Agenda
•
•
•
•
•
•
•
Introductions
Some assumptions
Basic neurobiology (that’s all I know anyways)
The effects of stress
Memory
Treatment implications
Teens and drugs
Premises and Assumptions
•
•
•
•
Unconscious
Evolutionary perspective
Influence of culture on genetic expression
Nature-nurture
Our Amazing Brain
• The brain - 100 billion neurons in a
complex net of continuous activity allows us our humanity. Each neuron
cell can have 5,000 to 10,000 synaptic
connections
• For each of us, our brain’s functioning is
a reflection of our experiences.
The Brain Does Not Come
“Ready Made With Batteries”
We are likely the species most
dependent for the longest
period of time following birth.
Our brains are exquisitely
designed to survive and adapt to
our changing environments.
Neocortex
Limbic
Abstract thought
Concrete Thought
Affiliation
"Attachment"
Sexual Behavior
Emotional Reactivity
Motor Regulation
"Arousal"
Appetite/Satiety
Diencephalon
Sleep
Blood Pressure
Heart Rate
Body Temperature
Brainstem
Dr. Bruce Perry
Input
Output
• Number of synapses for a "typical" neuron =
1,000 to 10,000
• 10 neurons can have 3,620,800 possible
permutations…
• so imagine that we have a central nervous
system that can have up to 100 billion
neurons
Brain structure and functioning
changes in response
to experience…
this is basic neuro-plasticity.
(experience-dependent change)
The Context within which
the Brain Development
Primary Caregiver
Family
Immediate Community
Extended Community
Cultural Changes
=
=
The “cook book” … but what does the
environment call for?
The Force
• This has changed, an continues to
change…
• Our brains have not changed that much
or at least not at the same rate
Stress - Performance Connection
We now have the ability to “create
stress” in our “minds”… but the body’s
endocrinology response does not
differentiate between “imagined” threat
and “real” threat
Parts of the brain responsible for the
detection of threat function outside of
“LOGIC”
The Stress Response System
• The autonomic nervous system (ANS)
Engine
Sympathetic system
(cortisol, epinephrine, norepinephrine)
Parasympathetic system
(oxytocin)
Brakes
Basic Physiology of Stress:
The Autonomic Nervous System
•
•
•
•
•
Sympathetic
Parasympathetic
The engine
Adrenaline, cortisol
heart rate
blood pressure
Pupils dilate
• The brakes
• Oxytocin, Vasopressin,
Prolactin
• Vagal tone (“nerve”)
The HPA axis
Hypothalamus - Pituitary - Adrenal cortex
• In humans, over exposure to cortisol,
and cell death, has been associated
with depression and trauma.
What the Research Shows
About the Effects of Stress
• Stress can have a negative and
permanent impact on neurological
development (PTSD type II).
• Prolonged exposure or activation of the
HPA axis (the engine) can lead to cell
death and atrophy of dendrites
(particularly in the hippocampus).
Types of stress
Short & Challenging
Short & Overwhelming
(ideal)
(traumatic)
Long & Challenging
Long & Overwhelming
(depleting-traumatic)
(very traumatic)
3 Year Old Children
Normal
CIVITAS ChildTrauma Programs
Extreme Neglect
© 1997, Bruce D. Perry, M.D., Ph.D
Dr. Bruce Perry
Stress Can Change the Way
We Think
Calm
Aroused
Overwhelmed
Abstract
Creative
Focused
Concrete
Emotional
Reactive
NeocortexSubcortex
Subcortex Limbic
Limbic –
Brainstem
Developmental
“Thinking Styles”
Children Regress Under Stress
Infant
Toddler
Preschool
School Aged
Adolescent
Sensorymotor
Egocentric
Magical
“Magical”
Concrete
Abstract
Magical
Egocentric
Implications
• Early intervention
• Talk therapy
• Policy
It works!
We need to reconsider
what “drives” our
therapeutic approach
Where are we spending
our money?!
Early Interventions
Program Type
• Regular Nurse visits pre
and post natal (help
mother and child)
• Programs that target lowbirth weight & premature
infants
• Early education (6wks to
5yr olds) with parental
involvement
Shore, 1997
Benefits
Employment
Save $
Abuse
IQ
Academic functionin
Spending on Programs to “Change the Brain”
Brain’s Capacity for Change
0
3
Headstart
6
Mental Health
Public Education
Age
Juvenile Justice
Substance Abuse Tx
20
Hippocampus
Responsible for the development of new
memories (an long term memories)
Amygdala
• Attaches emotional valence to stimuli
(good-bad)
• Not sophisticated in its ability to
discriminate
• Active in high road and low road to
fear
• The amygdala is involved in the experience
of emotion (especially negative emotions),
and also appears to be involved in storing
and perhaps recalling the emotional
components of memories.
