as a “spectrum” of disease
Common features are disordered perception, thought and judgment
An error in the ability to process “reality” in the form of sensory input
Synesthesia is another type of error in processing
An inability to distinguish internally generated data from external experience
Appears to require a defect in two areas
in the brain
Thalamus (sensory integration) (positive symptoms?)
Pre-frontal cortex (judgment) (negative symptoms?)
Appears to require a defect in two areas
in the brain
Thalamus (sensory integration) (positive symptoms?)
Pre-frontal cortex (judgment) (negative symptoms?)
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Thalamic &
Frontal Damage
Damage to the thalamus causes alterations to perceptions
Alterations in frontal lobe function makes patients believe the perceptions are real rather than internally
generated phenomena
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Crossroads In The Brain
Schizophrenia
Symptoms of Schizophrenia
Hallucinations
Delusions
Decreased focused attention
Disorganized thought
Cognitive impairment
Flattened affect
Withdrawal
Paranoia
Poverty of speech
Disorganized speech
Social anxiety
Dysexecutive syndrome
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Variants of Schizophrenia
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Problems Defining Schizophrenia
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The Many Symptoms of Schizophrenia
Decreased Focused Attention
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Attention Deficits
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Positive & Negative symptom clusters
Positive = delusions, hallucinations, paranoia (respond to medication)
Negative = apathy, social disfunction, withdrawal, flat affect (don’t respond)
The classical subtypes used in the DSM-IV, paranoid, disorganized, catatonic, undifferentiated,
residual have been removed from the DSM 5
Catatonic
Described in the past - not seen now - may have been due to brain injury
Schizoaffective
Mix of perceptual distortion and mood disorder
Schizophrenia research suffers from an inability to develop a stable set of diagnostic criteria
There are many places to look for disease
Chemical
Structural
Behavioral
Genetic
Developmental Congenital
We do not understand why schizophrenia presents so differently in different patients
Brain activity occurs in two modes, a background trickle and brief bursts
Schizophrenics have a hard time separating background information from the important bursts
They tend to find importance in trivial details
Nicotine helps them to focus on what’s real
Many mental disorders have attentional disruption as a core symptom
Nicotine helps the brain focus on important stimuli and ignore things that are unimportant
Nicotine activates areas in the brain that filter stimulation
“I’ll be surprised if there is not a co-therapy [for schizophrenia] that takes advantage of nicotine systems in
less than a decade”
Physical Brain Differences
Ventricular enlargement
Decreased volume
Small thalamus
Decreased volume
Small thalamus
Gliosis
Hypofrontality
Cell migration defects
Alterations in dopamine serotonin & glutamate
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Ventricular Enlargement
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Hypofrontality
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Hypofrontality In Identical Twins
New Evidence For Frontal Lobe Dysfunction
Decreased Hippocampal Volume
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Early Cortical Degeneration
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Neural Networks
Damaged In
Schizophrenia
This condition worsens with time as the brain continues to lose volume
Left side greater than the right
Alters memory formation
Increases confabulation
Temporal Lobe
Schizophrenia is a Dementia
Brain areas do not function separately from each other
Most mental illnesses occur on an “axis” or loop of several brain areas that are linked by neurons that
produce the same chemicals
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Emil Kraeplin &
Alois Alzheimer
Pioneering neurologists who thought both Alzheimer’s and schizophrenia were degenerative
Both considered these diseases as dementias
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Cellular Migration Defects
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Too Many Connections
Overactivity & Underactivity
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Schizophrenia Is ...
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Wouldn’t anyone be crazy if they saw or heard things that weren’t there?
Synesthesia
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Synesthesia
Synesthesia
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Causes of Synesthesia
Scans of Crossed Pathways
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Feeling Music
Cellular confusion
Too many cells in some areas
Too few in others
Glial cells that guide the patterning of cells are thought to be abnormal in schizophrenia
Some parts of the brain are overactive (temporal)
Some areas are underactive(frontal)
Resulting in a mix of perceptual and behavioral symptoms
An early defect in the thalamus that alters physical perception
Neurotransmitters that send signals are effected
Additional left-frontal damage prevents insight into perceptual errors
A rare genetic disorder that causes the brain to mix sensory perceptions
Synesthetes see music, taste sound, hear color etc.
