Download DM-ID-2: Growing Pains in Our Understanding of Psychiatric

DM-ID-2: Growing Pains in Our
Understanding of Psychiatric Disorders
among Persons with ID.
JARRET T BARNHILL MD DLFAPA, FAACAP, NADD -CC
UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE
What Exactly are Psychiatric Diagnoses?
Evolution of descriptive psychiatry- the idea of a categorical mode of syndrome
diagnosis
Discrete syndromes versus the dimensional nature of most disorders
Minimization of etiology as a contributing factor- movement away from a
psychodynamic approach to understanding mental disorders
Biology of mental disorders- evolution of genetics, molecular psychiatry,
neuroimaging technologies, “personalized medicine”
Each step towards trying to more tightly define mental disorders led to more
complex ideas about their nature
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: Trauma and Stressor related disorders and Disruptive Mood
Dysregulation Disorders
What Exactly Are Psychiatric Disorders- The Skeptics
View?
Collections of symptoms that hang together but are they syndromes?
Validity of discrete categories, distinct lesion-focused models; reality is a
continuum-severity/functional impairment?
Are all psychiatric disorders neurodevelopmental; gene-environmental
interactions, who ordered that?
Are genetics a boon or a curse- what do they tell us?
Is neuro-imaging the next phrenology?
Is the age of the discrete neurotransmitter a delusion; are we focusing on the
wrong things?
Has the Biopsychosocial Model Become a Cliché?
The original idea: move away from reductionist, simple cause-effect, brainbehavior relationships
Can the model avoid “reification of meaninglessness” and be adapted to our
neuroscience revolution?
Genetic, environmental psychological determinism, linear causality versus
transactional, epigenetic, and probability (Quantum revolution)
William James and the researchers fallacy- DA model of schizophrenia,
ecological/ethological alternatives
Can Categorical/Descriptive Approaches to Diagnosis
Ever Deal with Heterogeneity?
Disorder as final common pathways- rethinking to sources of psychopathology
Family traits- variation within families- biopsychosociology
Temperamental antecedents- risk factors, prodromal, states or traits
Genetic Risk factors- where do disconnection and imbalance between
excitatory/regulatory systems fit into our models for the inheritance of ID,
problem behaviors and mental illness- e. g. where to put behavioral phenotypes
What is the nature of environmental risk factors- transactional models, GXE
Biomarkers- where do they interact with ecological factors, neuro-ethological
models
DSM 5: Clinician’s Point of View
Uses a descriptive, categorical approach to establish phenomenological
subtypes- many have limited adaptability for the severe end of ID
Elimination of 5 axis model in the DSM-5 to align with ICD-11
Super category- Neurodevelopmental Disorders encompasses ASD, ID and other
disorders attributed to a childhood onset; many psychiatric disorders are
neurodevelopmental.
Broad categories, specifiers, lumping and clinical v research usefulness,
dimensionality and overlapping symptoms
Broadness of categories not adapted for patients with dual diagnoses
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
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
Diagnostic Approaches- Necessary Adjustments
Presentation- quality of diagnosis affected by level of ID, co-occurring genetic,
neurodevelopmental and neurological/medical disorders; ASD
Qualitative differences between borderline to mild/moderate and severe-profound ID;
boundary issues, dueling heterogeneities
Referrals- mostly due to behavioral issues not primary psychiatric complaints;
Assessment requires multiple sources; modifications dues to language and
communication deficits, capacity for self-reflection/reporting; modifications- MSE
Adaptations- diagnostic criteria, instruments not designed to define specific
endophenotypes
Consensus diagnosis; combining behavioral data with psychiatric assessment
Approach to Behavior Problems in Individuals with
Severe/Profound ID
S/P ID require qualitative changes; ASD adds to this need
Three axis model for the DC-ID:
Axis- level of ID; Axis II- causes of IDD; reversal of Axis III sequence, begin with
neurobiological-temperamental variability, problem behaviors; symptoms of
psychiatric disorders, associated DD
Attachment behaviors need to be included
Temperament- genetic, neurophysiological correlates; transactional model;
neuroticism, behavioral inhibition, novelty seeking, introversion/extroversion,
cognitive/emotional instability; internalizing/externalizing
Dx- relates to imbalances between multiple and often overlapping domains
Data CollectionIdeally from across multiple settings and ecological contexts
Longitudinal or developmental trajectory of symptoms- time line of
behavior/symptom development plotted against life events
Aberrant Behavior Checklist provides a methods of clustering target behaviors:
Irritability, lethargy, stereotypy, HA/noncompliance, inappropriate speech
(Inventory)- symptoms not Dx
Integrate data from previous assessment and functional behavioral analyses;
past treatments
Careful data monitoring can also be used as a diagnostic tool
What Can Behavioral Data Teach Us?