Pre-Frontal Cortex (PFC)
Memory
Declarative
Facts
Events
Nondeclarative
(implicit)
Skills Priming
C-Condit.
What Do We Address in Therapy…
Declarative Learning
• Engages hippocampus
• Demands morphological changes in
associated neurons
• These changes take place rapidly,
which demands protein synthesis
Memory
• Transition from short to long-term memory
(which can reflect hrs) is referred to as
consolidation
• Re-consolidation occurs when “old”
memories are “re-activated”… memories go
through another round of consolidation
dependent on certain protein synthesis
• Therapy might actually inhibit consolidation
and/or reconsolidation of memory
Neurobiology of Memory
• Experience alters the structure and
functioning of neurons
• This create memory traces
• Some pathology may reflect an
automated response to some type of
stimuli that evokes the memory trace
• Activation of an old memory returns it
to a labile state
• Memory storage is a repetitive
phenomena that re-occurs with every
use of the memory
• Reconsolidation favours memory
maintenance
Long Term Potentiation (LTP)
• LTP is associated with an increase in
synaptic connections and dendritic spines
• And synapses become more efficient at firing
each other
• LTP is triggered by brief periods of repetitive
excitation…(high frequency stimulation)
• 100-hz (100 beats per sec.)
Long Term Depression (LTD)
• LTD is promoted by low frequency
stimulation … 1-hz (one beat per
second… like your heart rate)
Long Term Potentiation
Stimulation
Response
Long Term Depression
Stimulation
Response
• Extinction is about laying down new
neural nets in response to a CS… the
CS comes to trigger a secondary
response
(the old response is not eliminated)
• Repeated exposure to CS without
significant event
• This new association is more labile
than the excitatory one
Perhaps therapy is about the re-structuring
maladaptive declarative and implicit
memories
• Focused consciousness can re-activate
previously “stored memory traces” …
thinking about something strengthens
learning (synapses changes in response)
Build Safety Nets for Stress
• You are the safety net
• What do you need to do for yourself to
be the “safety net” for your child
Post Traumatic Stress Disorder
Type I & II
(Intrusive Arousal Avoidance)
Depression
and Stress
Neurobiological Considerations
• High levels of cortisol receptors in the
Prefrontal Cortex, Hippocampus,
cingulate cortex
• ”Supersensitive" postsynaptic cortical
alpha2-adrenoceptors
• Memory bias toward negativity
Major Sites Affected by Stress
• Functioning of the HPA axis and SAM
• Hippocampal volume (not in children) and
functioning
• PFC functioning
• "Repeated exposure to traumatic
reminders without any adverse
consequences causes fear responses to
gradually disappear,"
• "Such reduction of fear appears to be an
active rather than passive process. It
doesn't erase the fear association from
memory, but generates a new memory for
safety."
• So treatment is about generating
experiences that allow for a person to
safely process traumatic experiences
We undo this…
And promote this….
The prefrontal cortex projects to the amygdala
and down regulates its response
Treatment Options
• Medication … can alleviate symptoms but
obviously does not specifically affect
environmental concerns
• Recent concerns regard risk of suicide…
which led to disclosure of limited efficacy
• Up to 75-76% of response to typical SSRIs is
duplicated in placebos
• 18% of response accounted for by
pharmacology
Of the Total Response Rate
(pass the clinical cut off)
SSRI 18%
Placebo 75%
Unaccounted 7%
These findings are from published results (Kirsch & Antonuccio FDA testimony,
2004)
Response rate SSRI 60%
Unaccounted for 40%
Response rate Placebo 40%
Unaccounted for 60%
Cheung, et al., CMAJ, 2006 (review, based on a 12 wk course)
Psychotherapy
• Psychological interventions are effective at
reducing the severity and number of
symptoms experienced (Cuijper & Dekker, 2005)
• Research is more supportive of problem
focused therapies, than the use of
medication for the treatment of paediatric
depression (Compton, et al.; Journal of the American
Academy of Child and Adolescent Psychiatry, 2004)
• It is the power of interpersonal
relationships that brings about change
• (Mayberg, 2003) study found that
psychotherapy was more effective than
medication for patients who experienced
early childhood trauma
Talk Therapy Changes the
Brain
• Compared treatment of depression with
Effexor or Paxil, and Interpersonal
therapy after 6 weeks.