The perceptual changes are stable for each person across their lifetime
The most common form is color-number
The next most common form is sound-color
The cause of synesthesia is a gene that causes two or more areas of the brain to respond to a single
sensation
May alter the chemical balance between two sensory systems
May alter the chemical balance between two sensory systems
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Feeling Music
Testing for Synesthesia
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Synesthesia
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Color Is In The Brain
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Understanding Schizophrenia
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Cognitive Therapy
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Etiology of Schizophrenia
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Genetic Defects
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The Genain Quadruplets
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39 Year Followup
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Is Schizophrenia Genetic?
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Polygenetic Inheritance
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Schizophrenia Is Not Simply Inherited
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A Developmental Disorder
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Etiology of Schizophrenia
Color Makes The Numbers Easy To See
Each synesthete is a little different and sees and hears a different set of sensations
Synesthetes were shown black and white cartoons that contained numbers
They reported seeing the numbers in color
The colors corresponded to their personal “palate”
Like synesthesia schizophrenia alters the brain’s ability to perceive the environment
The symptoms interfere with their ability to work and socialize
Unlike synesthesia patients have no insight into their perceptions
Synethetics have no damage to the frontal lobes
Strengthening the Frontal Lobe
The Genetic Defect Hypothesis
The Neurodevelopmental Hypothesis
Excitotoxcicity-Neurodegenerative Hypothesis
SZ clearly runs in families
There is a tenfold increase in risk in 1st degree relatives
There is little other evidence for direct genetic transmission
Every major genetic linkage study has failed
Symptoms of SZ do not even follow the Mendelian rules for inheritance
Identical quadruplets
All had schizophrenia but differed significantly in presentation
Risk was 1.5 billion to 1
Both parents were severely mentally ill
Cause of their disease still debated
Schizophrenia is not fully penetrant
50% of identical twins do not get the disease
Symptoms of schizophrenia can be causes by other means
Schizophrenia is not independent of environment
No genetic study has ever been completely successful
Probably not just one disease
Science, August 2008
“Thus, the tight one-to-one relationship that exists between disease gene and phenotype does not apply
to schizophrenia.”
Events that occur during critical periods of fetal growth can negatively impact brain development
In the 2nd trimester, neuronal migrations take place that form critical cortical connections
Many studies show that women exposed to trauma or pathogens at this time have a higher risk of having a
child with schizophrenia
As many as 13/15 in some studies
Many studies show that women exposed to trauma or pathogens at this time have a higher risk of having a
child with schizophrenia
As many as 13/15 in some studies
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Etiology of Schizophrenia
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Defects in Cortex Development
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Factor Analysis of Schizophrenia
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Haldol In The Brain
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The DSM 5
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Summary
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The Neurobiology of Anxiety
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What Is Anxiety?
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Stress & Survival
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Anxiety & Survival
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Pain & Survival
Update
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Anxiety Disorders
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Not Within Normal Limits
Damage to cortical sub-plate in the 2nd trimester of pregnancy
Some of the risk factors are:
Viruses
Malnutrition
Severe psychological stress
Obstetrical complications
Probably anything that interferes with growth and neuronal development
Cortex is formed as neurons migrate from the cortical plate through the intermediate zone
Excess neurons are produced and must die back
As much as 50% of initial neural growth
Defects in neuronal migration and cell death account for perturbed connections in the brain
Positive Symptoms (temporal lobe)
Delusions
Hallucinations
Negative Symptoms (frontal lobe)
Social withdrawal
Disorganized thought (frontal lobe)
Thalamus and Frontal Cortex
The overall definition of schizophrenia has not changed greatly in DSM 5
A patient must have at least 2 characteristic symptoms for at least one month
These include delusions, hallucinations, disorganized speech, abnormal psychomotor activity
There must be social/occupational dysfunction over a six-month duration
Schizophrenia appears to be a disorder of both genetic and environmental cause
Interference with cell death sends neurons to the wrong places
Sometimes triggered by infection, starvation or injury during pregnancy
A simultaneous loss of pre-frontal and thalamic function occurs interfering with sensory integration and
judgment about what is real and unreal
Paranoid personality disorder may be the frontal lobe/judgment deficit without the sensory errors
Fear and Loathing in the Brain
Anxiety is the brain & body’s natural response to threat
Anxiety is necessary for survival
Thus, a complex and sensitive system has evolved to alert us to danger
This system is deeply ingrained
When this natural system for self-preservation goes awry excess anxiety and panic may result
This system predates the development of cognition and so is based mostly in the midbrain and brainstem
Much of the brain exists to cause stress and anxiety
Historically these important emotions helped us survive
Without negative emotions humans do not live long
Anxiety and depression can be characterized as survival-related communication from the brain
People who lack fear and anxiety often do not live long
Gabby Gingras
In the DSM-IV diagnosed only when responses were judged to be out of proportion to the situation
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Not Within Normal Limits
Cultural Factors
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Expression of Emotion
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The Neurobiology of Fear
Anxious Dogs
Role of the Amygdala
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Role of the Amygdala
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It is generally believed that most, perhaps all, specific fears are learned through
experience. For example, monkeys in the wild are afraid of snakes but monkeys
raised in labs are indifferent to them.