Differences in world view- learning models provide insights but may not explain
why this disorders affects this individual
Associative CS+US= UR/CR, instrumental (ABC), neurobiology of learning,
forgetting and recovering
Factors that initiate a behavior may not be the same as those maintaining it
DSM- predisposing, precipitating, perpetuating, and protective (resilience)
A means of tracking treatment response
What do we learn from our failures?
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
Analysis of Function
Function of behavior- arousal, reactivity, motivational state, approachavoidance, autonomic regulation
Drive or craving, reward potential, hedonic drive
Neuroticism- emotional reactivity
Behavioral inhibition, conflict
Escape behaviors-sensitivity, threat perception
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
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)
DM-ID-2
Adapting DSM-5 criteria to the special needs of clinicians treating IDD, loss of
multi-axial format is problematic, much more data available
Accommodation with the basic issues related to borderline/mild v.
severe/profound IDD- not taking into account qualitative differences, nor
consideration of a novel approach to diagnosis
Not specifically adapted for the special problems posed by ASD- will we need a
new set of criteria or assessment algorithms
Serves as a textbook that includes an update and integrate on developmental
neurosciences with bio-psycho-social factors
Includes a section on behavioral phenotypes, but most is devoted to
phenomenological subtypes
Diagnostic Instruments- domains and a Clinician’s View
of their Research Value
Phenomenological “phenotypes” within individual syndromes; separation of
Bipolar Disorder from Depressive Disorders; development of Disruptive Mood
Dysregulation Disorder from prepubertal BD; Disruptive and Impulse control
disorders- integration of temperamental, neurobiological and neuro-ethological
phenotypes
ASD- use the specifiers to integrate RDoC criteria; borrow the DC-LD 3 axis
model; work with DM-ID development in symptom adaptation
Five factor model of personality disorders- operationalize that temperamental
profile analysis for problem behaviors and Disruptive, Impulse-Control and
Conduct Disorders
Summary
How do we handle general to specific modes of diagnosis- endophenotyping?
Current systems are phenomenological phenotypes (lumping, heterogeneity);
“neurobiological” endophenotyping (, splitting, etiology-based)
Specificity of neuropharmacology; where do ecological models, diversity systems
of therapy fit in? Improvement vs remission, what can we learn from pain
management- nociception, subjective pain, misery
In IDD, a comparisons behavioral phenotypes and primary psychiatric disorders ,
temperament and personality; genes as risk factors, influence the impact of
setting events; neuroplasticity, extinction and resilience.
What can individuals with severe/profound ID or severe ASD teach us about
diagnosis?
Conclusions
Diagnosis is a process; diagnoses are hypotheses that remain reductionist’s ; concept will change
over time
How do we monitor progress- ACA and a new synthesis
DSM-5 and DM-ID-2 are based more on a description of syndrome, phenomenological
endophenotypes,
Heterogeneity remains across many domains; Behavioral phenotypes are a step in the right
direction
Are all major psychiatric disorders neurodevelopmental