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

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1 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 the current controversy over prepubertal Bipolar disorder? How will we come to understand Trauma and Stress Related Disorder? Are these changes useful for clinicians dealing working in Dual Diagnosis? JARRETT BARNHILL MD DEPT OF PSYCHIATRY UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE Concept of Diagnostic Nomenclature Basic idea-how to standardize nomenclature by descriptive, categorical methodologies, minimizing the use of etiology in diagnosis From the DSM 3 onward these categories have been refined to match clinical research and statistical analyses. If 5-axis diagnoses seemed helpful and a step forward, why ditch it? GAF to the WHO-DAS; Two topics to illustrate the complex changes in two Neurodevelopmental Disorders: Autism Spectrum Disorders and Disruptive Mood Dysregulation Disorders Concept of Diagnostic Nomenclature Basic idea-how to standardize nomenclature by descriptive, categorical methodologies, minimizing the use of etiology in diagnosis From the DSM 3 onward these categories have been refined to match clinical research and statistical analyses. If 5-axis diagnoses seemed helpful and a step forward, why ditch it? GAF to the WHO-DAS; Two topics to illustrate the complex changes in two Neurodevelopmental Disorders: Autism Spectrum Disorders and Disruptive Mood Dysregulation Disorders What about Pre-pubertal onset Bipolar Disorder? Mood disorders are classified as discrete syndromes Although predominantly disorders of mood regulation, significant cognitive and behavioral changes are prominent Subtypes and Specifiers-represent attempts to fine tune diagnosis and increase the homogeneity of individuals Course and treatment response vary based on subtype-generally. Onset during childhood creates ongoing interaction between mood disorder and ongoing development- high levels of comorbidity Is POBD continuous into adulthood- trajectory effects of IDD Subtyping BD: Age of Onset Substantial percentage of adults with BD disorders report an onset during childhood Loading for bipolar and other mood disorders; rates of schizophrenia may also be higher Earlier age of onset associated with more complex typology, developmental course (continuity into adulthood); higher rates of comorbidity, variation in clinical treatment response Debate: 2 subtypes of mood/neurodevelopmental impulse control disorders versus one umbrella dx category 1

2 Current Model High degree of overlap with ADHD and disruptive/impulse-control disorder. Lack of apparent cycling (episode v cycles); mood labilityv ultra-rapid cycling, irritability, explosive behaviors, rage and aggressive behaviors, higher rates of comorbid disruptive disorders Classic cyclical mood disorder, recurrent, typological differences, comorbid anxiety disorders v. state related CD-like behaviors Treatments are basically the same, and this far there is no cure Disruptive Mood Dysregulation Disorder Developed to account for a subgroup of children with affective dysregulation, chronic irritability, aggressive behaviors, impulsivity but no clear cut cycles Family history neg for BD. Complex overlap with ADHD combine type, CD/ODD, Tourette s disorder-mainly externalizing symptoms Lacking callous un-emotionality and psychopathy Treatment algorthms- Longitudinal course-greater risk for MDD/Persistent Depression What s different? Temperamental features of DMDD- neuroticism, impulse dysregulation, emotional dysregulation and ADHD/ODD State v. Trait related-externalizing/internalizing disorders, longitudinal trajectory and continuity with BD v mood disorder IDD-boundary with Intermittent Explosive Disorder, Disruptive/Impulse Control and Conduct Disorder, ASD Neurocognitive disorders are often overlooked in individuals with IDD Treatment Models Rx of BD/DMDD overlap- mainly because of a recent separation Research into aggression suggests an overlap with ADHD, CD/ODD/ASPD, although many individuals with Tourette s disorder and TBI may share treatment modalities Relationship with other disorders of emotional dysregulation/ neuroticism/ impulse control disorders First treat co-morbidities; SSRIs/Li/AEDS/SGA There is little likelihood of a magic bullet How Do we make a Diagnosis in IDD? Basic temperamental traits-neuroticism, intense negative reactions, chronic over-reactivity, relationship to ADHD with emotional dysregulation Neural substrates-top down/bottom up; excitation/inhibition, sensitivity to affective information, awareness of emotions Overlap Intermittent Explosive Disorder but mood/irritability are not intermittent; ODD- two subtypes: irritable high levels of neuroticism; callous unemotionality, overt defiance resemble CD, and greater risk ASPD; BD-episodic euphoria/irritability with phasic shifts in mood, activity level, self appraisal and circadian/vegetative states What is a traumatic experience? Neuro-ethology fear/threat/stress responses: arousal, freezing, defensive aggression Stress and neurobiological risk factors Adaptive skills and executive functions Developmental lines of stress responses Fear conditioning/ learned helplessness: memory, sensitization and extinction IDD-vulnerability and maintenance 2

