Transcript Josh-Sizemores

Neuro Alignment: A
Monoamine Treatment
Approach
JOSH SIZEMORE, RN, MN, PMHNP
ORCA FALL CONFERENCE
11/05/2016
Disclaimers
• I love coffee, if a drug rep brings me one, I drink it.
Presentation Goal
TO CONSIDER DIFFERENT WAYS OF LOOKING AT
SYMPTOMS, DIAGNOSIS AND TREATMENT TO
ASSIST IN CONCEPTUALIZING THE MOST
COMPLICATED OF PATIENTS. INSTEAD OF
FOCUSING SOLELY ON CHIEF COMPLAINTS,
SYMPTOMS AND DIAGNOSIS IT TEACHES A WAY
OF ROOTING OUT THE UNDERLYING CAUSES OF
THE SYMPTOMS WHICH ALLOWS FOR RICHER
TREATMENT OPTIONS AND IMPROVED
OUTCOMES.
Does psychiatry need a different way of looking at
things?
Does psychiatry need a different way of looking at
things?
How do we do it now?
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Major Depressive Disorder
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Bipolar Disorder
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Attention Deficit Hyperactivity Disorder
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Obsessive Compulsive Disorder
Uh Oh?
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Major Depressive Disorder with Moderate to
Severe Anxious Distress
What about this?
What about this?
Major Depressive Disorder
What about this?
Major Depressive Disorder
Adjustment Disorder
What about this?
Borderline Personality Disorder
Major Depressive Disorder
Adjustment Disorder
What about this?
Borderline Personality Disorder
Major Depressive Disorder
PTSD
Adjustment Disorder
What about this?
Borderline Personality Disorder
Major Depressive Disorder
Disruptive Mood Dysregulation Disorder
PTSD
Adjustment Disorder
The 5 Core Areas of Focus
1) Nature - Biological predisposition – The way each
individuals brain was naturally made
2) Nurture – Non genetic influences
3) Limbic System activation/response
4) Sensory integration
5) Medical/Somatic signs and contributors
1) Nature - Biological Predisposition
Problems vs Disorders
 Everyone has problems: Which accounts for most of what
we encounter when working with children and adults.
 Psychiatric disorders are rare – most “true” psychiatric
disorders have an underlying organic cause or
component which when understood can lead to the best
treatment options and outcomes.
Monoamine Neurotransmitters
5HT
Serotonin
NE
Norepinephrine
Da+
Dopamine
Theoretical Monoamine Model
Bipolar I
Schizophrenia
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Bipolar II
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Psychotic Process/
Bipolar Episode
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Bipolar Brain
Bipolar
5HT
NE
Mood/Anxiety
ADHD
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Severe Mood
& Anxiety, OCD
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DA+
ADHD
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Severe Mood/Anxiety
Fibromyalgia/Aspergers
Autism/DD/TBI
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Medication Side Effects
 Medication side effects correlate (for the most part)
with underlying brain pathways (except for odd
metabolizers and certain gene mutations – it is still
true in these cases, just unpredictable unless you
have obtained and understand genetic testing).
Medication Side Effects Discussion
Bipolar I
Schizophrenia
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Bipolar II
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Psychotic Process/
Bipolar Episode
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Bipolar Brain
Bipolar
5HT
NE
Mood/Anxiety
ADHD
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Severe Mood
& Anxiety, OCD
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DA+
ADHD
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Severe Mood/Anxiety
Fibromyalgia/Aspergers
Autism/DD/TBI
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2) Nurture – Non Genetic Variables
Other variables that were not related to the way we were
biologically made.
* Trauma
* Attachment
* Sleep/Insomnia/Sleep Deprivation
* Nutrition,
* Medical problems (some crossover with 5th core
area, hypothyroidism, Vit D deficiency…)
* Social Relationships
* Coping skills
* Drugs
* others?
3) Limbic System Response (& Limbic Irritability)
Focus,
Cope, Adapt
& Learn
React
Anxiety
PTSD,
Fight or Flight
3) Limbic System Response (& Limbic Irritability)
Focus,
Cope, Adapt
& Learn
React
Anxiety
PTSD,
Fight or Flight
3) Limbic System Response (& Limbic Irritability)
Focus,
Cope, Adapt
& Learn
React
Reactive anger, reactive emotions, reactive bonds, reactive
hopelessness, reactive si/sib/hi, etc.
Anxiety
PTSD,
Fight or Flight
4) Sensory Integration
Two main processes (therefore 2 ways of evaluating & treating).
1: The amount that gets through (dependent on
level of dysfunction).
2: Our ability to process what gets through
(dependent on ability to focus, concentrate and organize).
5) Medical/Somatic Contributors
 Many medical problems are psychosomatic in nature
or found to be comorbid with psychiatric
contributors with the underlying causes being the
same for both (example MTHFR gene defect, chronic
pain, migraines, seizures, histaminosis…)
Case Study 1
17 year old male, past diagnosis: MDD w psychotic features, GAD, high functioning
Aspergers and ADHD. Hx of suicide attempts and sib, multiple past hosp. CC is
anxiety, depression and poor focus. MH tx for 2 years.