Primal Fear
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Amygdala
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Role of the Hippocampus
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Role of the Prefrontal Cortex
Appropriate response to a stressor varies by culture
American’s are very ambivalent regarding emotional reaction
We praise “human emotion” but do not want to deal with it in our families and ourselves
We medicate feelings that are normal expressions of emotions
Change Across Time
The amygdala processes fear, anxiety and rage
Specific fears are not innate, but are learned through experience
Lab monkeys are not afraid of snakes
The brain-stem response to fear is innate & includes sweaty palms, racing heart, shaking
In other words, people can be afraid of many different things, but how the emotion of fear is experienced
is always the same
Our old, primitive brain responses for survival can be triggered by modern events
For a neutral stimulus to begin produce the behavioral response of fear and anxiety, it is only necessary for
that stimulus to activate
the amygdala
The amygdala signals the rest of the brain to produce the response of fear
Individuals with an “overactive” amygdala will be more likely to respond to many things with fear
Electrical stimulation of the amygdala will also cause a classic fear response
Temporal lobe epilepsy
paranoia
The amygdala sends info to the hippocampus which is instrumental in assigning meaning to the stimulus
“Content conditioning”
Chronic stress has been found to be especially damaging to the hippocampus
Anxiety disorders may occur when a pre-stressed hippocampus too readily assigns a stimulus as
something to fear
Preparation to respond to threat requires integration between brains areas that assess and interpret a
stimulus (amygdala & hippocampus) and brain areas involved in judging how to respond (frontal lobe and
cingulate cortex)
Multiple studies have found PTSD and panic patients to have pre-existing prefrontal disfunction
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The Basic Fear Response
Pathway of Anxiety
Neurochemistry in Anxiety
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The Expression of Fear is Universal in Humans
3 Major Neurotransmitters
Noradrenalin
Dopamine
Serotonin
3 Minor chemical messengers
GABA (benzodiazepines)
Opioid peptides
Cholecystokinin (pain killers)
This was established by Darwin and was reported in his first book, The Expression of Emotion in Man and
Animals
Prior to this, emotions were not thought to be the same across cultures
This was established by Darwin and was reported in his first book, The Expression of Emotion in Man and
Animals
Prior to this, emotions were not thought to be the same across cultures
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Bodily Response in Fear
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The Eyes Express Fear
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Amygdaloid Overactivity
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Amygdaloid Damage
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William’s Syndrome
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Neurochemistry of Fear
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Etiology of Anxiety
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The DSM Anxiety Disorders
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Prevalence of Anxiety Disorders
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The Pattern of Normal Anxiety
Pounding heart
Dry mouth
Fidgeting
Apprehensive expectation
Upset stomach
Increased respiration
Scanning and vigilance
Jumpy, quick startle
Evacuation of bladder
Evacuation of bowels
More than any other part of the body, fear can be seen in the eyes
Adrenaline causes a widening of the eyes to gather more light and allow better judgment
Anxious subjects show extra activity in the amygdala
Mild damage to the amygdala can cause increased aggression
Severe damage causes decreased perception of danger or anger and blunts the behavioral response to
threat
Williams syndrome is characterized by medical problems, including cardiovascular disease and learning
disabilities. These occur side by side with striking verbal abilities, highly social personalities and an affinity for music.
They require supervision because they do not fear anything
Nor-adrenaline
Corticotropin Releasing Hormone
Neurosteroids
Arginine Vasopressin
Neuropeptide Y
Galanin
GABA
Dopamine
Serotonin
Benzodiazepines
Opioid peptides
Genetic studies show some genetic predisposition for excessive fear but little evidence for a specific
disease
A nonspecific vulnerability to anxiety appears to be inherited, but environment and experience may be
large factors in which type of anxiety is developed
PTSD, Panic Disorder and General Anxiety are more similar than different
Panic Disorder with/without Agoraphobia
Specific Phobia
Social Phobia
Obsessive-Compulsive Disorder
Post-traumatic Stress Disorder
Generalized Anxiety Disorder
30% of Americans will experience a diagnosable anxiety disorder some time in their lives
Panic affects 9-10 % of the population
Social phobia in 13% of the population
Simple phobias in 10-11% of the population
Generalized anxiety disorder in 5%
OCD found in 1-2% of the population
OCD found in 1-2% of the population
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The Pattern of Normal Anxiety
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Reconsolidation
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Extinction
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Extinction
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Risk Factors for Anxiety Disorder
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Initial stressor
Consolidation
Reconsolidation
Extinction
Whereby a prior experience can undergoes another round of placement into memory
It is the rule, rather than the exception that memories are reactivated by cues associated with the original
trauma or experience
Reconsolidation can cause a memory to strengthen, change or weaken
Medications can interfere with reconsolidation (Benzos-Beta blockers)
Can they be used to lessen anxiety without loss of other forms of learning?
