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ACquired Personality Disorders

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ACquired Personality Disorders

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  1. Oklahoma Academy of Physicians Assistants, October 2013 ACquired Personality Disorders Jeff Seaman, MD, MS, FAPM ABPN: Psychiatry (2000, 2010); Psychosomatic Medicine (2005) UCNS: Behavioral Neurology and Neuropsychiatry (2012)

  2. Acquired Personality Disorders • Relevant neuropsychiatry fundamentals • Common problem domains • Personality changes with diseases or injuries • “Family of Origin” Personality Disorders (DSM-4/5) • Not today, but available on website

  3. Relevant neuropsychiatry fundamentals Two Founding Fathers #1 L.S. Vygotsky (1896-1934) mentor to A.R. Luria “The task, then, is not to localize functions to limited areas but to ascertain which groups of concertedly working zones of the brain are responsible for the performance of complex mental activity; what contribution is made by each of these zones to the complex functional system, and how the relationship between these areas changes with development.”

  4. Relevant neuropsychiatry fundamentals • 2) A. R. Luria (1902-1977) • Psychologist and physician • Student of Vygotsky • Invented 1st lie-detector • Widespread studies of diverse patient populations • Father / creator of Neuropsychiatry after WW2

  5. Relevant neuropsychiatry fundamentals: Connectionism • . • Function = brain-driven cognition, activity, perception, or behavior • It is a simplified (often wrong) assumption that a disturbance in function localizes that missing function to the part of the brain destroyed. • A lesion in one area maymodify more than abolish function. • The functional system can also be disturbed differently by lesions in different locations. • Each area introduces its own particular factor essential to the performance of a function.

  6. Relevant neuropsychiatry fundamentals: Connectionism Structural foundations of cognitive & behavior domains take the form of partially overlapping large-scale networks organized around reciprocally interconnected cortical epicenters. Components of these networks can be divided into critical versus participating areas. Right-dominant spatial attn network Left-dominant language network Memory-emotion network Executive function-comportment network Face and object recognition network • .

  7. Relevant neuropsychiatry fundamentals: Connectionism • Right-dominant spatial attn network • Epicenters: dorsal posterior parietal cortex, frontal eye fields, cingulategyrus • Left-dominant language network • Epicenters: Wernickes and Broca’s • Memory-emotion network • Epicenters: Hippocampus-entorhinal regions and amygdala • Executive function-comportment network • Epicenters: dorsolateral prefrontal cortex (DLPFC), orbitofrontal PFC (OFPFC), posterior parietal cortex • Face and object recognition network • Epicenters: lateral temporal & temporopolar cortices • .

  8. Prefrontal Anatomy • Diverse inputs • Other Heteromodal Association Cortex • Temporal • Parietal • Limbic System (includes basal forebrain) • Hypothalamus • Brainstem Monoamine Nuclei

  9. Prefrontal Anatomy • Diverse Outputs • Motor System - Behavior • Reciprocal Connections - Amplify Information • Other Heteromodal Association Cortex • Temporal • Parietal • Limbic System • Hypothalamus • Brainstem Monoamine Nuclei

  10. Memory-emotion network epicenters: Hippocampus-entorhinal regions and amygdala

  11. Memory-emotion network epicenters: Hippocampus-entorhinal regions and amygdala

  12. Memory-emotion network: Pathways and Stations Grey Matter Nodes for processing emotions and memory Ventral Striatum The ventral striatum consists of NA and olfactory tubercle. Site for integration of signals with: • Emotional content (amygdala) • Contextual info (hippocampus) • Motivational significance (DA inputs) • info about state of arousal (midline thalamus); • Executive/cognitive info (prefrontal cortex – PFC).

  13. Memory-emotion network: Pathways and Stations Grey Matter Nodes for processing emotion and memory VentralPallidum Ventral Pallidumreceives DA inputs from the ventral tegmental area (VTA) & GABAergic inputs from the Nucleus Accumbens (NA) A relay nucleus from the NA to medial dorsal nucleus of the thalamus

  14. Memory-emotion network: Pathways and Stations Grey Matter Nodes for processing emotions and memory Ventral Striatum Outputs directly or via relays, to: • Lateral hypothalamus (feeding & drinking) • VTA and nigral DA neurons (motivational behavior) • Caudal mesencephalon (locomotor behavior) • To PFC via medial thalamic nuclei (more complex cognitive and executive functions)

  15. Memory-emotion network: Summary Cortical: • Hippocampus-entorhinal regions • (Amygdala) Subcortical: • Ventral Striatum (Nucleus Accumbens and olfactory tubercle) • Lateral hypothalamus • VTA and nigral DA neurons • Caudal mesencephalon(SN,Periaqueductal gray, Locus coeruleus +) • tracts to PFC via medial thalamic nuclei

  16. Relevant neuropsychiatry fundamentals: • Executive function-comportment network epicenters: • Dorsolateral prefrontal cortex (DLPFC) • Orbitofrontal prefrontal cortex (OFPFC) • (Posterior parietal cortex) • .