Brody, et. al, 2001
Martin, et. al, 2001
• Brain structure changes in response to
experience…this is basic neuroplasticity (experience-dependent
change).
Factors that Influence Outcome
30% Therapeutic Relationship
40%
30%
15% Expectancy of Change
15% Technique
40% Extraneous Factors
15%
15%
Lambert & Barley, 2001
What Is Involved in The
Therapeutic Alliance...
• An alliance involves three factors:
The important
1- a positive bond
stuff
2- consensus on the goals of
counseling
3- agreement about the plan to
achieve the goals
• 2 & 3 are guided by your theoretical
orientation and service mandate!
Attachment Based
Perspective
• Therapy functions as a secondary
attachment
• Provide a sense of relief from an
unmanageable state of arousal
• Such therapeutic relationships provide
corrective emotional experiences
Circle of Security
Parent Attending to the Child’s Needs
Or
Therapist Attending to Client’s Needs
I need
you to
I need
you to
 Watch over me
 Help me
 Enjoy with me
Support My
Exploration
I need
you to
I need
you to
 Protect me
 Comfort me
 Delight in me
 Organize my feelings
Welcome My
Coming To You
© 2000 - Cooper, Hoffman, Marvin & Powell
• Like a secure attachment, strong alliances
may also reflect a biological synchronicity
between client and therapist
• Close relationships provide physiological
regulation of the other’s rhythms
e.g. shared variation in heart rates between
married couples, and children and primary
care-givers
Interpersonal Relationships
Soothe (oxytocin)
• Oxytocin … hormone and neurotransmitter
(neuro-peptide)
• Associated with affiliative behaviour
• Down-regulates the stress system
(HPA & SAM)
Oxytocin
• Child birth, nursing
• Lowers blood pressure, heart rate, levels of
cortisol, increased effectiveness of digestion
• effects are long lasting
• self promoting…the release of oxytocin promotes
further production
• promotes social interaction and bonding
Therapists’ use Self in a
Soothing and Aggrandizing
Relationship
• Kohut’s self psychology and selfobjects
• We engage in interpersonal relationship
that provide for twinship, idealizing, and
mirroring needs of the client.
• We provide psychological structure to
clients through empathic attunement
• Affective attunement can lead to the
mutual release of oxytocin (Harvard studyunpublished).
• Animal studies demonstrate the long
term “calming” effects of
oxytocin…leads to enhanced sedation,
relaxation, reduced fearfulness and
decreased sympathetic activity!
Flow of the Alliance
Attunement
Breaks
Fostering the Bond
• Facilitated through non-verbal
communication… which is primarily
attended to by the right orbital frontal
lobe
• This occurs at an unconscious level
• Right orbital frontal lobe attends to the
emotional valence of communication
The Population
Consider the continuum...
The Presenting Concern
Distress
Pathology
The Function of the Relationship
Supportive
Intervention
2.Therapist’s right orbitofrontal lobe
attends to client’s presentation of
distress
3.Therapist seeks affective attunement
between frontal lobes through on-going
synchronous attending
1.Client Experiences Dysregulation
of HPA axis and Limbic system
4. Such physiological attunement
Soothes
6.Therapist attends to and amplifies
alternative states through
“aggrandizing comments”
5.Client’s HPA axis and
Limbic system is
downregulated
Developmental
Emotional Anchors
Health
Pathology
Birth
BACK TO LTP
Three Stages of LTP
• LTP 1 = lasts about 6hrs
• LTP 2 = lasts about 10hrs
• LTP 3 = lasts weeks
• We want to take advantage of the 40%
“extraneous factors” to further promote LTP
(and LTD)
40%
30%
15%
15%
Meeting once a week or once every two weeks may be more
of a gamble
Treatment Considerations
• 3 meetings week One
• 2 meetings Week Two
• 1 Meeting Week Three
• 1Meeting Week Four
• 1 Booster Session
• Frequently activated neurons increase their
supply and release of neurotransmitter
• LTP associated with increase in glutamate
secretion with each subsequent firing (an
excitatory neurotransmitter)
• The act of recalling an emotionally charged
experience returns the memory to a labile
state… from which it can be “tampered with”
• Genetic expression is required for
reconsolidation
• So a soothing and calm response to elicited
traumatic memories influences reconsolidation
The Process of Treatment
Treatment Process
Arousal
Time
Memory Lability
Treatment Process
Arousal
Time
Those moments in therapy ( ) are
opportunities for corrective emotional
experiences!