Extinction occurs when an event recurs without a negative consequence
After a while the fear lessens
Immersion therapy uses extinction to reduce the brain’s response to a specific fear
Immersion works well with classic phobias
When immersion therapy fails it may be because the stated trigger for fear is incorrect
Women who claim to be afraid of flying are often actually fearful of depriving their children of care
Immersion therapy using airplane interiors will fail in these cases
Damaged/poorly functioning amygdala
Damaged/poorly functioning hippocampus
Damaged/poorly functioning prefrontal cortex
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Nosology
of
Anxiety Disorders
The Neuroses
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The Neuroses
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DSM-3
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Diagnostic Difficulties
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Newer Data on Anxiety
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The Cycle of Panic Disorder
Panic Disorder
Early Psychiatry referred to anxiety as “anxiety neurosis”
The neuroses were defense mechanisms created in childhood to adapt to imperfect parenting
Most people were thought to have some form of neurosis
Caused by poor parenting
Psychotherapy treats neuroses by providing increased insight reducing the need for immature (fearful)
responses to stress
Measures of neuroticism are excellent predictors for the development of anxiety disorders and PTSD later
in life
Neuroses were removed as a diagnostic category in 1980
The anxiety disorders were put in their place
The older categories were based more on Freudian concepts then empirical research
Few medications were available and the focus was on therapy
Unlike schizophrenia our current classification of anxiety disorders is not based on modern knowledge of
neurophysiology or even treatment response
This makes the relationship between DSM anxiety disorders and a specific neuro-pathway difficult to
establish
As research develops we may change our vocabulary about anxiety disorders
New data suggests that Panic Disorder is a genetically based alteration in the brain’s perception of threat
A standardized symptom profile for Generalized Anxiety Disorder has yet to be established
Criteria for PTSD have been expanded in DSM 5 to include seeing stressful events on television
Social phobia and PTSD may be more of a pre-existing personality disorder triggered by an environmental
stressor
Prevalence is 4% of population
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Panic Disorder
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Social Anxiety
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Generalized Anxiety Disorder
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Post-traumatic Stress Syndrome
Prevalence is 4% of population
Genetic predisposition - 11p
50% of patients have a chronic relapsing-remitting pattern
No known biomarkers
Still, easier to diagnose as symptoms are more specific
Highest response to medications
SSRIs and imipramine first line
MAOIs are second line agents
Response to cognitive behavior therapy almost as high as medication treatment
Best recovery rate of all anxieties
Individuals with social anxiety have over-active amygdalas that fire when the person is stressed
This can be in situations that ordinary people do not find stressful
Groups of people, public speaking etc.