  17. Executive function-comportment network • Inputs from PFC, BG and Limbic system • Output to PFC & Association Cortex Crucial role in: • Attention • Planning & Organization • Abstract thinking • Multi-tasking • Active (working) memory • Complex judgment & problem solving • Capacity for medical compliance Grey Matter Node for processing:Dorsomedial Thalamus

  18. Dorsolateral PFC Dysexecutive Syndromes have diverse etiology as lesions occur at varied locations across the PFC-BG-midbrain circuit

  19. ExecutiveDysexecutive • Integration of multimodal sensory input • Generation of multiple response alternatives • Maintenance of set and goal-directedness • Modification of behavior as conditions change • Self-evaluation • Top-down influence on working memory of all domains • Inability to integrate disparate sensory elements into a coherent whole • A stereotyped or limited repertoire • Easy loss of task set • Perseveration, stimulus-bound, inflexibility • Poor self monitoring of errors

  20. Dysexecutive • Failure to modify behavior to fit novel contexts • Reduced ability to internally program, select, and sequence responses • Failure to manipulate existing information rather than failure to perceive

  21. Orbitofrontal PFC • Limbic Input • TBI-vulnerable • Selection of appropriate behaviors • Adjustment of behavior in response to feedback • Tests: • Best: olfactory tests • 2nd Best: Iowa Gambling Task • +/- Stroop • +/- Go/No Go tasks

  22. Orbitofrontal PFC Syndrome Limbic Input to OFPFC: • Allows visceral / emotional valence to bias behavior choices and guide rapid decision making • Damage – become less responsive to the consequences of their actions, reduced learning, failure to learn from experience • Special note: frontal release signs rare, and only when lesion extends to motor-premotor frontal cortex

  23. Orbitofrontal PFC Syndrome • Lesions lead to: • Reduced insight • Impaired planning • Social impropriety • Reduced empathy • Poorly modulated emotional responses

  24. Orbitofrontal PFC Syndrome Phineas Gage: passage of an iron bar through the head • John M. Harlow M.D. • 3 June 1868

  25. Superior Medial PFC Syndrome Sequelae of lesions to cingulumand its connections • Apathy • APATHY IS NOT DEPRESSION ! • USUAL ANTIDEPRESSANTS WILL NOT WORK FOR APATHY SYNDROMES !

  26. APATHY: Levy & Dubois (2006) 3 Subtypes • Cognitive (DLPFC) • Emotional-affective (OFPFC) • Auto-activation (SMPFC) • Neurodegenerative diseases (esp PD, PSP, HD) • Direct lesions of PFC-basal ganglia circuit except… • Lesions to ventral striatum (NA) do not result in apathy syndrome – why? • Reduction of hedonic tone is associated with increased reward-dependence / compulsive pursuit of reward

  27. APATHY: Levy & Dubois (2006) Cognitive • “cognitive inertia” • Planning, organizing, sequencing, rule-finding, & set-shifting are needed to engage the environment • “Loss of self-activation of cognitive strategies may quantitatively impoverish behavior” • Dorsal Caudate – DLPFC segregation of fibers • Lesions of dorsal caudate  massive apathetic syndrome

  28. APATHY: Levy & Dubois (2006) Emotional-affective • Emotions are necessary to decode the context of behavior and provide its motivational value… • Disruption of this circuitry can reduce “the willingness to perform actions and maintain them to their completion” • “Decreased reactivity to emotion and sensitivity to reward” leads to an “inability to accurately evaluate the consequences of their choices on an emotional basis” • OFPFCventromedial caudate & ventral striatum (NA) ventromedialpallidum SN and amygdala and medial-dorsal thalamus  OFPFC

  29. Frontal Poles • Receives highly processed info from other PFC areas • Awareness of one’s internal states / self-knowing / mindfullness • Abstraction • Process future plans / real-world multi-tasking

  30. Diverse Illness States associated with Acquired Personality Disorders • Neurocognitive Disorders (formerly known as Dementia) • Subcortical and Cortical Vascular Dementia • Frontotemporal Dementias (FTD): • Corticobasal degeneration • Progressive Supranuclear Palsy • Progressive SubcorticalGliosis • Frontotemporal lobar degeneration • Primary Progressive Aphasia • DAT (Alzheimers) • Parkinson’s Disease and Lewy Body Disease • Chronic ETOH (diffuse atrophy) OR marijuana use (VMPFC atrophy)

