MH ID: Misuse of Psychotropic Medications. Jarrett Barnhill MD UNC School of Medicine Jarrett November 19, 2013

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1 MH ID: Misuse of Psychotropic Medications Jarrett Barnhill MD UNC School of Medicine Jarrett November 19, 2013

2 Goals To explore the complex relationship between challenging behaviors and psychiatric disorders To look into the relationship between psychopharmacological and behavioral interventions behavioral pharmacology Use findings from both to address the problems of treatment resistance

3 What We Know? Basic elements of brain development Earlier onset has a greater impact of subsequent development Challenging behaviors are heterogeneous conditions Psychiatric disorders pose real challenges for children with ID

4 What We Don't Know Causes of mental disorders and IDD Exact mechanisms of drug action we know what we have studied and can measure Long term impact on brain development, especially in young children

5 What We Need to Remember The brain is adaptive organ, is constantly rewiring itself, functions in an integrated, hierarchical fashion No single transmitter or lesion Psychopharmacological agents are generally "dirty" agents whose effects are still under investigation

6 Developmental Issues Primer on brain development it matters what, where, and when something goes awry Problems with defining psychiatric disorders hitting a moving target Pharmacokinetic v. pharmacodynamics Placebos, families, and learning curves

7 IDD Brain Development Mild ID environmental stimulation, nutrition, gestational problems, exposure to toxins (FAS), genetic disorders Severe ID frequent brain developmental abnormalities, epilepsy, motor disorders are more common Degenerative disorders may cross boundaries

8 Behavior and Brain Abnormalities Disruption of emerging skills deficits Decreased top down regulation of affect or impulse control excesses Temperamental factors lesions less relevant today than coherence issues Behavioral phenotypes effects of specific genetic disorders on substrate

9 Brain and Psychiatric Disorders Dual heterogeneity of psychiatric disorders, epigenesis Multiple brain networks and systems are involved lesions rarely reproduce a primary psychiatric disorder Single neurotransmitter abnormalities are not causes of psychiatric disorders Brains disorders presentation, course, and prognosis

10 Another Look at Antecedents and Behavior Antecedents or trigger events, positive/negative experience, setting, memory, conditioning experiences, social factors Classical conditioning (initiating) CS/CR impact motivation (escape); intensity of reward potential (approach); Temperamental and presence of psychiatric disorders Fear conditioning LTP (panic disorder)

11 Other Factors Affecting Consequences Ease of conditioning, extinction, reversal learning Operant learning valence of reinforcer Extinction LTD (long term depression) Extinction spurt or increased appetitive behaviors Multiple layers of conditioning panic disorder with agoraphobia

12 Analysis of Function Function of behavior arousal, reactivity, motivational state, approach avoidance, autonomic regulation Drive or craving, reward potential, hedonic drive Neuroticism emotional reactivity Behavioral inhibition, conflict Escape behaviors sensitivity, threat perception

13 Analysis of Functional Behavioral Analysis Function: approach avoidance, intensity of drive, valence of reinforcement, arousal, positive negative affective state Antecedents: assessment of stimulus/setting, pos/neg affective valence Behaviors: careful subtyping Consequences: ease of reinforcement; resistance to extinction

14 Pharmacology of Learning Motivational states reward potential (BFS), inhibition (BIS) Linkage to VTA n accumbens: reward pathways Septo hippocampal system, memory circuitry, LTP/LTD MPF/orbital cortex top down regulation Attachment/social pathways

15 Theories Intrinsic reinforcement shift from positive to negative maintenance strategies; what happens to endorphins Factors that trigger SIB stress, urge to act, balance between aggression and SIB when restricted; craving and HPA axis Problem with extinction requires learning at a molecular biological level, LTD; Glutamate/NMDA activity; ACTH/AVP

16 Challenging Behavior Treatment Issues Limited success finding drugs for specific behaviors Most challenging behaviors are extremely heterogeneous conditions Functional Behavioral Analysis is a critical step but more information is needed Relationship between brain function, neurochemistry, and target behavior

17 Challenging Behaviors and Syndromes SIB Aggression ADHD Tic repetitive behavior spectrum Anxiety disorders Mood disorders Psychoses

18 SIB: A Diverse Collection of Behaviors Topography, typology, intensity, frequency, setting and trigger events Functional Behavioral Analysis is a critical tool but has limits Relationship to genetic disorders specific topographies Developmental models do not always address special vulnerabilities

19 SIB: Behavioral Pharmacological Dissection Why do some people develop progressive SIB when others in the same environment don t? Why does it persist in spite of pain, tissue destruction? What initiates and maintains this particular typography? What gets in the way of extinction self restraint?