3 Basics of Stress Response Event related variables- traumatic event Fear conditioning, generalization and extinction; anhedonia/dysphoria SNS, HPA, Limbic over activation, deficits in top down regulation (prefrontal, cortical, cingulate) Memory disorder-gaps for events (dissociation); autobiographical/explicit Reactive Attachment Disorder Moved to stress related disorders: risk and developmental antecedent; Ainsworth and pattern of attachments; S/PIDD RAD (Inhibited) and Disinhibited Social Engagement Disorder IDD impacts the evolution of attachment, may prolong the period of time dependent on caregivers-challenging behaviors and attachment Acute Stress Reaction 1 mo. duration gone (DSM-V); dissociation will be an optional criteria Boundary with Adjustment disorder, RAD, PTSD Intrusion, negative mood, avoidance and arousal and dissociative phenomena Risk factor for transition to PTSD Preventative interventions at this stage Adjustment disorder Clear connection between stress and symptoms; wanes after 3 months, genetic vulnerability to mental disorders. Chronic-related to some of the factors that lead to chronic PTSD. Vulnerability to triggering psychiatric disorders Boundary with PTSD-adaptive skills, executive function, support systems, What is PTSD? A chronic condition that arise from a kidnapped stress response system. Descriptive Dx-multi-factorial syndrome that is relatively resistant to most treatment programs- why is relapse so common? Risk factors-acute stress reaction, dissociation, autonomic dysregulation, neuroendocrine changes, age and repeated events. Complex PTSD-neuropsychiatric comorbidity Developmental course towards PTSD Phase I-acute stress (1 month)-dissociation, anxiety, obsessive preoccupation, stress induced analgesia (trauma addiction) Phase II-locus of control, autonomic over-arousal/exaggerated startle, avoidance, anger outbursts Transformation-isolation, chronic, learned helplessness, complications and comorbidity 3

4 Interesting things about PTSD Acute stress disorder, dissociation, and co-existing anxiety/depression increase risk. Females are far more likely to develop than males Age, repeated trauma, tendency towards avoidance patterns of behavior increase the risk, SUD, traumatic brain injury 10-20% develop PTSD; 18% recovery (5 yrs) Why only 10-20%? Acute stress disorder is a precursor to PTSD Relationship to temperament, neuroticism, early entrainment of stress response system, age of trauma, repeat events, risk for psychiatric disorders, IQ/adaptive skills Neuropsychological features of resilience, fear conditioning, neuroendocrine and genetic risk factors. Trauma addiction, repetition neurosis What leads to Chronic PTSD? Gender-F>M, past history of trauma, co-existing mental disorder, SUD Neurophysiology-SNS/PNS, CRH, genetic factors (5HTTPr; MAO-a; COMT); GABA/NPY High level of avoidance behaviors-proneness of high neuroticism; top-down regulation Fear conditioning: CS-US>> escape, freezing, defensive aggression, learned helplessness IDD Extremely high rates of traumatization, Should be high rates of PTSD; SPID attachment needs, markedly reduced adaptive and communication skills-behavior may be the most noticeable feature Baseline exaggeration, diagnostic overshadowing Boundary issues Fear and fear conditioning Key feature of PTSD-a form of associative conditioning (US-CS linkage). Repeated activation-intensity, sensitization, LTP Amygdala and Hippocampus play a role-central nucleus of the amygdala is the key. Frontal-temporal and occipito-parietal cortices are key players in extinction; topdown regulation. Fear and fear conditioning Key feature of PTSD-a form of associative conditioning (US-CS linkage). Repeated activation-intensity, sensitization, LTP Amygdala and Hippocampus play a role-central nucleus of the amygdala is the key. Frontal-temporal and occipito-parietal cortices are key players in extinction; topdown regulation. 4

5 Sensitization: learning run amok Repeated events change neurophysiology Opposite of tolerance or habituation; rewiring increase probability that CS will expand to include other stimuli (generalization); context and arousal as trigger. Increased CRH triggers panic/fear conditioned responses Kindling-eventually original conditioned stimulus may no longer be needed. Sensitization: learning run amok Repeated events change neurophysiology Opposite of tolerance or habituation; rewiring increase probability that CS will expand to include other stimuli (generalization); context and arousal as trigger. Increased CRH triggers panic/fear conditioned responses Kindling-eventually original conditioned stimulus may no longer be needed. IDD Extremely high rates of traumatization, Should be high rates of PTSD; SPID attachment needs, markedly reduced adaptive and communication skills-behavior may be the most noticeable feature Baseline exaggeration, diagnostic overshadowing Boundary issues Conclusions The RDC and endophenotype/subtype analysis based on neurobiological markers, we cannot forget that psychiatric disorders are expressions of a multi-directional interaction between neuro-ethological and ecological that present as social behavior We need to remain cautious of determinism, reification and our capacity for myth making No nomenclature can capture the complexity of human behavior We picked the wrong organ to study and try to understand 5

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

MH ID: Misuse of Psychotropic Medications Jarrett Barnhill MD UNC School of Medicine Jarrett Barnhill@med.unc.edu November 19, 2013 Goals To explore the complex relationship between challenging behaviors