  31. Diverse Illness States associated with Acquired Personality Disorders • Neurocognitive Disorders (formerly known as Dementia) • With ALS • With Epilepsy • With Wilson’s Disease • With Huntington’s Disease • With Autoimmune Encephalopathy • With PANDAS and variants • Traumatic Brain Injury (TBI) • “mild” (mTBI) • Chronic Traumatic Encephalopathy (CTE)

  32. Subcortical Vascular Demenia • Subcortical dementia 1st described in 1976: Folstein and McHugh with Huntington’s Dz • Next advanced – Krishnan: degeneration of Striatal-Cortical DA effectively denervates PFC • Most commonly misDx as DAT

  33. Subcortical VAD • Who? • DM / HTN / CAD / lipids / “vasculopaths” • How? • Lentiform a. occlusions • Insidiuous, NOT Multi-CVA process • Variable progression • Often combined with lacunar CVA, cortical CVA, • Can still have DAT / LBD • Nasty misnomer: “psudeodementia”

  34. Chronic lesions of vascular dementia are best visualized on T2 and FLAIR MRI sequences as hyperintense lesions the periventricular white matter consistent with ischemic cerebral injury.

  35. FIGURE 25–14. Frequency of neuropsychiatric symptoms in vascular dementia. Neuropsychiatric symptoms are common in vascular dementia (Figure 25–14). Relative to Alzheimer’s disease and mild cognitive impairment, vascular dementia has the highest incidence of new-onset depression, and the mood changes are more refractory to therapy. AMB=aberrant motor behavior. Source. Adapted from Lyketsos et al. 2000.

  36. Diverse Illness States associated with Acquired Personality Disorders Parkinson’s Disease and Lewy Body Disease

  37. Diverse Illness States associated with Acquired Personality Disorders • Frontotemporal Dementias (FTD) • Progressive decline of frontal – temporal function • Before or after abnormal motor signs • Postural • Rigidity • Amyotropy • these diseases share deposits of abnormal proteins in neuroectodermic cells, and severe cell loss with atrophy of vulnerable cortical and subcortical structures. In most patients, brain atrophy is asymmetric. • Bugiani 2007 NeurolSci

  38. Diverse Illness States associated with Acquired Personality Disorders • FTD is quite a complex disease entity with high clinical and neuropathologicvariability, extended genetic contribution, involvement of multiple proteins and neurodegenerationmost likely due to changes in cytoskeletal structure and in ubidependent protein degradation activity. • To date, seven loci (chromosomes 3p, 9q, and 17q24, one locus each; 9p and 17q21, two loci each), four genes (MAPT, PGRN, VCP, CHMP2B) and several proteins (tau, PGRN, VCP, CHMP2B, TDP43, ubiquitin, ubi-associated proteins and the intermediate neurofilamentsystem) have been related to FTD,

  39. Diverse Illness States associated with Acquired Personality Disorders • Primary Progressive Aphasia • greater atrophy of right lateral orbitofrontal cortex (OFC) in PPA patients with anxiety, apathy, irritability/lability and abnormal appetite/eating disorders • greater atrophy of left OFC in those with disinhibition. • Areas involved beyond OFC included right dorsolateral prefrontal cortex (apathy), right cingulate (irritability/lability) and left anterior superior and medial temporal lobe (disinhibition). Rohrer & Warren 2010 J NeurolSci

  40. Diverse Illness States associated with Acquired Personality Disorders DAT (Alzheimers)

  41. Diverse Illness States associated with Acquired Personality Disorders Traumatic Brain Injury Two NCNB measures (motivation and emotional regulation) were found to significantly predict outcome at 1-year follow-up, accounting for 53% of the variance in MPAI total scores. NCNB variables (motivation, disinhibition, social perception, irritability and emotional regulation) MPAI = Mayo-Portland Adaptability Inventory Brain Injury, October 2011; 25(11): 1035–1046

  42. Personality Change Post-TBI the model of best fit included the BMQ-R (motivation) and the BREQ-R (regulation of emotion) and accounted for 53% of the variance in outcome (MPAI score) at 1-year follow-up PTA was not found to make a significant contribution to the multiple regression model and was therefore excluded.

  43. Personality Change Post-TBI

  44. Personality Change with Epilepsy

  45. Personality Change with Autoimmune Encephalitis

  46. Personality Change with Rare Neurologic Illness • ALS • Wilsons • Huntington’s

  47. Acquired Personality Disorder Summary You are not likely going to cure them. Medications will not cure them. Top-tier integrated rehabilitative therapy with occupational therapy, PMR, and neuropsychiatry might be the most effective long-term approach, but no such center exists nor would it be paid for by CMS / commercial payors. Brief psychotherapies can helptemporarilycontain and limit the disruptive impact.

  48. Family of Origin Personality Disorder Please see the OAPA website for this slideshow