We Access; Attenuate; Alter…
Then reconsolidate
Oxytocin Again
• Oxytocin impairs learning, consolidation,
and re-consolidation
• Again… our alliance attenuates
sympathetic responses and may impinge
re-consolidation when upsetting memories
are recalled
Psychological Wellbeing Scale
100
80
60
40
20
0
Sess. 1
2
3
4
5
6
In Session Considerations
• Discuss past challenging life events related
to presenting problem
• Bring them forth in as much detail as is
SAFE (they need to feel)
• Use self as reliable, unconditional soothing
object
• Send your voice with them
Homework
• Thinking Tasks
• Exercise
• Exercise and Affirmations
• Exercise and Anticipation of Success
• Utilizing lived experiences to challenge past
assumptions (undoing distortions)
Simple Homework Tasks
• Brain Derived Neurotrophic Factor
(BDNF) can be up-regulated in the
hippocampus through exercise, which
promotes neuronal growth
• So … have clients “exercise and think”
• Focused consciousness can re-activate
previously “stored memory traces” …
thinking about something strengthens
learning (synapses changes in response)
What is Adolescence?
• Transition between childhood and
adulthood
• Common across many mammalian species
• Biology supports this transition
Adolescent Development
Early
Mid
 Body changes
 Behaviour less  Long term
influenced by
consolidation
peer group
 Less reliant on  More realistic
peer group to
perspectives
regulate self
of self and
esteem
other
 Cognitive skills
increase
 Maintain
coherent self
image
 Increase in
impulses
Late
So What Happens to
Teenagers...
• Bodily changes… (need to fit in!)
• Fluctuations in self-image and self-esteem
• Develop an appreciation of others’ thoughts
(slowly!)
• Frontal lobes (emotional centres mature earlier)
Risk Taking...Novelty Seeking
• Moves them out of the home! (serves evolution!)
• Adolescent brain influenced by drive for rewards
(but takes more to get them excited)
• Immediate gratification (those frontal lobes!)
• They can effectively appraise risk…but
Changes in the Limbic system related to
increase in rewards as motivators
Also need more bucks for the same bang!
Increase in hormone levels
(impulses)
Self regulation is related to gradual changes in
the prefrontal lobes:
•increase in myelination
•second wave of pruning (sculpting the
network)
This part of the brain’s functioning is related
to impulse control, planning, prioritizing,
abstract thinking
Competing Emotional States
•Appetitive (seeking obtaining rewards)
•Aversive (threat avoidance)
Short term
Long term
Immediate gains
Desires
Immediate
gratification
Fears
Factors that Influence Decisions
to Engage in “Risky Behaviour”
• Fear of rejection
• Anxiety of being caught
• Excitement in the moment
• Desire to satisfy urge
Developmental Vulnerabilities
•
•
•
•
•
Risk taking!
Need for peer support
early onset of puberty
increase in impulses and impulsiveness
poor cortical influence on decision
making in the moment
Distorted Developmental
Considerations
BIO
BIO
Dual Diagnosis
• SA & MH are different symptomatic
expressions of the same underlying
neurobiological vulnerabilities
• SA leads to MH
• SA reflects efforts to self medicate,
regardless of which came first
• The comorbidity observed between SA
and MH is chance
Dopamine Networks
• Most psychoactive drugs activate
mesolimbic dopamine networks, either
directly or indirectly
• Plays a primary role in responsereinforcement…this good do it again!
• Adolescence brings with it a spike in
dopamine receptors followed by a period
of pruning (remember…more bang to enjoy
things)
Milder Forms of Hedonism that
May Appeal to those Dx with an
MH Concern
•
•
•
•
Relief of tension
reduction of fatigue
increased arousal (fun factor)
Belonging
Relapse and Mental Health
Concerns
• Symptoms evoke relapse
• Relapse exacerbates symptoms
Remember, we seek pleasure and avoid
displeasure.
Intervention Considerations
• Research suggests that adolescents are
not very different from adults with
regards to risk perception and appraisal!
• Pharmacological treatment of the MH
concerns can reduce rate of relapse.
• Abstinence can worsen mental health
symptoms.
• Avoid the cues of use
• Distraction
• Engagement
• Should treatment demand sobriety?
Rationale
• Avoid “pin-ball effect”
• Need to be engaged, sitting in an office
offers little hedonistic pleasure
• What are we waiting for?
• Might such interventions “raise” their
bottoms!? :-)
• Need to provide a continuum of care!
• There is an ethical responsibility to
offer something based on our
knowledge base
• Should treatment demand sobriety?
(culture of MH vs. Drug Treatment?)
The richness of human experience is
not found in the application of
temporally defined “effective
treatments” of mental health
concerns, but rather attending to the
complexity of the human experience
reflected in our very biology