20 Behavioral Pharmacology of Self Injurious Behaviors Complex relationship between SIB, behavioral phenotypes, and environment Gene expression is continually influenced by environmental events and learning Temperamental style influences helps shape life experiences and learning environment Think in terms of an ecosystem

21 Behavioral Pharmacology of Self Injurious Behaviors Complex relationship between SIB, behavioral phenotypes, and environment Gene expression is continually influenced by environmental events and learning Temperamental style influences helps shape life experiences and learning environment Think in terms of an ecosystem

22 Basics of psychopharmacology Drug mechanisms more complex than originally described Pharmacokinetics how do the drugs get there; genetic differences in rates Pharmacodynamics what the drugs do when they get there; genetics of receptor variability Pharmaco genomics

23 Anxiety Disorders

24 Anxiety: Fear Anxiety a ubiquitous human affective cognitive response to threat Fears change during development Life experiences plus temperament shape personality Neurobiology of threshold, reactivity, self regulation, sensitivity to distress

25 Anxiety Disorders Development, age of onset, severity Duration or frequency of symptoms Genetic risk OCD, panic disorder Trauma, abuse/neglect, attachment Regulation top down regulation of limbic system, cortical activation

26 Common Anxiety Disorders Separation anxiety exaggerated attachment distress, age limits? Social anxiety social cues Phobias panic attacks PTSD: fear conditioning, sensitization OCD, repetitive behaviors, tics PTSD

27 Treatment Issues Attachment behaviors Panic fear phobia Anticipatory, conditioned fear Hypervigilance GAD, social anxiety, BDD, AN Avoidance behaviors Mood disorders

28 Mood Disorders

29 Mood Disorders Biological risk factors family history, early losses Gender differences, effects of puberty Genetic risks BD>MDD Polarity, severity, comorbidity, longitudinal course Psychopharmacology

30 Major Depressive Disorder (MDD) High rates of comorbidity with anxiety disorders, CD/ADHD, trauma Neg affect plus anhedonia in MDD M=F prior to puberty, high rates ADHD 50 75% relapse within 5 years 20% develop BD

31 MDD ID Recognition irritability and endocrine, cortical asymmetry, epilepsy and RX Primary sleep v mood disorders Life experiences, temperament, self regulation, educational/social stresses Recurring disorder SAD, comorbid anxiety, externalizing symptoms Parent recognition

32 Treatment Approaches Medication trials, high placebo response, cognitive interpersonal Rx Environmental/ecological, iatrogenic issues SSRIs mainstay, drug interactions, disinhibition,? prolonged Rx course Recurrence, duration of RX, remission

33 Psychotic Disorders

34 What are Psychoses? Severe disturbances in brain function Disorders of thought, mood, behavior, motivational states Hallucinations, delusions, bizarreness, affective changes Genetic risk, timing of insults Continuity with adult disorders

35 Schizophrenias Childhood onset forms rare Common features with autistic spectrum disorders Ontogeny of symptoms emergence of secondary features Genetic risk Temporal profile clinical course

36 Treatment Issues Positive symptoms APDs work best Negative symptoms EPS related v. core features schiz, cognition, chronicity Comorbidity OC, anxiety, mood disorders, aggression, SIB Complications obesity, TD

37 What exactly is a nonresponder? Wrong person, wrong diagnosis or learning model, wrong drug or intervention Incomplete functional behavioral analysis Incomplete understanding of the bio behavioral issues Drug issues wrong dose; theory of drug effect and connection between it and behaviors is incomplete

38 Conclusions The assessment is the most important part of psychopharmacology Medication selection evidence, experience Limited knowledge of neuropharmacology There are no cures, improvement is far more common than remission there are no silver bullets More is not better All drugs are poison with positive side effects.

4/28/2014. Goals. A glimpse into the world of naming something. Concept of Diagnostic Nomenclature. Concept of Diagnostic Nomenclature

4/28/2014. Goals. A glimpse into the world of naming something. Concept of Diagnostic Nomenclature. Concept of Diagnostic Nomenclature A glimpse into the world of naming something Goals Explore the evolution of the classification of mental disorders and our journey to define mental disorders in individuals with IDD How do we deal with