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Nature - Genetic diathesis: Paternal: Anxiety, Depression, Social Skill Deficits
(suggestive of Aspergers). Maternal: Anxiety, Depression and ADHD. Presents
with vibrating keen anxiety, non stop motion, bouncing leg, distractible, verbally
impulsive but pleasant and likable. Highly intelligent in electronics...
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Nurture – Negative trauma hx, social skill deficits, mild hx of being bullied,
trouble falling asleep, anxiety leads to poor school attendance. Past medication
trials: 4 SSRIs, partial response, excess physical and mental sedation at moderate
doses. Stimulant led to increase in anxiety, anger and irritability but helped focus.
Clonazepam helpful, not fully effective – only current med, can’t be without.
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Limbic Response; reactive, poor ability to adapt, focus, cope and learn.
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Sensory Integration: Mild sensitivity to noise, touch, texture & light which greatly
improved since childhood, used to be moderate to severe. In quiet/neutral
environment able to focus but only on things he enjoys.
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Medical/somatic – diagnosis of fibromyalgia, chronic back, knee, joint pain,
multiple MRIs with no findings, 1 unremarkable exploratory joint procedure,
allergy to food dyes resulting in extreme behavioral reactions.
Case Study 1 Results
 Treatment plan made to trial Cymbalta and/or amantadine with prior
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provider before I met client, however, medications not started until
under my care – not instinct.
Began Cymbalta and increased to 30 mg twice daily, within 2 months
mood and anxiety stabilized, continued to struggle with ADHD
symptoms, mild reactivity, pain, anxiety and mood symptoms.
Began Amantadine and increased to 100 mg twice daily and started
decrease in clonazepam, within 2 months (by month 4) all symptoms
stabilized and rarely taking clonazepam.
By month 6 off clonazepam. Remained psychiatrically stable on
medications, without changes, for the past 1.5 years, no lasting pain
issues.
Full time college student, double majoring, working and involved with
student clubs – purposeful sleep issues continue.
Case Study 2
56 year old female, past diagnosis of: PTSD, Major Depressive Disorder and Bipolar Disorder.
Hx of suicide attempt in early 20s during major depressive episode. CC is depression, med side
effects and sleep. Most recent diagnosis: PTSD and Bipolar I Disorder (which was diagnosed
when hallucinating and in a delusional state after being placed on a steroid).
1)
Nature – Genetic diathesis – Maternal – all women struggle with depression and anxiety.
Paternal – alcohol and substance abuse. Presents moderately depressed with mild anxiety
and physically restless, needs to stand due to restlessness not anxiety.
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Nurture – Hx of domestic violence, no ongoing trauma, extensive past PTSD treatment
which she feels was as effective as it could be and denies any lasting concerns. Past
medication trials: Was fully stable on Prozac for over 20 years but stopped working, on
Zoloft for 2-3 years, helpful, not fully effective but stopped working. Changed over to
Cymbalta which helpful but caused anxiety, then placed on effexor which has also caused
anxiety and restlessness. Placed on Abilify when hospitalized and given bipolar diagnosis 5
years ago. Currently on Abilify and Effexor which is not working, causing weight gain,
anxiety, irritability and restlessness. but has not been able to get off due to withdrawal side
effects. Struggle falling asleep, tired but can’t shut down thoughts.
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Limbic Response; Mild reactivity, surprisingly low given PTSD history.
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Sensory Integration: Unremarkable.
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Medical/somatic – Obesity, diabetes, chronic ankle, shoulder and back pain from past car
accident, diabetic neuropathy, constipation.
Case Study 2 Discussion
autoreceptor
Case Study 2 Results
 Treatment plan made to trial Viibryd and get off Abilify and Effexor
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(with assistance of Pristiq).
Over a 2 month period used Pristiq to get off of Effexor which
decreased side effects and minimally helped mood, then titrated over to
Viibryd.
Within 2 months (by month 4) depressive symptoms completely
stabilized with only side effects being looser stools which was tolerated
and even helpful due to hx of constipation.
At 5 months decreased and discontinued Abilify with only side effect
mildly worse sleep initiation which stabilized with use of Prazosin.
Has been stable the past 2 years on Viibryd and Prazosin without any
lasting side effects and has lost 30 lbs which helped to stabilize her
diabetes. Pain improved through pain management and is more
tolerable due to improved mood, coping and decreased med side
effects.
Look outside the box
 The brain is stupid, the mind is intelligent (example
sleep deprivation).
 Try to look at symptoms from a more evolutionary
standpoint (examples ADHD, melatonin).
 If you are following treatment recommendations for
a given disorder and it is NOT working – DON’T
keep doing it – reassess if you have the right
diagnosis. (Examples; OCD vs ADHD, ADHD, True
ADHD and an ADHD Brain)
Perspective
Questions?
[email protected]