5% prevalence rate
More females than males
Characterized by chronic persistent anxiety
30% concordance in identical twins
Genetic markers found in serotonin and norepinephrine systems
Most people exposed to severe stress never show symptoms of PTSD
Individuals with PTSD show evidence of hypofrontality on PET scans
They were functioning within their limits until a major stressor required more frontal coping ability than
they were capable of maintaining
Subjects were no longer able to use the frontal lobe to modulate their amygdala
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PTSD
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Genetic Variations
Genes Interact With Environment
Treatments For Anxiety
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History of Treatment for Anxiety
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Trans-cortical Magnetic Stimulation
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Benzodiazepines for Anxiety
PTSD is the anxiety disorder that is hardest to treat
Perhaps because the brain is responding to a real threat
Individuals with smaller hippocampi are at higher risk of developing PTSD if they experience a trauma
Anxiety Can Be Conquered
Treatment
Cognitive-behavior therapies work by improving frontal judgment to reassign new meaning to previously
feared stimuli i.e. increasing frontal inhibition of amygdala response
Drug therapies work by using chemicals to reverse or quiet overactive brain areas
New drugs may be developed that can be specific to the amygdala or hippocampus
TMS may also be used to increase frontal lobe function and inhibit anxiety
Prior to 1950, psychotherapy was the only option
In the 1950s benzodiazepines were discovered
In the late 1980s the SSRIs introduced
Buspar came shortly thereafter
In the 1990s, anticonvulsants and SNRIs were developed
Transcortical magnetic stimulation is in development
This treatment uses an electromagnet to stimulate the brain in specific areas
It is being used to treat depression, OCD and anxiety
Benzodiazepines (Valium, Ativan) were the first medications found to be effective in treating symptoms of
anxiety
They work by reducing activity in the sub-cortex and frontal lobes
This reduction in activity can also treat seizures
Disadvantages include memory and cognitive loss in the elderly
They work by reducing activity in the sub-cortex and frontal lobes
This reduction in activity can also treat seizures
Disadvantages include memory and cognitive loss in the elderly
Also muscle weakness and disinhibition in everyone
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Benzo-diazapines
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Tricyclic Antidepressants
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Anti-convulsants for Treatment of Anxiety
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SNRI
Librium (1960)
Valium (1963)
Ativan
Klonopin
Serax
Halcion
Xanax
A large class of chemical agents that effect the serotonin system
Proven effective in treating anxiety but ….
Many have significant side-effects and are no longer recommended
Valproic Acid
Gabapentin
Lamictal
Topiramate
Serotonin Norepinephrine Reuptake Inhibitor
Venlafaxin
(Effexor)
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RIMAs
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The Tricyclic Antidepressants
Common Side-effects of TCAs
Reversible inhibitors of monoamine A
Similar in action to MAOIs but reversible and do not require a special diet
Not available in the USA
Found in tobacco!
Dry-mouth
Constipation
Urinary retention
Confusion
Blurred vision
Orthostatic hypotension
Sedation
Cardiac arrhythmia's
Muscle weakness
Increased glaucoma
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Attitudes About Psychotherapy
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Anxiety Spectrum Disorder
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Hoarding
"We are in a society that is enamored of high tech. So people think that psychotherapy is just handholding
—that it cannot actually have a serious impact on a person or his brain. This is one of the reasons it is so
important to get scientific results that lend credibility to
psychotherapy as a real treatment"
Glen Gabbard, MD
Menninger Clinic
A proposed method of regarding the wide breadth of symptoms associated with the term anxiety
It recognizes that anxiety can be a normal response to expected life stressors
Anxiety would exist on a continuum rather then be present or absent
In the past, hoarding behavior has been classed as a variant of OCD
Recent research using fMRI has revealed that hoarders brains resemble bereavement and pathological
grief
In the past, hoarding behavior has been classed as a variant of OCD
Recent research using fMRI has revealed that hoarders brains resemble bereavement and pathological
grief
hoarders appear to be suffering from chronic loss
Hoarding is now in the DSM 5
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DSM 5
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A Look Into The Future
Beta Blockers
&
PTSD
Classification of anxiety disorders did not change dramatically in DSM 5
Generalized anxiety disorder has been renamed generalized anxiety and worry disorder
Time frames have been lessened from 6 months to 3 months for symptom duration
Criteria for PTSD has been softened and will increase diagnosis
DSM 5 allows me to witness to disaster or even reactions to learning about a disaster at a later date to
qualify for a diagnosis of PTSD
Taking propranolol directly after a frightening event prevented the development of fear but did not appear
create amnesia for the event
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Future Treatments for Anxiety?
Transcranial Magnetic Stimulation
Summary
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Summary
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Questions
Major References
Mental Illness is the most common cause of disability in the US
Mental illness is not mental
The brain comes in three parts
Each has its own type of memory & processing using different chemicals and pathways in the brain
Mental health requires smooth integration of all three areas
Damage to parts of the limbic system create misperceptions of reality
Emotional Illness appears to be caused by a dysfunction in the limbic system coupled with a dysfunction in
the frontal lobe areas for reasoning and judgment
These two defects create disturbed perception along with the inability to gain insight
Treatments can focus on altering the chemical messengers in the limbic system or increasing frontal
function through insight
Both types of treatments are equally valid
Both result in physical changes in the brain
1. The Neurobiology of Mental Illness
Dennis Charney, Eric Nestler
2. The Frontal Lobes & Neuropsychiatric Illness
Stephen Salloway, Paul Malloy, James Duffy
3. Neuropsychiatry & Behavioral Neuroscience
Jeffery Cummings, Michael Mega
4. Neuroscience (2nd Edition)
Mark Bear, Barry Connors, Michael Paradiso